WikiMD


W8MD Diet | COVID-19 portal | Vitamin D | Vaccine | Keto

WikiMD is the world's largest medical encyclopedia with
28,888 pages, 4,107,223 edits & 35,652,376 views.

Free unbiased diet, health and wellness info!

Antineoplastic agents c

From WikiMD's free health, diet & wellness encyclopedia
Jump to navigation Jump to search
  • C/ebp beta antagonist st101 - A peptide antagonist of the transcription factor CCAAT/enhancer-binding protein beta (C/EBP beta), with potential antineoplastic activity. Upon administration, C/EBP beta antagonist ST101 targets and inhibits the activity of C/EBP beta. This prevents the expression of C/EBP beta target genes and proteins, including the anti-apoptotic protein B-cell lymphoma 2 (Bcl-2), cyclins and inhibitor of differentiation (ID) family of proteins, which are involved in cell proliferation, differentiation, and cell cycle regulation. This may lead to apoptosis in tumor cells. C/EBP beta is overexpressed in many cancers and plays an important role in the regulation of cell differentiation; its expression is associated with tumor cell survival and proliferation.
  • Cabazitaxel - A semi-synthetic derivative of the natural taxoid 10-deacetylbaccatin III with potential antineoplastic activity. Cabazitaxel binds to and stabilizes tubulin, resulting in the inhibition of microtubule depolymerization and cell division, cell cycle arrest in the G2/M phase, and the inhibition of tumor cell proliferation. Unlike other taxane compounds, this agent is a poor substrate for the membrane-associated, multidrug resistance (MDR), P-glycoprotein (P-gp) efflux pump and may be useful for treating multidrug-resistant tumors. In addition, cabazitaxel penetrates the blood-brain barrier (BBB).
  • Cabiralizumab - A humanized monoclonal antibody directed against the tyrosine kinase receptor colony stimulating factor 1 receptor (CSF1R; CSF-1R), also known as macrophage colony-stimulating factor receptor (M-CSFR) and CD115 (cluster of differentiation 115), with potential antineoplastic activity. Upon administration, anti-CSF1R monoclonal antibody FPA008 binds to CSF1R expressed on monocytes, macrophages, and osteoclasts and inhibits the binding of the CSF1R ligands colony-stimulating factor-1 (CSF-1) and interleukin-34 (IL-34), to CSF1R. This prevents CSF1R activation and CSF1R-mediated signaling in these cells. This blocks the production of inflammatory mediators by macrophages and monocytes and reduces inflammation. By blocking the recruitment to the tumor microenvironment and activity of CSF1R-dependent tumor-associated macrophages (TAMs), FPA008 enhances T-cell infiltration and antitumor T-cell immune responses, which inhibits the proliferation of tumor cells. Additionally, FPA008 prevents the activation of osteoclasts and blocks bone destruction. TAMs play key roles in immune suppression and promoting inflammation, tumor cell proliferation and survival.
  • Cabozantinib - An orally bioavailable, small molecule receptor tyrosine kinase (RTK) inhibitor with potential antineoplastic activity. Cabozantinib strongly binds to and inhibits several RTKs, which are often overexpressed in a variety of cancer cell types, including hepatocyte growth factor receptor (MET), RET (rearranged during transfection), vascular endothelial growth factor receptor types 1 (VEGFR-1), 2 (VEGFR-2), and 3 (VEGFR-3), mast/stem cell growth factor (KIT), FMS-like tyrosine kinase 3 (FLT-3), TIE-2 (TEK tyrosine kinase, endothelial), tropomyosin-related kinase B (TRKB) and AXL. This may result in an inhibition of both tumor growth and angiogenesis, and eventually lead to tumor regression.
  • Cabozantinib s-malate - The s-malate salt form of cabozantinib, an orally bioavailable, small molecule receptor tyrosine kinase (RTK) inhibitor with potential antineoplastic activity. Cabozantinib strongly binds to and inhibits several RTKs, which are often overexpressed in a variety of cancer cell types, including hepatocyte growth factor receptor (MET), RET (rearranged during transfection), vascular endothelial growth factor receptor types 1 (VEGFR-1), 2 (VEGFR-2), and 3 (VEGFR-3), mast/stem cell growth factor (KIT), FMS-like tyrosine kinase 3 (FLT-3), TIE-2 (TEK tyrosine kinase, endothelial), tropomyosin-related kinase B (TRKB) and AXL. This may result in an inhibition of both tumor growth and angiogenesis, and eventually lead to tumor regression.
  • Cab-ror2-adc ba3021 - An antibody-drug conjugate (ADC) composed of a conditionally active biologic (CAB) antibody against receptor tyrosine kinase-like orphan receptor 2 (ROR2) conjugated to an as of yet undisclosed cytotoxic agent, with potential antineoplastic activity. Upon administration of CAB-ROR2-ADC BA3021, the anti-ROR2 antibody becomes activated through an as of yet not fully elucidated process, only under the unique microphysical conditions that are present in the tumor microenvironment (TME) as a result of the glycolytic metabolism of cancer cells and not in the microenvironment of normal, healthy tissues. Upon binding to ROR2-expressing cancer cells and internalization, the cytotoxic agent kills the cancer cells through an as of yet undisclosed mechanism of action (MoA). ROR2, highly expressed during embryonic development while only minimally expressed on certain normal, healthy cells, is involved in Wnt signal transduction and is overexpressed on certain cancer cells. It plays a key role in cancer cell proliferation, migration and invasion. High levels of ROR2 expression often correlates with poor prognosis. The CAB antibody allows for efficient binding to ROR2-expressing cancer cells only, thereby maximizing efficacy while minimizing toxicity by avoiding activation and thus binding of the antibody to normal, healthy ROR2-expressing cells under normal conditions.
  • Cactinomycin - A chromopeptide antineoplastic antibiotic isolated from the bacterium Streptomyces chrysomallus. Cactinomycin binds to DNA by intercalating between guanine and cytosine, forming stable antibiotic-DNA complexes that inhibit RNA and protein synthesis.
  • Caffeic acid phenethyl ester - The phenethyl alcohol ester of caffeic acid and a bioactive component of honeybee hive propolis, with antineoplastic, cytoprotective and immunomodulating activities. Upon administration, caffeic acid phenethyl ester (CAPE) inhibits the activation of nuclear transcription factor NF-kappa B and may suppress p70S6K and Akt-driven signaling pathways. In addition, CAPE inhibits PDGF-induced proliferation of vascular smooth muscle cells through the activation of p38 mitogen-activated protein kinase (MAPK) and hypoxia-inducible factor (HIF)-1alpha and subsequent induction of heme oxygenase-1 (HO-1).
  • Caix inhibitor dtp348 - An orally bioavailable, nitroimidazole-based sulfamide, carbonic anhydrase IX (CAIX) inhibitor with potential antineoplastic activity. Upon administration, CAIX inhibitor DTP348 inhibits tumor-associated CAIX, a hypoxia-inducible transmembrane glycoprotein that catalyzes the reversible reaction and rapid interconversion of carbon dioxide and water to carbonic acid, protons, and bicarbonate ions. This prevents the acidification of the tumor's extracellular microenvironment and decreases the intracellular pH. This results in increased cell death in CAIX-expressing, hypoxic tumors. In addition, DTP348, through its nitroimidazole moiety, is able to sensitize hypoxic tumor cells to irradiation. CAIX is overexpressed in various tumors and plays a key role in intra- and extracellular pH regulation, cancer cell progression, survival, migration and invasion.
  • Caix inhibitor slc-0111 - A sulfonamide carbonic anhydrase inhibitor with potential antineoplastic activity. Upon administration, CAIX inhibitor SLC-0111 inhibits tumor-associated carbonic anhydrase IX (CAIX), an hypoxia-inducible transmembrane glycoprotein that catalyzes the reversible reaction and rapid interconversion of carbon dioxide and water to carbonic acid, protons, and bicarbonate ions. This prevents both the acidification of the tumor's extracellular microenvironment and cytoplasmic alkalization. This increases cell death in CAIX-expressing, hypoxic tumors. CAIX is overexpressed in various tumors and plays a key role in intra- and extracellular pH regulation, cancer cell progression, survival, migration and invasion; it is also involved in resistance to both chemo- and radiotherapy.
  • Calaspargase pegol-mknl - An intravenous formulation containing E.coli-derived L-asparaginase II conjugated with succinimidyl carbonate monomethoxypolyethylene glycol (SC-PEG), with potential antineoplastic activity. Upon administration of calaspargase pegol-mknl L-asparaginase hydrolyzes L-asparagine to L-aspartic acid and ammonia, thereby depleting cells of asparagine; asparagine depletion blocks protein synthesis and tumor cell proliferation, especially in the G1 phase of the cell cycle and ultimately induces tumor cell death. Asparagine is critical to protein synthesis in acute lymphoblastic leukemia (ALL) cells which, unlike normal cells, cannot synthesize this amino acid due to the absence of the enzyme asparagine synthase. Pegylation decreases enzyme antigenicity and increases its half life. SC is used as a PEG linker to facilitate attachment to asparaginase and enhances the stability of the formulation.
  • Calcitriol - A synthetic physiologically-active analog of vitamin D, specifically the vitamin D3 form. Calcitriol regulates calcium in vivo by promoting absorption in the intestine, reabsorption in the kidneys, and, along with parathyroid hormone, regulation of bone growth. A calcitriol receptor-binding protein appears to exist in the mucosa of human intestine. Calcitriol also induces cell cycle arrest at G0/G1 phase of the cell cycle, cell differentiation, and apoptosis, resulting in inhibition of proliferation of some tumor cell types. This agent may be chemopreventive for colon and prostate cancers.
  • Calcium release-activated channel inhibitor cm4620 - A calcium (Ca2+) release-activated channel (CRAC) inhibitor, with potential anti-inflammatory and protective activities. Upon administration, CM4620 targets, binds to and inhibits the calcium release-activated calcium channel protein 1 (Orai1), which forms the pore of CRAC, and is expressed on both parenchymal cells and immune cells. This prevents the transport of extracellular Ca2+ into the cell and inhibits the subsequent activation of Ca2+-mediated signaling and transcription of target genes. This may prevent Ca2+ entry-mediated cell death. It may also inhibit the proliferation of immune cells and prevents the release of various inflammatory cytokines in immune cells, such as interleukin-2 (IL-2) and tumor necrosis factor-alpha (TNF-a). This may lead to a reduction of inflammatory responses in inflammatory-mediated diseases. CRACs, specialized plasma membrane Ca2+ ion channels composed of the plasma membrane based Orai channels and the endoplasmic reticulum (ER) stromal interaction molecules (STIMs), mediate store operated Ca2+ entry (SOCE) and play a key role in calcium homeostasis. CRACs are overactivated in a variety of cell types, especially certain immune cells during inflammation, including T-lymphocytes, neutrophils and macrophages.
  • Calcium release-activated channels inhibitor rp4010 - A calcium (Ca2+) release-activated channel (CRAC) inhibitor, with potential antineoplastic activity. Upon administration, RP4010 binds to and inhibits CRACs, thereby preventing the transport of extracellular Ca2+ into the cell and inhibiting the subsequent activation of Ca2+-mediated signaling and transcription of target genes. CRACs, specialized plasma membrane Ca2+ ion channels composed of the plasma membrane based Orai channels and the endoplasmic reticulum (ER) stromal interaction molecules (STIMs), play key roles in calcium homeostasis and are over-activated in a number of cancer cell types. Aberrant activation of CRACs leads to increased cancer cell proliferation.
  • Calcium saccharate - The calcium salt form of glucaric acid, a natural substance found in many fruits and vegetables, with potential anti-cancer property. One of the key processes in which the human body eliminates toxic chemicals as well as hormones (such as estrogen) is by attaching glucuronic acid to them in the liver and then excreting the complex in the bile. When beta-glucuronidase breaks the bond, it prolongs the stay of the hormone or toxic chemical in the body. Elevated beta-glucuronidase activity has been implicated to be associated with an increased risk for hormone-dependent cancers like breast, prostate, and colon cancers. Therefore, supplementing calcium glucarate may suppress the developments of hormone-dependent cancers.
  • Calculus bovis/moschus/olibanum/myrrha capsule - An orally available traditional Chinese medicine (TCM)-based capsule formulation containing Calculus bovis, the dried gallstones of cattle, Moschus, also referred to as deer musk, the resin Olibanum and the resin Myrrha, with potential antineoplastic and chemopreventive activities. Although the exact mechanisms of action through which the active ingredients in the Calculus bovis/Moschus/Olibanum/Myrrha capsule elicit their effects have yet to be fully elucidated, they may, upon intake, exert their antineoplastic activity through modulation of the immune system, inhibition of tumor cell proliferation and induction of apoptosis.
  • Calicheamicin gamma 1i - An oligosaccharide enediyne antitumor antibiotic isolated from Micromonospora echinospora ssp. Calichensis. Calicheamicin Gamma 1I binds to the minor groove of DNA, resulting in site-specific double-strand breaks and apoptosis.
  • Calr exon 9 mutant peptide vaccine/montanide isa-51 - A peptide vaccine consisting of a calreticulin (CALR) mutant peptide, CALRLong36, and montanide ISA 51 with potential antineoplastic activity. Upon vaccination, the CALR exon 9 mutant peptide vaccine may stimulate the host immune system to mount a cytotoxic T-lymphocyte (CTL)-mediated response against tumor cells harboring mutations in exon 9 of the calreticulin gene. CALR, an endoplasmic reticulum chaperone protein that normally facilitates protein folding, immune response, and hematopoiesis, is often mutated in patients with chronic myeloproliferative neoplasms. In its mutant form, CALR is secreted into the plasma, where it binds to and activates the thrombopoietin receptor MPL and initiates downstream JAK/STAT signaling. Montanide ISA-51, also known as incomplete Freund's adjuvant or IFA, is a stabilized water-in-oil (w/o) emulsion adjuvant containing mineral oil with mannide oleate added as a surfactant that non-specifically stimulates cell-mediated immune responses to antigens.
  • Camidanlumab tesirine - An immunoconjugate consisting of a human immunoglobulin (Ig) G1 monoclonal antibody directed against the alpha subunit of the interleukin-2 receptor (IL-2R alpha or CD25) and conjugated, via a cleavable linker, to a synthetic, cross-linking agent pyrrolobenzodiazepine (PBD) dimer that targets DNA minor grooves, with potential antineoplastic activity. The monoclonal antibody portion of the anti-CD25 antibody-drug conjugate (ADC) ADCT-301 specifically binds to the cell surface antigen CD25. This causes the internalization of ADCT-301 and the subsequent release of the cytotoxic PBD moiety. The imine groups of the PBD moiety bind to the N2 positions of guanines on opposite strands of DNA. This induces interstrand cross-links in the minor groove of DNA and inhibits DNA replication, which inhibits the proliferation of CD25-overexpressing tumor cells. CD25, a transmembrane receptor and tumor-associated antigen (TAA), is expressed on certain cancer cells.
  • Camptothecin - An alkaloid isolated from the Chinese tree Camptotheca acuminata, with antineoplastic activity. During the S phase of the cell cycle, camptothecin selectively stabilizes topoisomerase I-DNA covalent complexes, thereby inhibiting religation of topoisomerase I-mediated single-strand DNA breaks and producing potentially lethal double-strand DNA breaks when encountered by the DNA replication machinery. (NCI)
  • Camptothecin analogue tlc388 - A synthetic analogue of camptothecin with potential antineoplastic and radio-sensitizing activities. Camptothecin analogue TLC388 selectively stabilizes topoisomerase I-DNA covalent complexes during S-phase, thereby inhibiting religation of topoisomerase I-mediated single-strand DNA breaks and producing potentially lethal double-strand DNA breaks when encountered by the DNA replication machinery. Topoisomerase I relaxes negative super-coiled DNA during replication and transcription. This agent has been chemically modified to enhance the potency and stability of camptothecin.
  • Camptothecin glycoconjugate bay 38-3441 - A water-soluble camptothecin derivative conjugated to a carbohydrate moiety exhibiting antineoplastic activity. BAY 56-3722 stabilizes the topoisomerase I-DNA covalent complex and forms an enzyme-drug-DNA ternary complex. As a consequence of the formation of this complex, both the initial cleavage reaction and religation steps are inhibited and subsequent collision of the replication fork with the cleaved strand of DNA results in inhibition of DNA replication, double strand DNA breakage and triggering of apoptosis. The peptide carbohydrate moiety of this agent stabilizes the lactone form of camptothecin in blood.
  • Camptothecin sodium - The sodium salt of camptothecin, an alkaloid isolated from the Chinese tree Camptotheca acuminata, with antineoplastic activity. During the S phase of the cell cycle, camptothecin selectively stabilizes topoisomerase I-DNA covalent complexes, thereby inhibiting religation of topoisomerase I-mediated single-strand DNA breaks and producing potentially lethal double-strand DNA breaks when encountered by the DNA replication machinery. The sodium salt of camptothecin is more water-soluble than the parent molecule.
  • Camptothecin-20(s)-o-propionate hydrate - The hydrated, crystalline propionate ester (attached in position C-20) prodrug of camptothecin, an alkaloid isolated from the Chinese tree Camptotheca acuminata, with potential antineoplastic activity. Upon entry into cells, camptothecin-20(S)-O-propionate is hydrolyzed by esterases into the active form camptothecin. Camptothecin selectively stabilizes topoisomerase I-DNA covalent complexes, thereby inhibiting religation of topoisomerase I-mediated single-strand DNA breaks and producing potentially lethal double-strand DNA breaks when encountered by the DNA replication machinery, thus inhibiting DNA replication and triggering apoptotic cell death. Camptothecin readily undergoes hydrolysis at physiological pH, changing its conformation from the active, S-configured lactone structure to an inactive carboxylate form. The ester chain in the vicinity of the S-configured lactone moiety, a key determinant for the chemotherapeutic efficacy of the camptothecins, inhibits protein binding, rendering this agent resistant to hydrolysis and prolonging its half-life.
  • Camrelizumab - A monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed death-1 (PD-1, PCD-1,) with immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1 monoclonal antibody SHR-1210 binds to and blocks the binding of PD-1, expressed on activated T-lymphocytes, B-cells and natural killer (NK) cells, to its ligands programmed cell death ligand 1 (PD-L1), overexpressed on certain cancer cells, and programmed cell death ligand 2 (PD-L2), which is primarily expressed on antigen presenting cells (APCs). This prevents the activation of PD-1 and its downstream signaling pathways. This restores immune function through the activation of cytotoxic T-lymphocytes (CTLs) and cell-mediated immune responses against tumor cells or pathogens. Activated PD-1 negatively regulates T-cell activation and plays a key role in tumor evasion from host immunity.
  • Camsirubicin - A synthetic non-cardiotoxic analogue of the anthracycline antibiotic doxorubicin with potential antineoplastic activity. Camsirubicin intercalates DNA and impedes the activity of topoisomerase II, inducing single and double-stranded breaks in DNA; inhibiting DNA replication and/or repair, transcription, and protein synthesis; and activating tumor cell apoptosis.
  • Canarypox-hil-12 melanoma vaccine - A vaccine consisting of a replication-defective recombinant canarypox virus (ALVAC) that encodes the gene for human interleukin-12 (hIL-12). Produced mainly by B-cells, IL-12 is an endogenous cytokine that activates natural killer (NK) cells, promotes cytotoxic T lymphocyte (CTL) responses, induces the release of interferon-gamma (IFN-gamma), and may exhibit antitumor and anti-angiogenic effects. Vaccination with canarypox-hIL-12 melanoma vaccine may stimulate the host immune system to mount an immune response against tumor cells, thereby inhibiting tumor growth and/or metastasis.
  • Cancell - Cancell (Entelev or Cantron), is a liquid that has been produced in various forms, principally by two manufacturers, since the late 1930s. The exact composition of Cancell/Entelev is unknown, but the U.S. Food and Drug Administration (FDA) has listed the components as inositol, nitric acid, sodium sulfite, potassium hydroxide, sulfuric acid, and catechol. NCI studies determined that the mixture lacked substantial antitumor activity. (from CancerNet)
  • Cancer peptide vaccine s-588410 - A cancer peptide vaccine containing five human leukocyte antigen (HLA)-A*2402-restricted epitope peptides derived from as of yet not disclosed oncoantigens, with potential immunostimulating and antineoplastic activities. Upon administration of the cancer peptide vaccine S-588410, the peptides may stimulate a cytotoxic T-lymphocyte (CTL) response against cancer cells expressing the antigens. This decreases proliferation of susceptible tumor cells.
  • Canerpaturev - A non-engineered, naturally oncolytic, replication-competent spontaneous herpes simplex virus (HSV) type I mutant variant. Upon intratumoral injection, canerpaturev transfects, replicates in, and lyses rapidly dividing cells such as tumor cells. In addition, this agent may increase host immune responses that may kill non-infected tumor cells.
  • Canertinib dihydrochloride - The hydrochloride salt of an orally bio-available quinazoline with potential antineoplastic and radiosensitizing activities. Canertinib binds to the intracellular domains of epidermal growth factor receptor tyrosine kinases (ErbB family), irreversibly inhibiting their signal transduction functions and resulting in tumor cell apoptosis and suppression of tumor cell proliferation. This agent also acts as a radiosensitizing agent and displays synergistic activity with other chemotherapeutic agents.
  • Canfosfamide - A modified glutathione analogue and nitrogen mustard prodrug, with potential antineoplastic activity. Canfosfamide is selectively activated by glutathione S-transferase P1-1 into an alkylating metabolite that forms covalent linkages with nucleophilic centers in tumor cell DNA, which may induce a cellular stress response and cytotoxicity, and decrease tumor cell proliferation. Glutathione S-transferase P1-1 is an enzyme that is overexpressed in many human malignancies.
  • Canfosfamide hydrochloride - The hydrochloride salt of a modified glutathione analogue with potential antineoplastic activity. Canfosfamide is selectively activated by glutathione S-transferase P1-1 into an alkylating metabolite that forms covalent linkages with nucleophilic centers in tumor cell DNA, which may induce a cellular stress response and cytotoxicity, and decrease tumor proliferation. S-transferase P1-1 is an enzyme that is overexpressed in many human malignancies.
  • Cannabidiol - A phytocannabinoid derived from Cannabis species, which is devoid of psychoactive activity, with analgesic, anti-inflammatory, antineoplastic and chemopreventive activities. Upon administration, cannabidiol (CBD) exerts its anti-proliferative, anti-angiogenic and pro-apoptotic activity through various mechanisms, which likely do not involve signaling by cannabinoid receptor 1 (CB1), CB2, or vanilloid receptor 1. CBD stimulates endoplasmic reticulum (ER) stress and inhibits AKT/mTOR signaling, thereby activating autophagy and promoting apoptosis. In addition, CBD enhances the generation of reactive oxygen species (ROS), which further enhances apoptosis. This agent also upregulates the expression of intercellular adhesion molecule 1 (ICAM-1) and tissue inhibitor of matrix metalloproteinases-1 (TIMP1) and decreases the expression of inhibitor of DNA binding 1 (ID-1). This inhibits cancer cell invasiveness and metastasis. CBD may also activate the transient receptor potential vanilloid type 2 (TRPV2), which may increase the uptake of various cytotoxic agents in cancer cells. The analgesic effect of CBD is mediated through the binding of this agent to and activation of CB1.
  • Cantrixil - A cyclodextrin-encapsulated, third generation super-benzopyran (SBP) compound with potential antineoplastic activity. Upon intraperitoneal (IP) administration, cantrixil enhances the activation and expression of c-Jun, downregulates phosphorylated extracellular signal-regulated kinase (p-ERK) and induces activation of caspase-3, -7 and -9, thereby inducing tumor cell apoptosis. c-Jun, an activator protein-1 (AP-1) transcription factor component, is involved in a wide range of cellular processes including cell cycle progression, differentiation, cell transformation and apoptosis.
  • Cantuzumab ravtansine - An immunotoxin of a humanized monoclonal antibody C242 (MoAb HuC242) conjugated to a derivative of the cytotoxic agent maytansine, DM4, with potential antitumor activity. Cantuzumab ravtansine is generated from MoAb C242, which is raised against a cell surface superantigen, CA242, found in a variety of human tumor cells. Upon binding and entry, the immunoconjugate releases the maytansinoid agent DM4, which binds to tubulin, thereby affecting microtubule assembly/disassembly dynamics. As a result, this agent prevents cell division and reduces cell growth of cancer cells that express CA242.
  • Capecitabine - A fluoropyrimidine carbamate belonging to the class of antineoplastic agents called antimetabolites. As a prodrug, capecitabine is selectively activated by tumor cells to its cytotoxic moiety, 5-fluorouracil (5-FU); subsequently, 5-FU is metabolized to two active metabolites, 5-fluoro-2-deoxyuridine monophosphate (FdUMP) and 5-fluorouridine triphosphate (FUTP) by both tumor cells and normal cells. FdUMP inhibits DNA synthesis and cell division by reducing normal thymidine production, while FUTP inhibits RNA and protein synthesis by competing with uridine triphosphate for incorporation into the RNA strand.
  • Capecitabine rapidly disintegrating tablet - A rapidly disintegrating film-coated tablet composed of the fluoropyrimidine carbamate antimetabolite capecitabine with antineoplastic activity. As a prodrug, capecitabine is converted to 5'-deoxy-5-fluorocytidine (5'-DFCR) by hepatic carboxylesterase and then to 5'-deoxy-5-fluorouridine (5'-DFUR) by cytidine deaminase and is eventually activated by thymidine phosphorylase to its cytotoxic moiety, 5-fluorouracil (5-FU); subsequently, 5-FU is metabolized to two active metabolites, 5-fluoro-2-deoxyuridine monophosphate (FdUMP) and 5-fluorouridine triphosphate (FUTP). FdUMP inhibits DNA synthesis and cell division by reducing normal thymidine triphosphate production, while FUTP inhibits RNA and protein synthesis by competing with uridine triphosphate for incorporation into the RNA strand. Capecitabine rapidly disintegrating tablet (RDT) contains the water insoluble, disintegrating agent crospovidone which very rapidly disperses and swells in water making this RDT easier to swallow than the traditional capecitabine tablet.
  • Capivasertib - A novel pyrrolopyrimidine derivative, and an orally available inhibitor of the serine/threonine protein kinase AKT (protein kinase B) with potential antineoplastic activity. Capivasertib binds to and inhibits all AKT isoforms. Inhibition of AKT prevents the phosphorylation of AKT substrates that mediate cellular processes, such as cell division, apoptosis, and glucose and fatty acid metabolism. A wide range of solid and hematological malignancies show dysregulated PI3K/AKT/mTOR signaling due to mutations in multiple signaling components. By targeting AKT, the key node in the PIK3/AKT signaling network, this agent may be used as monotherapy or combination therapy for a variety of human cancers.
  • Capmatinib - An orally bioavailable inhibitor of the proto-oncogene c-Met (also known as hepatocyte growth factor receptor (HGFR)) with potential antineoplastic activity. Capmatinib selectively binds to c-Met, thereby inhibiting c-Met phosphorylation and disrupting c-Met signal transduction pathways. This may induce cell death in tumor cells overexpressing c-Met protein or expressing constitutively activated c-Met protein. c-Met, a receptor tyrosine kinase overexpressed or mutated in many tumor cell types, plays key roles in tumor cell proliferation, survival, invasion, metastasis, and tumor angiogenesis.
  • Captopril - A sulfhydryl-containing analog of proline with antihypertensive activity and potential antineoplastic activity. Captopril competitively inhibits angiotensin converting enzyme (ACE), thereby decreasing levels of angiotensin II, increasing plasma renin activity, and decreasing aldosterone secretion. This agent may also inhibit tumor angiogenesis by inhibiting endothelial cell matrix metalloproteinases (MMPs) and endothelial cell migration. Captopril may also exhibit antineoplastic activity independent of effects on tumor angiogenesis.
  • Car t-cells amg 119 - A preparation of T-lymphocytes that are genetically engineered to express a chimeric antigen receptor (CAR) that targets an as of yet unidentified tumor-associated antigen (TAA), with potential immunomodulatory and antineoplastic activities. Upon administration of the CAR T-cells AMG 119, the T-cells target, bind to and induce selective cytotoxicity in tumor cells expressing the TAA.
  • Caracemide - An agent derived from acetohydroxamic acid with potential antineoplastic activity. Caracemide inhibits ribonuclease reductase, resulting in decreased DNA synthesis and tumor growth; it also inhibits acetylcholinesterase. In vivo, caracemide contributes to the formation of the neurotoxin methyl isocyanate; this effect, along with the agent's acetylcholinesterase activity, may be responsible for the severe central nervous system toxicity observed in clinical trials.
  • Carbendazim - A broad-spectrum benzimidazole antifungal with potential antimitotic and antineoplastic activities. Although the exact mechanism of action is unclear, carbendazim appears to binds to an unspecified site on tubulin and suppresses microtubule assembly dynamic. This results in cell cycle arrest at the G2/M phase and an induction of apoptosis.
  • Carbetimer - Carbetimer (carboxyimamidate) is a low molecular weight derivatized copolymer of ethylene and maleic anhydride. It has demonstrated antitumor activity against several animal models. It has calcium chelation activity but seems to inhibit growth of sensitive cells by disrupting nucleoside uptake and metabolism.
  • Carbogen - An inhalant consisting of hyperoxic gas (95%-98% oxygen and 2%-5% carbon dioxide) with radiosensitizing properties. Inhaled carbogen reduces diffusion-limited tumor hypoxia, increasing tumor radiosensitivity due to the increased availability of molecular oxygen for cytotoxic radiation-induced oxygen free radical production.
  • Carbon c 14 eribulin acetate - A radioconjugate containing the acetate salt of eribulin, labeled with the beta particle-emitting radioisotope carbon C 14, with radioisotopic and potential antineoplastic activities. Upon administration, eribulin binds to the vinca domain of tubulin and inhibits the polymerization of tubulin and the assembly of microtubules, resulting in inhibition of mitotic spindle assembly, induction of cell cycle arrest at G2/M phase, and, potentially, tumor regression. The radioisotope moiety of this agent acts as a radioactive tracer.
  • Carbon c 14 ombrabulin - A synthetic water-soluble analogue of combretastatin A4, derived from the South African willow bush (Combretum caffrum), labeled with carbon C 14 with potential antineoplastic activity. The ombrabulin moiety of carbon C 14 ombrabulin binds to the colchicine binding site of endothelial cell tubulin, thereby inhibiting tubulin polymerization and inducing mitotic arrest and apoptosis in endothelial cells. As apoptotic endothelial cells detach from their substrata, tumor blood vessels collapse; the acute disruption of tumor blood flow may result in tumor necrosis. The radioisotope moiety of this agent acts as a radioactive tracer.
  • Carbon c 14-pamiparib - An orally bioavailable radioconjugate composed of pamiparib, a nuclear enzyme poly(ADP-ribose) polymerase (PARP) inhibitor, radiolabeled with the radioisotope carbon C 14, with potential use for evaluating the pharmacokinetic profile of pamiparib. Pamiparib targets, binds to and inhibits PARP, which results in the inhibition of tumor cell proliferation and survival. Labeling of pamiparib with the radioactive tracer carbon C 14 allows for the evaluation of pamiparib's pharmacokinetic profile, including its absorption, distribution, metabolism and excretion (ADME).
  • Carbon c11 temozolomide - A radioconjugate composed of temozolomide, a imidazotetrazine analog of dacarbazine, labeled with the radioisotope carbon C11, with potential positron emission tomography (PET) imaging activity. As a cytotoxic alkylating agent, temozolomide is hydrolyzed at physiologic pH to the pharmacologically active compound, 5-(3-methyl-(triazen-1-yl)-imidazole)-4-carboxamide (MTIC). MTIC is further hydrolyzed to 5-aminoimidazole-4-carboxamide (AIC) and a methyldiazonium cation. The cation is able to methylate DNA, particularly at the O6 and N7 positions of guanine residues, resulting in cell cycle arrest, inhibition of DNA replication and the induction of apoptosis. Temozolomide is metabolized to MITC at all sites, crosses the blood-brain-barrier and penetrates well into the central nervous system. Upon PET, the biodistribution, uptake in cancer cells and the efficacy of temozolomide can be assessed.
  • Carbon c-14 dacomitinib - A radioconjugate consisting of an orally bioavailable small-molecule inhibitor of the epidermal growth factor receptor (erbB or HER) family of tyrosine kinases radiolabeled with carbon-14 with potential antineoplastic and beta-emitting radioisotope activity. PF-00299804 specifically and irreversibly binds to and inhibits human Her-1, Her-2, and Her-4, resulting in the proliferation inhibition and apoptosis of tumor cells that overexpress these receptors. The HER receptor family of tyrosine kinases, often overexpressed by a variety of tumor cell types, may contribute to tumor cell proliferation, differentiation, migration, and survival. PF-00299804 radiolabeled with carbon C-14 may be used as a radiotracer in pharmacological studies of PF-00299804 metabolism.
  • Carbon-11 acetate - The acetate salt of the radioisotope carbon-11. Although the mechanism is unclear, carbon-11 acetate preferentially accumulates in tumor tissue, serving as a tracer for imaging tumors with positron emission tomography (PET).
  • Carboplatin - A second-generation platinum compound with a broad spectrum of antineoplastic properties. Carboplatin contains a platinum atom complexed with two ammonia groups and a cyclobutane-dicarboxyl residue. This agent is activated intracellularly to form reactive platinum complexes that bind to nucleophilic groups such as GC-rich sites in DNA, thereby inducing intrastrand and interstrand DNA cross-links, as well as DNA-protein cross-links. These carboplatin-induced DNA and protein effects result in apoptosis and cell growth inhibition. This agent possesses tumoricidal activity similar to that of its parent compound, cisplatin, but is more stable and less toxic.
  • Carboquone - An aziridinylbenzoquinone-based alkylating agent with potential antineoplastic activity. The alkylating group in carboquone becomes activated upon reduction of quinone to the hydroquinone form. This eventually results in the alkylation and crosslinking of DNA, thereby inhibiting DNA replication followed by an induction of apoptosis. In addition, reactive oxygen species may form during redox cycling which may contribute to this agent's cytotoxic activity.
  • Carboxyamidotriazole - An orally-active agent with potential antineoplastic activity. Carboxyamidotriazole binds to and inhibits non-voltage-operated Ca2+ channels, blocking both Ca2+ influx into cells and Ca2+ release from intracellular stores and resulting in the disruption of calcium channel-mediated signal transduction and inhibition of vascular endothelial growth factor (VEGF) signaling, endothelial proliferation, and angiogenesis. This agent may also inhibit tumor cell growth, invasion and metastasis.
  • Carboxyamidotriazole orotate - The orotate salt form of carboxyamidotriazole (CAI), an orally bioavailable small molecule with potential antiangiogenic and antiproliferative activities. Carboxyamidotriazole binds to and inhibits non-voltage-operated calcium channels, blocking both Ca2+ influx into cells and Ca2+ release from intracellular stores, resulting in the disruption of calcium channel-mediated signal transduction. CAI inhibits PI3 activity and vascular endothelial growth factor (VEGF) signaling. This may inhibit endothelial proliferation, tumor cell growth, invasion and metastasis.
  • Carboxyphenyl retinamide - A synthetic phenylretinamide analogue of retinol (vitamin A) with potential antineoplastic and chemopreventive activities. Carboxyphenyl retinamide induces cell differentiation and inhibits tumor cell growth and carcinogenesis. This agent may also induce cell cycle arrest in the G1 phase in some cancer cell types.
  • Carcinoembryonic antigen peptide 1 - A nine amino acid peptide fragment of carcinoembryonic antigen (CEA), a protein that is overexpressed in several cancer cell types, including gastrointestinal, breast, and non-small cell lung. Autologous vaccination with activated autologous dendritic cells (DC) or peripheral blood mononuclear cells (PBMC) which have been exposed to CEA peptide 1 in vitro may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against tumor cells expressing CEA, thereby inhibiting tumor growth.
  • Carcinoembryonic antigen peptide 1-6d - A 9-residue human leukocyte antigen (HLA)-restricted fragment of carcinoembryonic antigen (CEA). Vaccination with carcinoembryonic antigen peptide 1-6D, which has the amino acid sequence YLSGANLNL, may elicit a cytotoxic T lymphocyte (CTL) immune response against tumors expressing CEA.
  • Carcinoembryonic antigen peptide 1-6d virus-like replicon particles vaccine - A cancer vaccine, consisting of alphavirus vector-derived virus-like replicon particles expressing the 9-amino-acid carcinoembryonic antigen peptide (CAP) 1-6D, with potential antineoplastic activity. Vaccination with this agent may elicit a cytotoxic T lymphocyte (CTL) immune response against CEA-expressing tumor cells.
  • Carcinoembryonic antigen-expressing measles virus - An attenuated oncolytic Edmonston (Ed) strain of measles virus (MV) encoding the soluble extracellular N-terminal domain of human carcinoembryonic antigen (CEA) (MV-CEA) with potential antineoplastic activity. The cellular receptor of MV is human CD46 antigen, a type 1 integral membrane glycoprotein found on nearly all human tissues and overexpressed on many cancer cell types. Mediated through CD46, both haemagglutinin and fusion glycoproteins of MV are required for the attachment to and fusion of host cell membranes, thereby leading to syncytia and cell lysis. The expressed CEA, a tumor associated antigen, can be detected in serum and used as a sensitive marker to monitor viral gene expression in order to easily optimize individual therapy. Compared to wild-type MV, the Ed strain of MV has a lower affinity for the MV receptor signaling lymphocyte-activation molecule (CD150), mainly expressed in B- and T-lymphocytes, but a higher affinity for CD46.
  • Carfilzomib - An epoxomicin derivate with potential antineoplastic activity. Carfilzomib irreversibly binds to and inhibits the chymotrypsin-like activity of the 20S catalytic core subunit of the proteasome, a protease complex responsible for degrading a large variety of cellular proteins. Inhibition of proteasome-mediated proteolysis results in an accumulation of polyubiquinated proteins, which may lead to cell cycle arrest, induction of apoptosis, and inhibition of tumor growth.
  • Caricotamide/tretazicar - A combination therapy consisting of the prodrug tretazicar and the enzyme co-substrate caricotamide with potential antineoplastic activity. In the presence of separately and simultaneously administered caricotamide, tretazicar is converted to the short-lived cytotoxic DNA cross-linking agent dinitrobenzamide by NAD(P)H quinine oxidoreductase 2 (NQO2), resulting in the inhibition of DNA replication and the induction of apoptosis. NQO2 has been found to be elevated in certain cancers such as hepatocellular carcinoma (HCC).
  • Carlumab - A human IgG1 kappa monoclonal antibody directed against human CC chemokine ligand 2 (CCL2) with potential antineoplastic activity. Carlumab binds to and inhibits CLL2, which may result in inhibition of angiogenesis and, so, tumor cell proliferation. Endothelium-derived CLL2 (monocyte chemoattractant protein; MCP1) is a member of the beta-chemokine family, can stimulate monocyte/macrophage migration and smooth muscle cell (SMC) proliferation, and plays a role in angiogenesis and tumor cell migration; CCL2 induction of angiogenesis may involve the upregulation of hypoxia-inducible factor 1 alpha (HIF-1 alpha) gene expression which, in turn, induces vascular endothelial growth factor-A (VEGF-A) gene expression.
  • Carmofur - An antimetabolite (pyrimidine analogue) antineoplastic derivative of 5-fluorouracil. (NCI)
  • Carmustine - An antineoplastic nitrosourea. Carmustine alkylates and cross-links DNA during all phases of the cell cycle, resulting in disruption of DNA function, cell cycle arrest, and apoptosis. This agent also carbamoylates proteins, including DNA repair enzymes, resulting in an enhanced cytotoxic effect. Carmustine is highly lipophilic and crosses the blood-brain barrier readily.
  • Carmustine implant - A synthetic, biodegradable wafer containing the agent carmustine with antineoplastic activity. Used to deliver drug directly into a brain tumor site and typically implanted post-surgically, the wafer is made of a biodegradable poly-anhydride copolymer and contains the nitrosourea carmustine. As an antineoplastic nitrosourea, carmustine alkylates and cross-links DNA during all phases of the cell cycle, resulting in disruption of DNA function, cell cycle arrest, and apoptosis. Carmustine also carbamoylates proteins, including DNA repair enzymes, resulting in an enhanced cytotoxic effect. Carmustine is highly lipophilic and crosses the blood-brain barrier readily.
  • Carmustine in ethanol - A formulation containing carmustine dissolved in ethanol for intra-tumoral administration that allows carmustine to enter both aqueous and lipid compartments of the target tissue. As an antineoplastic nitrosourea, carmustine alkylates and cross-links DNA during all phases of the cell cycle, resulting in disruption of DNA function, cell cycle arrest, and apoptosis. Carmustine also carbamoylates proteins, including DNA repair enzymes, resulting in an enhanced cytotoxic effect. Carmustine is highly lipophilic and crosses the blood-brain barrier readily.
  • Carmustine sustained-release implant wafer - A sustained release (SR) implant wafer containing the lipophilic nitrosourea carmustine (BCNU) with antineoplastic activity. Upon intracranial administration of the implant wafer and subsequent release of BCNU from the wafer, this agent alkylates and cross-links DNA during all phases of the cell cycle, resulting in the disruption of DNA function, cell cycle arrest, and apoptosis. This wafer contains the biodegradable copolymer PLGA (poly(lactide-co-glycolide) as the major drug delivery vehicle which is slowly degraded into water and carbon dioxide thereby continously releasing BCNU over approximately 3-4 weeks. Compared to systemic administration of BCNU alone, this local SR formulation is able to maintain higher drug concentrations locally over a longer period of time while minimizing exposure to other tissues.
  • Carotuximab - A human/murine chimeric monoclonal antibody directed against endoglin (CD105) with potential antiangiogenic and antineoplastic activities. Carotuximab binds to endoglin, which may result in inhibition of tumor angiogenesis and decreased tumor cell proliferation. The glycoprotein endoglin is a transforming growth factor beta-1 (TGF beta-1) accessory receptor that is highly expressed on tumor vessel endothelial cells and appears to be essential for angiogenesis.
  • Carrageenan-containing gel - A water-based, vaginal moisturizing gel containing a mixture of lambda- and kappa- carrageenans, sulfated polysaccharides derived from red seaweed (Chondrus crispus), with potential microbicidal activity against various viruses, including human papillomavirus (HPV), human immunodeficiencyvirus (HIV) and human herpes simplex virus (HSV). Upon vaginal insertion via an applicator, carrageenan specifically binds to the viral capsids, which prevents the binding of virions to heparan sulfate proteoglycan (HSPG) receptors or other, as of yet not fully identified, cellular proteins. In addition, the viral binding of carrageenan may also interfere with conformational changes within the virions after cellular attachment. This inhibits viral infection. Certain HPV types cause cervical cancer; therefore, the prevention of HPV infection by this gel may subsequently prevent the development of cervical cancer.
  • Carubicin - An anthracycline antineoplastic antibiotic isolated from the bacterium Actinomadura carminata. Carubicin intercalates into DNA and interacts with topoisomerase II, thereby inhibiting DNA replication and repair and RNA and protein synthesis.
  • Carubicin hydrochloride - The hydrochloride salt of the anthracycline antineoplastic antibiotic carubicin. Carubicin intercalates into DNA and inhibits topoisomerase II, thereby inhibiting DNA replication and ultimately, interfering with RNA and protein synthesis.
  • Carzelesin - A cyclopropylpyrroloindole prodrug analogue and DNA minor groove binding agent, with antineoplastic activity. After hydrolysis, the cyclopropyl group of carzelesin alkylates N3-adenine in a sequence-selective fashion. This results in tumor growth inhibition.
  • Carzinophilin - An ethylenimine antineoplastic antibiotic isolated from the bacterium Streptomyces sahachiroi. Carzinophilin forms interstrand DNA cross-links, thereby inhibiting DNA synthesis.
  • Cationic liposome-encapsulated paclitaxel - A cationic liposome preparation of paclitaxel with antineoplastic activity. Paclitaxel, the active ingredient in cationic liposome-encapsulated paclitaxel, binds to tubulin and inhibits the disassembly of microtubules, resulting in the inhibition of mitosis and cellular proliferation, and apoptosis. Cationic liposome encapsulation of paclitaxel allows the delivery of high doses of paclitaxel to target tissues while minimizing systemic toxicity. Tumor endothelial cells may preferentially bind and internalize cationic liposomes.
  • Cationic peptide cream cypep-1 - A topical cream containing Cypep-1, a cationic lytic peptide of 27 amino acids, with potential antineoplastic activity. Upon topical administration, Cypep-1 selectively targets tumor cells with negatively charged cell membranes and ruptures the cell membranes. This leads to tumor cell lysis and the release of neoantigens into the tumor microenvironment (TME) and circulation. This elicits a specific and potent cytotoxic T-lymphocyte (CTL) response against tumor cells expressing these neoantigens. Warts are benign skin tumors caused by human papilloma virus (HPV).
  • Catumaxomab - A trifunctional bispecific monoclonal antibody with potential antineoplastic activity. Catumaxomab has two antigen-recognition sites: one for human CD3, a T cell surface antigen; and one for human epithelial cell adhesion molecule (EpCAM), a cell surface antigen expressed by a variety of epithelial tumor cells. In addition, the modified Fc portion of this antibody binds Fc receptors on antigen presenting cells (APCs) such as macrophages and dendritic cells (DCs). Catumaxomab brings T cells, EpCAM-expressing epithelial tumor cells and APCs together into tricellular complexes, which may result in a potent cytotoxic T-lymphocyte (CTL) response against EpCAM-expressing epithelial tumor cells. Fc-mediated binding of APCs in the tricellular complex potentiates EpCAM antigen presentation to T cells and the activation of anti-tumor cytotoxic T cell functions.
  • Cbp/beta-catenin antagonist pri-724 - A potent, specific inhibitor of the canonical Wnt signaling pathway in cancer stem cells with potential antineoplastic activity. Wnt signaling pathway inhibitor PRI-724 specifically inhibits the recruiting of beta-catenin with its coactivator CBP (the binding protein of the cAMP response element-binding protein CREB); together with other transcription factors beta-catenin/CBP binds to WRE (Wnt-responsive element) and activates transcription of a wide range of target genes of Wnt/beta-catenin signaling. Blocking the interaction of CBP and beta-catenin by this agent prevents gene expression of many proteins necessary for growth, thereby potentially suppressing cancer cell growth. The Wnt/beta-catenin signaling pathway regulates cell morphology, motility, and proliferation; aberrant regulation of this pathway leads to neoplastic proliferation.
  • Ccl21-expressing h1944 cell vaccine - A cancer cell vaccine comprised of the allogeneic human lung adenocarcinoma cell line H1944 that has been transduced ex vivo with adenoviral vector encoding human cytokine chemokine C-C motif ligand 21 (CCL21), with potential immunomodulating and antineoplastic activities. Upon administration, CCL21-expressing H1944 cell vaccine expresses the chemokine CCL21, which may induce an antitumoral cytotoxic T-lymphocyte immune response in the tumor microenvironment. CCL21 has been shown to attract antigen presenting cells (APCs), like leukocytes and DCs, and natural killer (NK) cells and their T-cell effectors to induce a cytotoxic immune response. H1944 cells contain tumor-associated antigens (TAAs) overexpressed in non-small cell lung cancer (NSCLC).
  • Ccr2 antagonist ccx872-b - An orally available human C-C chemokine receptor type 2 (CCR2) antagonist, with potential immunomodulating and antineoplastic activities. Upon oral administration, CCR2 antagonist CCX872-B specifically binds to CCR2 and prevents the binding its cognate endothelium-derived chemokine ligand CCL2 (monocyte chemoattractant protein-1 or MCP1). This may result in the inhibition of both CCR2 activation and CCR2-mediated signal transduction, which may inhibit inflammatory processes, angiogenesis, tumor cell migration, and tumor cell proliferation. The G-protein coupled receptor CCR2 is expressed on the surface of monocytes and macrophages, and stimulates their migration and infiltration; it plays a key role in inflammation. CCR2 is overexpressed in certain cancer cell types, where it is involved in angiogenesis, tumor cell migration and proliferation.
  • Ccr2 antagonist pf-04136309 - An orally available human chemokine receptor 2 (CCR2) antagonist with potential immunomodulating and antineoplastic activities. Upon oral administration, CCR2 antagonist PF-04136309 specifically binds to CCR2 and prevents binding of the endothelium-derived chemokine ligand CLL2 (monocyte chemoattractant protein-1 or MCP1) to its receptor CCR2, which may result in inhibition of CCR2 activation and signal transduction. This may inhibit inflammatory processes as well as angiogenesis, tumor cell migration, and tumor cell proliferation. The G-protein coupled receptor CCR2 is expressed on the surface of monocytes and macrophages, stimulates the migration and infiltration of these cell types, and plays an important role in inflammation, angiogenesis, and tumor cell migration and proliferation.
  • Ccr2/ccr5 antagonist bms-813160 - An antagonist of both human C-C chemokine receptor types 2 (CCR2; CD192) and 5 (CCR5; CD195), with potential immunomodulating and antineoplastic activities. Upon administration, CCR2/CCR5 antagonist BMS-813160 specifically binds and prevents the activation of both CCR2 and CCR5. This inhibits the activation of CCR2/CCR5-mediated signal transduction pathways and may inhibit inflammatory processes, angiogenesis, tumor cell migration, tumor cell proliferation and invasion. The G-protein coupled chemokine receptors CCR2 and CCR5 are expressed on the surface of monocytes and macrophages, and stimulate their migration and infiltration; they play key roles in inflammation and autoimmune disease. CCR2 and CCR5 are overexpressed in certain cancer cell types, and are also involved in angiogenesis, and in tumor cell migration, proliferation and metastasis.
  • Ccr4 inhibitor flx475 - An orally available, small molecule antagonist of C-C chemokine receptor type 4 (CCR4) with potential immunomodulatory and antineoplastic activities. Upon oral administration, FLX475 inhibits the binding of CCR4 to its signaling molecules, thereby blocking the recruitment of regulatory T-cells (Tregs) to the tumor microenvironment (TME). This may abrogate the immunosuppressive effects of Tregs and promote an effective anti-tumor immune response. CCR4, a chemokine receptor normally expressed on circulating and tissue-resident T-cells, is highly expressed on circulating Tregs and is associated with poor prognosis in certain cancers.
  • Cd105/yb-1/sox2/cdh3/mdm2-polyepitope plasmid dna vaccine - A plasmid DNA vaccine containing the mammalian expression vector pUMVC3 (pNGVL3) encoding epitopes of CD105 (Endoglin), Y-box binding protein 1 (Yb-1), SRY-box 2 (SOX2), cadherin 3 (CDH3), and murine double minute 2 (MDM2) proteins, with potential immunomodulating and antineoplastic activities. Upon intradermal administration of pUMVC3-CD105/Yb-1/SOX2/CDH3/MDM2-epitopes plasmid DNA vaccine, the plasmid transfects cells and the peptides are expressed. This generates a specific memory Th1 (T-helper) cell immune response, stimulates secretion of cytokines by the T cells and leads to a cytotoxic T-lymphocyte (CTL) response against CD105/Yb-1/SOX2/CDH3/MDM2-expressing tumor cells. CD105/Yb-1/SOX2/CDH3/MDM2 proteins are highly immunogenic tumor associated antigens that are overexpressed in breast cancer. Additionally, these antigens are associated with breast cancer stem cells and with epithelial to mesenchymal transformation (EMT).
  • Cd11b agonist gb1275 - An orally bioavailable small molecule agonist of CD11b (integrin alpha-M; ITGAM; integrin alpha M chain), with potential immunomodulating activity. Upon administration, CD11b agonist GB1275 targets and binds to CD11b, thereby activating CD11b. This leads to CD11b-mediated signaling and promotes pro-inflammatory macrophage polarization while suppressing immunosuppressive macrophage polarization. This reduces influx of tumor-associated macrophages (TAMs) and myeloid-derived suppressor cells (MDSCs) in the tumor microenvironment (TME), promotes anti-tumor immune responses, induces cytotoxic T-lymphocytes (CTLs) and suppresses tumor growth. CD11b, a member of the integrin family of cell adhesion receptors highly expressed on immune system cells, is a negative regulator of immune suppression and activates anti-tumor innate immunity.
  • Cd123-cd33 compound car t cells - A preparation of T-lymphocytes transduced with a lentiviral vector expressing a compound chimeric antigen receptor (cCAR) containing two distinct units of CARs, one specific for the CD123 (interleukin-3 receptor alpha chain or IL3RA) antigen and one specific for the CD33 antigen, with potential immunomodulating and antineoplastic activities. Upon administration, the CD123-CD33 cCAR T cells specifically and simultaneously target and bind to tumor cells expressing CD123 and/or CD33. This induces selective toxicity in tumor cells that express the CD123 antigen and/or the CD33 antigen. CD123 is normally expressed on committed blood progenitor cells in the bone marrow; its overexpression is associated with increased leukemic cell proliferation and aggressiveness. CD33 is expressed on normal non-pluripotent hematopoietic stem cells and is overexpressed on myeloid leukemia cells. Targeting two different antigens may improve coverage and protect against antigen escape and relapse as it is less likely for tumor cells to lose both antigens. Additionally, the CD123-CD33 cCAR T cells express CD52 on the cell surface. This allows the depletion of the CD123-CD33 cCAR T cells with the administration of the anti-CD52 monoclonal antibody alemtuzumab, in case of unacceptable side effects.
  • Cd123-specific targeting module tm123 - A preparation of soluble adapter molecules consisting of an antigen-binding moiety targeting CD123 linked to a peptide motif recognizable by UniCAR02-T, that may be used to activate UniCAR02-T. Upon administration of CD123-specific targeting module (TM) TM123, and upon co-administration of UniCAR02-T, the antigen-binding moiety of TM123 targets and binds to cancer cells expressing CD123, and the binding domain of UniCAR02-T binds to the nuclear antigen motif of TM123. This activates UniCAR02-T, and induces selective toxicity in and causes lysis of CD123-expressing tumor cells. CD123 is normally expressed on committed blood progenitor cells in the bone marrow; its overexpression is associated with both increased leukemic cell proliferation and aggressiveness.
  • Cd133 antigen peptide-pulsed autologous dendritic cell vaccine - A cell-based cancer vaccine comprised of autologous dendritic cells (DCs) pulsed with human leukocyte antigen (HLA)-A2-restricted peptides derived from the CD133 antigen, with potential antineoplastic activity. Upon intradermal administration, the CD133 antigen peptide-pulsed autologous DC vaccine may stimulate an anti-tumoral cytotoxic T-lymphocyte (CTL) response against CD133-expressing tumor cells, resulting in tumor cell lysis. CD133, a cancer stem cell marker, is expressed on hematopoietic stem and progenitor cells and overexpressed on many types of cancer cells; it is associated with resistance to chemotherapy and increased cancer survival. HLA-A2 is an MHC class I molecule that presents antigenic peptides to CD8+ T-cells. Epitope design that is restricted to those epitopes that bind most efficiently to HLA-A2 may improve antigenic peptide immunogenicity.
  • Cd137l/epstein-barr virus-targeting autologous dendritic cell vaccine - A cell-based cancer vaccine composed of in vitro generated, highly potent, CD137 ligand (CD137L)-dendritic cells (CD137L-DCs), pulsed with Epstein-Bar Virus (EBV) antigen peptides, with potential antineoplastic and immunostimulatory activities. Upon administration, CD137L-DCs induce potent CD8+ T-cell responses against EBV+ target cells. DCs stimulated with CD137L enhance cytotoxic T-lymphocyte proliferation and activation to a greater extent compared to non-CD137L-stimulated DCs.
  • Cd138car-cd137/tcrzeta-expressing t lymphocytes - T-lymphocytes transduced with a retroviral vector expressing a chimeric antigen receptor (CAR) specific for syndecan-1 (CD138) (CART-138 T cells) coupled to the signaling domain of 4-1BB (CD137), and the zeta chain of the T-cell receptor (TCRzeta), with potential immunomodulating and antineoplastic activities. Upon transfusion, CD138CAR- CD137/TCRzeta -expressing T lymphocytes directs the T-lymphocytes to syndecan-1-expressing tumor cells and induces selective toxicity in those tumor cells. The 4-1BB co-stimulatory molecule signaling domain enhances activation and signaling after recognition of syndecan-1. Syndecan-1, a type 1 transmembrane proteoglycan and tumor associated antigen, is overexpressed in a variety of cancer cells. It plays a key role in the regulation of cell growth, differentiation, and adhesion, and its expression is correlated with poor prognosis.
  • Cd16/il15/cd33 trispecific killer cell engager - A trispecific killer engager (TriKE) molecule containing an anti-cluster of differentiation 16 (CD16; FcgammaRIII) single-chain variable fragment (scFv) to engage natural killer (NK) cells, an anti-CD33 scFv to engage myeloid cells and a human modified interleukin-15 (IL-15) linker, that links the two scFv, with potential immunomodulating and antineoplastic activities against CD33-expressing tumor cells. Upon administration of the CD16/IL15/CD33 TriKE, the simultaneous binding to CD16 on NK cells and CD33 on tumor cells will induce NK cell cytotoxicity specifically against CD33-expressing tumor cells. The cytokine IL-15 linker promotes NK cell proliferation, activity, survival and expansion. CD33 is expressed on normal non-pluripotent hematopoietic stem cells and is overexpressed on myeloid leukemia cells.
  • Cd19car-cd28-cd3zeta-egfrt-expressing tcm-enriched t-lymphocytes - A preparation of genetically modified central memory (Tcm) enriched T-cells transduced with a replication incompetent lentiviral vector expressing a chimeric antigen receptor (CAR), containing a CD28 signaling domain fused to both CD3 zeta, which targets the CD19 antigen, and a truncated form of the human epidermal growth factor receptor (EGFRt), with potential immunostimulating and antineoplastic activities. Upon intravenous administration, CD19CAR-CD28-CD3zeta-EGFRt-expressing Tcm-enriched T cells are directed to CD19-expressing tumor cells, thereby inducing a selective toxicity in CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies. Devoid of both ligand binding domains and tyrosine kinase activity, EGFRt both facilitates in vivo detection of the administered T-cells and can promote elimination of those cells upon a cetuximab-induced antibody dependent cellular cytotoxicity response. The costimulatory signaling domain enhances proliferation of T cells and antitumor activity.
  • Cd19car-cd28-cd3zeta-egfrt-expressing tn/mem-enriched t-lymphocytes - A preparation of genetically modified lymphocytes comprised of CD62L-positive naïve and memory T-cells (Tn/mem), that are transduced ex vivo with a self-inactivating (SIN) lentiviral vector expressing a hinge-optimized chimeric antigen receptor (CAR) specific for the CD19 antigen and containing CD28 and CD3 zeta signaling domains, and a truncated form of the human epidermal growth factor receptor (EGFRt), with potential immunostimulating and antineoplastic activities. Upon isolation of peripheral blood lymphocytes (PBLs), transduction of the CD62L-positive T-lymphocytes, expansion ex vivo and administration, the CD19R(EQ)-CD28-CD3zeta-EGFRt-expressing Tn/mem-enriched T-cells target CD19-expressing tumor cells, thereby inducing selective toxicity in CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies. Devoid of both ligand binding domains and tyrosine kinase activity, EGFRt both facilitates in vivo detection of the administered T-cells and can promote elimination of those cells upon a cetuximab-induced antibody dependent cellular cytotoxicity response. Tn/mem T-cells include naïve T-cells, central memory T-cells (Tcm) and stem cell memory T-cells (Tscm). CD19R(EQ) contains two point mutations in the immunoglobulin (Ig) G4 spacer region, thereby preventing recognition of the CAR by Fc receptors (FcRs).
  • Cd19car-cd28zeta-4-1bb-expressing allogeneic t lymphocytes - Allogeneic T-lymphocytes transduced with a retroviral vector expressing a chimeric antigen receptor (CAR) consisting of an anti-CD19 scFv (single chain variable fragment) coupled to the costimulatory signaling domain CD28, the signaling domain of 4-1BB (CD137), and the zeta chain of the T-cell receptor (TCR), with potential immunomodulating and antineoplastic activities. Upon transfusion, CD19CAR-CD28 zeta-4-1BB-expressing allogeneic T lymphocytes directs the T-lymphocytes to and induces selective toxicity in CD19-expressing tumor cells. CD28, a T-cell surface-associated co-stimulatory molecule, is required for T-cell activation, proliferation, and survival. The 4-1BB co-stimulatory molecule signaling domain enhances activation and signaling after recognition of CD19. Furthermore, inclusion of the 4-1BB signaling domain may increase the antitumor activity compared to the inclusion of the CD28 costimulatory domain and TCR zeta chain alone. CD19 antigen is a B-cell specific cell surface antigen, which is expressed in all B-cell lineage malignancies.
  • Cd19car-cd3zeta-4-1bb-cd28-expressing autologous t-lymphocytes - Autologous T-lymphocytes transduced with a retroviral vector expressing a chimeric antigen receptor (CAR) consisting of an anti-CD19 scFv (single chain variable fragment) coupled to three co-stimulatory signaling domains derived from CD28, 4-1BB (CD137), and the zeta chain of the T-cell receptor (TCR)/CD3 complex (CD3-zeta), with potential immunomodulating and antineoplastic activities. Upon transfusion, the CD19CAR-CD3zeta-4-1BB-CD28-expressing autologous T-lymphocytes direct the T-lymphocytes to CD19-expressing tumor cells and induce their selective toxicity. CD28, a T-cell surface-associated co-stimulatory molecule, is required for T-cell activation, proliferation, and survival. The 4-1BB co-stimulatory molecule signaling domain enhances activation and signaling after recognition of CD19. CD3-zeta is a transmembrane signaling adaptor polypeptide that regulates the assembly of TCR complexes, modulates the expression of the complex on the cell surface and plays a key role in antigen recognition. CD19 antigen, a B-cell specific cell surface antigen, is expressed in all B-cell lineage malignancies.
  • Cd19car-cd3zeta-4-1bb-expressing allogeneic t-lymphocyte cells - Allogeneic T-lymphocytes transduced with a modified lentiviral vector expressing a chimeric antigen receptor (CAR) consisting of an anti-CD19 scFv (single chain variable fragment) and the zeta chain of the TCR/CD3 complex (CD3-zeta), coupled to the signaling domain of 4-1BB (CD137), with potential immunomodulating and antineoplastic activities. Upon transfusion, CD19CAR-CD3zeta-4-1BB-expressing allogeneic T-lymphocyte cells direct the T-lymphocytes to CD19-expressing tumor cells, thereby inducing a selective toxicity in CD19-expressing tumor cells. The 4-1BB co-stimulatory molecule signaling domain enhances activation and signaling after recognition of CD19 and the inclusion of this signaling domain may increase the antitumor activity compared to the inclusion of the CD3-zeta chain alone. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies.
  • Cd19car-cd3zeta-expressing autologous t lymphocytes - Autologous T-lymphocytes transduced with a modified lentiviral vector expressing a chimeric antigen receptor (CAR) consisting of an anti-CD19 scFv (single chain variable fragment) and the zeta chain of the TCR/CD3 complex (CD3-zeta), with potential immunomodulating and antineoplastic activities. Upon transfusion, CD19CAR-CD3zeta-expressing autologous T-lymphocytes are directed to CD19-expressing tumor cells, thereby inducing a selective toxicity only in these tumor cells. The CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies. CD3-zeta (or CD247) is a transmembrane signaling adaptor polypeptide that regulates the assembly of complete T-cell receptor complexes and their expression on the cell surface.
  • Cd20-cd19 compound car t cells - A preparation of T-lymphocytes transduced with a lentiviral vector expressing a compound chimeric antigen receptor (cCAR) containing two distinct units of CARs, one specific for the tumor-associated antigen (TAA) cluster of differentiation 20 (CD20) and one specific for the TAA CD19, with potential immunomodulating and antineoplastic activities. Upon administration, the CD20-CD19 cCAR T cells specifically and simultaneously target and bind to tumor cells expressing CD20 and/or CD19. This induces selective toxicity in tumor cells that express CD20 and/or CD19. Both CD19 and CD20 are B-cell-specific cell surface antigens overexpressed in B-cell lineage malignancies. Targeting two different antigens may improve coverage and protect against antigen escape and relapse as it is less likely for tumor cells to lose both antigens.
  • Cd24 extracellular domain-igg1 fc domain recombinant fusion protein cd24fc - A recombinant fusion protein composed of the extracellular domain of the mature human glycoprotein CD24 linked to a human immunoglobulin G1 (IgG1) Fc domain, with potential immune checkpoint inhibitory, anti-inflammatory and antineoplastic activities. Upon administration, the CD24 extracellular domain-IgG1 Fc domain recombinant fusion protein CD24Fc binds to injured cell components, also called DAMPs (Danger-Associated Molecular Patterns), thereby preventing the interaction of DAMPs with toll-like receptors (TLRs) and inhibiting both nuclear factor-kappa B (NFkB) activation and secretion of inflammatory cytokines. In addition, CD24Fc binds to and activates Siglec G/10, a sialic acid-binding immunoglobulin-type lectin, and stimulates SHP-1-mediated inhibitory signaling, while also preventing NFkB activation and secretion of inflammatory mediators, which further prevents inflammatory responses. DAMPs activate the innate immune system. CD24 binds to both DAMPs and Siglec G/10 to regulate immune responses.CD24/Siglec G/10 interaction plays a key role in a number of immune-mediated diseases including graft-versus-host disease (GvHD), multiple sclerosis and rheumatoid arthritis.
  • Cd28/icos antagonist alpn-101 - An Fc fusion protein comprised of a human inducible T-cell costimulator ligand (ICOSL) variant immunoglobulin domain (vIgD) that binds to both inducible T-cell costimulator (ICOS; CD278) and cluster of differentiation 28 (CD28), with potential immunomodulating activity. Upon administration, CD28/ICOS antagonist ALPN-101 targets and binds to both CD28 and ICOS expressed on certain T-cells. This prevents the activation of CD28 and ICOS by its ligands, thereby blocking the two T-cell costimulatory pathways and the resulting T-cell activation. CD28 is involved in initiation of the pathogenic process in graft versus host disease (GVHD). Following initial activation, CD28 is often downregulated while ICOS is upregulated, possibly sustaining GVHD. Dual blockade of CD28 and ICOS may be superior to individual blockade of CD28 or ICOS alone.
  • Cd28car/cd137car-expressing t-lymphocytes - Third generation, chimeric antigen receptor (CAR) cells composed of T-lymphocytes transduced with a lentiviral vector expressing a CAR consisting of an a single chain variable fragment specific for a particular antigen, coupled to the two co-stimulatory signaling domains Cluster of Differentiation 28 (CD28) and Cluster of Differentiation 137 (CD137; 4-1BB), and the zeta chain of the T-cell receptor (TCR)/CD3 complex (CD3-zeta), with potential immunomodulating and antineoplastic activities. Upon transfusion, CD28CAR/CD137CAR-expressing T-lymphocytes are directed to, and induce selective toxicity in tumor cells expressing the particular antigen. CD28, a T-cell surface-associated co-stimulatory molecule, is required for T-cell activation, proliferation, and survival. The 4-1BB co-stimulatory molecule signaling domain enhances activation and signaling after recognition of the antigen. Furthermore, inclusion of the 4-1BB signaling domain may increase the antitumor activity when compared to the inclusion of the CD28 co-stimulatory domain and CD3-zeta alone.
  • Cd3/cd28 costimulated autologous t-cells - A population of T cells that have been sensitized to vaccine tumor antigen(s) in vivo; collected from the patient; co-stimulated with antibodies to the T-cell cell surface proteins CD3 and CD28 and expanded ex vivo; and then infused into the same patient. CD3, part of the T cell receptor complex, and CD28, a T-cell surface-associated co-stimulatory molecule, are both required for full T-cell activation. Adoptive transfer of CD3/CD28 costimulated vaccine-primed autologous T-cells may induce the production of interferon-gamma (IFN-gamma) and granulocyte-macrophage colony-stimulating factor (GM-CSF) and associated antitumor effects and a graft-versus-tumor (GVT) response.
  • Cd30 car-expressing autologous t lymphocytes - A preparation of autologous T-lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) specific for the CD30 antigen, with potential immunostimulating and antineoplastic activities. Upon administration, the CD30 CAR-expressing autologous T-lymphocytes specifically recognize and bind to CD30-expressing tumor cells, resulting in tumor cell lysis. CD30, a cell surface receptor and a member of the tumor necrosis factor (TNF) receptor superfamily, is transiently expressed on activated lymphocytes and is constitutively expressed in hematologic malignancies.
  • Cd33car-cd3zeta-4-1bb-expressing autologous t-lymphocytes - Autologous T-lymphocytes transduced with a retroviral vector expressing a chimeric antigen receptor (CAR) consisting of an anti-CD33 scFv (single chain variable fragment) coupled to the signaling domain of 4-1BB (CD137) and the zeta chain of the T-cell receptor (TCRzeta), with potential immunomodulating and antineoplastic activities. Upon transfusion, CD33-specific CAR retroviral vector-transduced autologous T lymphocytes target CD33-expressing tumor cells and induce selective toxicity in CD33-expressing tumor cells. Following binding to CD33, the 4-1BB co-stimulatory molecule signaling domain enhances both activation and signaling. Inclusion of the 4-1BB signaling domain may also increase the antitumor activity when compared to the inclusion of the CD3-zeta chain alone. CD33 is expressed on normal non-pluripotent hematopoietic stem cells as well as on myeloid leukemia cells.
  • Cd33-specific car lentiviral vector-transduced autologous t-lymphocytes - Autologous T-lymphocytes transduced with a lentiviral vector expressing a chimeric antigen receptor (CAR) specific for the CD33 antigen, with potential immunomodulating and antineoplastic activities. Upon transfusion, CD33-specific CAR lentiviral vector-transduced autologous T-lymphocytes target and induce selective toxicity in CD33-expressing tumor cells. CD33 is expressed on normal non-pluripotent hematopoietic stem cells and on myeloid leukemia cells.
  • Cd40 agonist monoclonal antibody cp-870,893 - A fully human monoclonal antibody (mAb) agonist of the cell surface receptor CD40 with potential immunostimulatory and antineoplastic activities. Similar to the CD40 ligand (CD40L or CD154), CD40 agonist monoclonal antibody CP-870,893 binds to CD40 on a variety of immune cell types, triggering the cellular proliferation and activation of antigen-presenting cells (APCs), activating B cells and T cells, and enhancing the immune response; in addition, this agent may activate CD40 present on the surfaces of some solid tumor cells, resulting in apoptosis and decreased tumor growth. CD40, a member of the tumor necrosis factor (TNF) receptor superfamily, is expressed on various immune cells, many B-cell malignancies, and some solid tumors, mediating both indirect tumor cell killing through the activation of the immune system and direct tumor cell apoptosis.
  • Cd44 targeted agent spl-108 - A proprietary agent that targets the cancer stem cell (CSC) antigen CD44, with potential antineoplastic activity. Although the mechanism of action has not been elucidated, following subcutaneous administration, CD44 targeted agent SPL-108 binds to CD44 and prevents the activation of various CD44-mediated signal transduction pathways, which may lead to reduced proliferation of CD44-expressing tumor stem cells. CD44, a transmembrane glycoprotein and hyaluronic acid receptor, is expressed in healthy tissue and overexpressed in numerous cancer cell types; it plays a key role in the proliferation, migration and survival of tumor cells.
  • Cd44v6-specific car t-cells - A preparation of genetically modified T-lymphocytes transduced with a lentiviral vector encoding a fourth-generation specific chimeric antigen receptor (4SCAR) specific for CD44 variant domain 6 (CD44v6), with potential immunomodulating and antineoplastic activities. Upon administration, CD44v6-specific CAR T-cells specifically recognize and kill CD44v6-expressing tumor cells. CD44, a transmembrane glycoprotein and hyaluronic acid receptor, is expressed in healthy tissue and overexpressed in numerous cancer cell types. CD44v6, the isoform containing the variant domain 6 of CD44 gene, plays a key role in tumor cell invasion, proliferation and metastasis.
  • Cd47 antagonist alx148 - A variant of signal regulatory protein alpha (SIRPa) that antagonizes the human cell surface antigen CD47, with potential phagocytosis-inducing, immunostimulating and antineoplastic activities. Upon administration, ALX148 binds to CD47 expressed on tumor cells and prevents the interaction of CD47 with its ligand SIRPa, a protein expressed on phagocytic cells. This prevents CD47/SIRPa-mediated signaling and abrogates the CD47/SIRPa-mediated inhibition of phagocytosis. This induces pro-phagocytic signaling mediated by the binding of the pro-phagocytic signal calreticulin (CRT), which is specifically expressed on the surface of tumor cells, to low-density lipoprotein (LDL) receptor-related protein (LRP), expressed on macrophages. This results in macrophage activation and the specific phagocytosis of tumor cells. In addition, blocking CD47 signaling activates both an anti-tumor cytotoxic T-lymphocyte (CTL) immune response and T cell-mediated killing of CD47-expressing tumor cells. CD47, also called integrin-associated protein (IAP), is a tumor-associated antigen (TAA) expressed on normal, healthy hematopoietic stem cells (HSC) and overexpressed on the surface of a variety of cancer cells. Expression of CD47, and its interaction with SIRPa, leads to the inhibition of macrophage activation and protects cancer cells from phagocytosis, which allows cancer cells to proliferate.
  • Cd4-specific telomerase peptide vaccine ucpvax - A therapeutic peptide vaccine containing the human telomerase reverse transcriptase catalytic subunit (hTERT)-derived universal cancer peptides 2 (UCP2) and 4 (UCP4), and combined with the immunoadjuvant Montanide ISA 51 VG, with potential immunostimulating and antineoplastic activities. Vaccination with the CD4-specific telomerase peptide vaccine UCPVax activates the immune system to mount a T-helper 1 (TH1) CD4-positive T-lymphocyte immune response against and ultimately killing telomerase-expressing cells. Telomerase, a reverse transcriptase normally repressed in healthy cells, is overexpressed in most cancer cells and plays a key role in cellular proliferation.
  • Cd73 inhibitor ab680 - A small molecule, competitive inhibitor of the ectoenzyme CD73 (cluster of differentiation 73; 5'-ecto-nucleotidase; 5'-NT; ecto-5'-nucleotidase), with potential immunomodulating and antineoplastic activities. Upon administration, CD73 Inhibitor AB680 targets and binds to CD73, leading to clustering of and internalization of CD73. This prevents CD73-mediated conversion of adenosine monophosphate (AMP) to adenosine and decreases the amount of free adenosine in the tumor microenvironment (TME). This prevents adenosine-mediated lymphocyte suppression and increases the activity of CD8-positive effector cells and natural killer (NK) cells. This also activates macrophages and reduces the activity of myeloid-derived suppressor cells (MDSCs) and regulatory T-lymphocytes (Tregs). By abrogating the inhibitory effect on the immune system and enhancing the cytotoxic T-cell-mediated immune response against cancer cells, tumor cell growth decreases. In addition, clustering and internalization of CD73 decreases the migration of cancer cells and prevents metastasis. CD73, a plasma membrane protein belonging to the 5'-nucleotidase (NTase) family, upregulated on a number of cancer cell types, catalyzes the conversion of extracellular nucleotides, such as AMP, to membrane-permeable nucleosides, such as adenosine; it plays a key role in adenosine-mediated immunosuppression within the TME.
  • Cd73 inhibitor ly3475070 - An orally bioavailable inhibitor of the ectoenzyme CD73 (cluster of differentiation 73; 5'-ecto-nucleotidase; 5'-NT; ecto-5'-nucleotidase), with potential immunomodulating and antineoplastic activities. Upon oral administration, CD73 inhibitor LY3475070 targets and binds to CD73, leading to clustering of and internalization of CD73. This prevents CD73-mediated conversion of adenosine monophosphate (AMP) to adenosine and decreases the amount of free adenosine in the tumor microenvironment (TME). This prevents adenosine-mediated lymphocyte suppression and increases the activity of CD8-positive effector cells and natural killer (NK) cells. This also activates macrophages and reduces the activity of myeloid-derived suppressor cells (MDSCs) and regulatory T-lymphocytes (Tregs). By abrogating the inhibitory effect on the immune system and enhancing the cytotoxic T-cell-mediated immune response against tumor cells, tumor cell growth decreases. In addition, clustering and internalization of CD73 decreases the migration of cancer cells and prevents metastasis. CD73, a plasma membrane protein belonging to the 5'-nucleotidase (NTase) family, catalyzes the conversion of extracellular nucleotides, such as AMP, to membrane-permeable nucleosides, such as adenosine. It is upregulated in a number of cancer cell types and plays a key role in adenosine-mediated immunosuppression within the TME.
  • Cd8+ and cd4+ donor memory t-cells-expressing ha1-specific tcr - A preparation of CD4+ and CD8+ central memory (CM) T-lymphocytes isolated from the peripheral blood of a transplant donor and transduced with a lentiviral vector (LV) (pRRLSIN) expressing a minor H antigen (HA-1(H); HA1(H)) T-cell receptor (TCR) containing the suicide gene inducible caspase 9 (iCasp9 or iC9)-HA1 TCR2-RQR-CD8 transgene (pRRLSIN iC9-HA1 TCR2-RQR-CD8; HA-1 TCR LV), with potential immunostimulating and antineoplastic activities. Upon intravenous administration and after allogeneic hematopoietic stem cell transplantation (HSCT), the CD8+ and CD4+ donor memory T cells-expressing HA1-specific TCR are directed to and induce selective toxicity in HA1-expressing tumor cells. iCasp9 consists of a human FK506 drug-binding domain with an F36V mutation (FKBP12-F36V) linked to human caspase 9. If administration of the T-cells lead to unacceptable side effects, a dimerizing agent rimiducid (AP1903), which binds to the FKBP12-F36V drug-binding domain and activates caspase 9, can be administered; caspase-9 activation results in the apoptosis of the administered TCR-modified T-cells. HA1(H) is a tumor-associated antigen (TAA) that is selectively and highly expressed on leukemic stem cells and blasts, but not in normal non-hematopoietic cells. RQR includes a CD20 epitope, and a CD34 epitope that facilitates both purification and cell tracking of the transduced T-cells with an anti-CD34 monoclonal antibody.
  • Cd8+nkg2d+ akt cell - A preparation of human CD8-positive tumor-specific T-lymphocytes engineered to express the natural killer cell activating receptor group 2D (NKG2D) and the serine/threonine kinase AKT, with potential immunomodulating and antineoplastic activities. Upon administration of CD8+NKG2D+ AKT cells, these cells target and kill tumor cells. AKT-mediated signaling enhances the activation, differentiation, proliferation and cytokine production of tumor specific T-cells, which enhances their anti-tumor effects; AKT activity in T-cells is often downregulated in the tumor environment. NKG2D, a stimulatory lymphocyte receptor, mediates the recognition of tumors cells and promotes T-cell activation and T-cell-mediated tumor cell killing; NKG2D ligands are expressed on cancer cells, while they are minimally expressed by or absent from normal, healthy cells.
  • Cd80-fc fusion protein alpn-202 - A fusion protein composed of the N-terminal Ig variable-like (IgV) domain of CD80 fused to a human immunoglobulin G1 (IgG1) Fc fragment, with potential immunostimulatory, immune checkpoint inhibitory and antineoplastic activities. Upon administration, CD80-Fc fusion protein ALPN-202 targets and binds to programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) expressed on tumor cells, which blocks its binding to and activation of its receptor programmed cell death 1 (PD-1; cluster of differentiation 279; CD279), and leads to PD-L1-dependent CD28 binding and co-stimulation in the local tumor microenvironment (TME). This reverses T-cell inactivation caused by PD-1/PD-L1 signaling, leads to the co-stimulation of T-cell responses including the activation of naïve and memory T-cells in the TME and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. In addition, ALPN-202 targets and binds to CTL-associated antigen 4 (CTLA4; CTLA-4) expressed on T-cells. This prevents the binding of CTLA-4 to endogenous CD80, thereby enabling CD80-CD28 engagement, CD28 signaling, and T-cell activation. This further promotes T-cell activity. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1 on T-cells suppresses the immune system and results in immune evasion. CD80 is a co-stimulatory molecule expressed on activated antigen presenting cells (APCs) that plays a key role in T-cell activation upon binding to CD28 on T-cells. On the other hand, binding of CD80 to CTLA-4 prevents CD80-CD28 engagement, thereby inhibiting T-cell activity and immune activation. CTLA-4 is a member of the immunoglobulin superfamily (IgSF) and an inhibitory molecule upregulated by T-cells following T-cell activation. It plays a key role in the downregulation of the immune system.
  • Cd80-fc fusion protein fpt155 - A recombinant fusion protein composed of the extracellular domain (ECD) of human CD80 (B7.1) fused to a human immunoglobulin G1 (IgG1) Fc fragment, with potential immunostimulatory, immune checkpoint inhibitory and antineoplastic activities. Upon administration of CD80-Fc fusion protein FPT155, the CD80 moiety targets and binds to CD28, which in the presence of antigenic T-cell receptor (TCR) signaling, leads to the co-stimulation of T-cell responses including the activation of naïve and memory T-cells. This leads to a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells, thereby killing cancer cells. FPT155 also targets and binds to CTL-associated antigen 4 (CTLA4; CTLA-4), preventing the binding of CTLA-4 to endogenous CD80, thereby enabling CD80-CD28 engagement, CD28 signaling, and T-cell activation in the tumor microenvironment. CD80 is a co-stimulatory molecule expressed on activated antigen presenting cells that plays a key role in T-cell activation upon binding to CD28 on T-cells. On the other hand, binding of CD80 to CTLA-4 prevents CD80-CD28 engagement, thereby inhibiting T-cell activity and immune activation. CTLA-4 is a member of the immunoglobulin superfamily (IgSF) and an inhibitory molecule upregulated by T-cells following T-cell activation. It plays a key role in the downregulation of the immune system.
  • Cdc7 kinase inhibitor bms-863233 - An orally bioavailable cell division cycle 7 homolog (CDC7) kinase inhibitor with potential antineoplastic activity. CDC7 kinase inhibitor BMS-863233 binds to and inhibits the activity of CDC7, which may result in the inhibition of DNA replication and mitosis, the induction of tumor cell apoptosis, and the inhibition of tumor cell proliferation in CDC7-overexpressing tumor cells. CDC7, a serine-threonine kinase overexpressed in a variety of tumor cell types, plays an essential role in the initiation of DNA replication by activating origins of replication.
  • Cdc7 kinase inhibitor ly3143921 hydrate - The hydrated form of an orally bioavailable inhibitor of cell division cycle 7 (CDC7) kinase, with potential antineoplastic activity. Upon administration of CDC7 kinase inhibitor LY3143921 hydrate, LY3143921 targets, binds to and inhibits the activity of CDC7, which may result in the inhibition of DNA replication and mitosis, the induction of tumor cell apoptosis, and the inhibition of tumor cell proliferation in CDC7-overexpressing tumor cells. The serine-threonine kinase CDC7 plays a key role in DNA replication by binding to and phosphorylating serine (Ser)-40 and 53 of MCM2 (minichromosome maintenance complex component 2), which is required for the initiation of DNA replication. Although expressed at low levels in healthy, normal cells, CDC7 is expressed at much higher levels in cancer cells.
  • Cdc7 kinase inhibitor nms-1116354 - An orally bioavailable cell division cycle 7 homolog (CDC7) kinase inhibitor with potential antineoplastic activity. CDC7 kinase inhibitor NMS-1116354 binds to and inhibits the activity of CDC7, which may result in the inhibition of DNA replication and mitosis, the induction of tumor cell apoptosis, and the inhibition of tumor cell proliferation in CDC7-overexpressing tumor cells. The serine-threonine kinase CDC7 initiates DNA replication by phosphorylating MCM2 (minichromosome maintenance complex component 2) at Ser40 and Ser53.
  • Cdk inhibitor at7519 - An orally bioavailable small molecule with potential antineoplastic activity. AT7519M selectively binds to and inhibits cyclin dependent kinases (CDKs), which may result in cell cycle arrest, induction of apoptosis, and inhibition of tumor cell proliferation. CDKs are serine/threonine kinases involved in regulation of the cell cycle and may be overexpressed in some types of cancer cells.
  • Cdk inhibitor r547 - An orally bioavailable diaminopyrimidine compound and a cyclin-dependent kinase (CDK) inhibitor with potential antineoplastic activity. CDKs are ATP-dependent serine/threonine kinases that are important regulators of cell cycle progression and are frequently overexpressed in cancerous cells. R547 selectively binds to and inhibits CDKs, especially CDK1/cyclin B, CDK2/cyclin E, and CDK4/cyclin D1. The inhibition of CDKs results in cell cycle arrest, inhibition of tumor cell proliferation, and induction of apoptosis. By inhibiting CDK activity, R547 also reduces phosphorylation of the retinoblastoma (Rb) protein, thereby preventing activation of transcription factor E2F and leading to further suppression of tumor cell proliferation.
  • Cdk inhibitor sns-032 - A small aminothiazole molecule and cyclin dependent kinase (CDK) inhibitor with potential antineoplastic activity. SNS-032 binds to and prevents the phosphorylation of cyclin-dependent kinases, especially CDK2, 7, and 9 that regulate cell cycle progression. Inhibition of CDKs leads to cell cycle arrest and induces apoptosis. As a result, this agent causes cytotoxicity and prevents further tumor cell growth.
  • Cdk1 inhibitor bey1107 - An orally bioavailable, cyclin dependent kinase 1 (CDK1) inhibitor, with potential antineoplastic activity. Upon administration, CDK1 inhibitor BEY1107 targets, binds to and inhibits the activity of CDK1. This may inhibit cancer stem cell (CSC) division, cause cell cycle arrest, and induce apoptosis. This may inhibit tumor cell proliferation. CDK1, an ATP-dependent serine/threonine kinase, plays a key role in regulating cell division, cell cycle progression and proliferation. It is frequently overexpressed in tumor cells.
  • Cdk1/2/4 inhibitor ag-024322 - A cyclin-dependent kinase (CDK) inhibitor with antineoplastic activity. AG-024322 selectively inhibits cyclin-dependent kinases (particularly CDK1,2 and 4), enzymes that regulate cell cycle progression. Inhibition of CDK may result in cell cycle arrest, induction of apoptosis, and inhibition of DNA replication and tumor cell proliferation.
  • Cdk2 inhibitor pf-07104091 - An orally bioavailable inhibitor of cyclin-dependent kinase 2 (CDK2), with potential antineoplastic activity. Upon administration, CDK2 inhibitor PF-07104091 selectively targets, binds to and inhibits the activity of CDK2. This may lead to cell cycle arrest, the induction of apoptosis, and the inhibition of tumor cell proliferation. CDKs are serine/threonine kinases that are important regulators of cell cycle progression and cellular proliferation and are frequently overexpressed in tumor cells. CDK2/cyclin E complex plays an important role in retinoblastoma (Rb) protein phosphorylation and the G1-S phase cell cycle transition. CDK2/cyclin A complex plays an important role in DNA synthesis in S phase and the activation of CDK1/cyclin B for the G2-M phase cell cycle transition.
  • Cdk2/4/6/flt3 inhibitor fn-1501 - A small molecule multi-kinase inhibitor of cyclin-dependent kinase (CDK) subtypes 2 (CDK2), 4 (CDK4), and 6 (CDK6) and FMS-related tyrosine kinase 3 (FLT3, FLK2, STK1), with potential antineoplastic activity. Upon intravenous administration, CDK2/4/6/FLT3 inhibitor FN-1501 binds to and inhibits CDK2, CDK4, and CDK6, as well as FLT3. This may induce apoptosis and inhibit tumor cell proliferation in cancer cells that overexpress these kinases. CDKs are serine/threonine kinases that assist in cell cycle regulation and cellular proliferation. FLT3, a class III tyrosine kinase receptor, is overexpressed or mutated in many cancer types.
  • Cdk4 inhibitor p1446a-05 - A protein kinase inhibitor specific for the cyclin-dependent kinase 4 (CDK4) with potential antineoplastic activity. CDK4 inhibitor P1446A-05 specifically inhibits CDK4-mediated G1-S phase transition, arresting cell cycling and inhibiting cancer cell growth. The serine/threonine kinase CDK4 is found in a complex with D-type G1 cyclins and is the first kinase to become activated upon mitogenic stimulation, releasing cells from a quiescent stage into the G1/S growth cycling stage; CDK-cyclin complexes have been shown to phosphorylate the retinoblastoma (Rb) transcription factor in early G1, displacing histone deacetylase (HDAC) and blocking transcriptional repression.
  • Cdk4/6 inhibitor bpi-16350 - An orally bioavailable inhibitor of cyclin-dependent kinase (CDK) types 4 (CDK4) and 6 (CDK6), with potential antineoplastic activity. Upon administration, CDK4/6 inhibitor BPI-16350 selectively inhibits CDK4 and CDK6, which inhibits the phosphorylation of retinoblastoma protein (Rb) early in the G1 phase, prevents CDK-mediated G1-S-phase transition and leads to cell cycle arrest. This suppresses DNA replication and decreases tumor cell proliferation. CDK4 and 6 are serine/threonine kinases that are upregulated in many tumor cell types and play a key role in the regulation of both cell cycle progression from the G1-phase into the S-phase and tumor cell proliferation.
  • Cdk4/6 inhibitor cs3002 - An orally bioavailable selective inhibitor of cyclin-dependent kinase (CDK) types 4 (CDK4) and 6 (CDK6), with potential antineoplastic activity. Upon oral administration, CDK4/6 inhibitor CS3002 selectively targets and inhibits CDK4 and CDK6, which inhibits the phosphorylation of retinoblastoma protein (Rb) early in the G1 phase, prevents CDK-mediated G1-S-phase transition and leads to cell cycle arrest. This suppresses DNA replication and decreases tumor cell proliferation. CDK4 and 6 are serine/threonine kinases that are upregulated in many tumor cell types and play a key role in the regulation of both cell cycle progression from the G1-phase into the S-phase and tumor cell proliferation.
  • Cdk4/6 inhibitor fcn-437 - An orally bioavailable inhibitor of cyclin-dependent kinase (CDK) types 4 (CDK4) and 6 (CDK6), with potential antineoplastic activity. Upon administration, CDK4/6 inhibitor FCN-437 selectively inhibits CDK4 and CDK6, which inhibits the phosphorylation of retinoblastoma protein (Rb) early in the G1 phase, prevents CDK-mediated G1/S transition and leads to cell cycle arrest. This suppresses DNA replication and decreases tumor cell proliferation. CDK4 and 6 are serine/threonine kinases that are upregulated in many tumor cell types and play key roles in the regulation of both cell cycle progression from the G1-phase into the S-phase and cell proliferation.
  • Cdk4/6 inhibitor hs-10342 - An orally bioavailable, small molecular, selective inhibitor of cyclin-dependent kinase (CDK) types 4 (CDK4) and 6 (CDK6), with potential antineoplastic activity. Upon oral administration, CDK4/6 inhibitor HS-10342 selectively inhibits CDK4 and CDK6, which inhibits the phosphorylation of retinoblastoma protein (Rb) early in the G1 phase, prevents CDK-mediated G1-S-phase transition and leads to cell cycle arrest. This suppresses DNA replication and decreases tumor cell proliferation. CDK4 and 6 are serine/threonine kinases that are upregulated in many tumor cell types and play a key role in the regulation of both cell cycle progression from the G1-phase into the S-phase and tumor cell proliferation.
  • Cdk4/6 inhibitor shr6390 - A cyclin-dependent kinase (CDK) inhibitor with potential antineoplastic activity. Upon administration, CDK4/6 inhibitor SHR6390 selectively inhibits cyclin-dependent kinase 4 (CDK4) and 6 (CDK6). This inhibits retinoblastoma (Rb) protein phosphorylation early in the G1 phase, which prevents CDK-mediated G1-S phase transition and leads to cell cycle arrest. This suppresses DNA replication and decreases tumor cell proliferation. CDK4 and 6 are serine/threonine kinases that are upregulated in many tumor cell types and play a key role in the regulation of cell cycle progression.
  • Cdk4/6 inhibitor tqb3616 - An orally bioavailable, selective inhibitor of cyclin-dependent kinase (CDK) types 4 (CDK4) and 6 (CDK6), with potential antineoplastic activity. Upon oral administration, CDK4/6 inhibitor TQB3616 selectively inhibits CDK4 and CDK6, which inhibits the phosphorylation of retinoblastoma protein (Rb) early in the G1 phase, prevents CDK-mediated G1-S-phase transition and leads to cell cycle arrest. This suppresses DNA replication and decreases tumor cell proliferation. CDK4 and 6 are serine/threonine kinases that are upregulated in many tumor cell types and play a key role in the regulation of both cell cycle progression from the G1-phase into the S-phase and tumor cell proliferation.
  • Cdk7 inhibitor sy-5609 - An orally bioavailable, selective inhibitor of cyclin-dependent kinase 7 (CDK7), with potential antineoplastic activity. Upon oral administration, SY-5609 selectively targets, binds to and inhibits the activity of CDK7, thereby inhibiting CDK7-mediated signaling. Specifically, inhibition of CDK7 prevents phosphorylation of the carboxy-terminal domain (CTD) of RNA Polymerase II, thereby preventing transcription of important cancer-promoting genes. In addition, it prevents phosphorylation of the cell cycle kinases CDK1, 2, 4, and 6, thereby disrupting uncontrolled cell cycle progression. Altogether, this may induce apoptosis, cause cell cycle arrest, inhibit DNA damage repair and inhibit tumor cell proliferation in certain cancers that are dependent on CDK7-mediated transcriptional regulation and signaling. CDK7, a serine/threonine kinase, plays a role in controlling cell cycle progression, transcriptional regulation, and promotes the expression of key oncogenes such as c-Myc and beta-catenin, through the phosphorylation of RNA polymerase II.
  • Cdk8/19 inhibitor sel 120 - An orally bioavailable inhibitor of cyclin-dependent kinases 8 and 19 (CDK8/19), with potential antineoplastic and chemoprotective activities. Upon oral administration, CDK8/19 inhibitor SEL 120 targets, binds to and inhibits the activity of CDK8/19, which prevents activation of CDK8/19-mediated oncogenic signaling pathways, blocks selective transcription of various tumor-promoting genes, and inhibits proliferation of CDK8/19-overexpressing tumor cells. CDK8/19, serine/threonine kinases involved in the regulation of the cell cycle, are overexpressed in certain cancer cell types and play key roles in tumor cell proliferation.
  • Cea/tetanus toxoid t helper epitope fusion protein-expressing dna plasmid vaccine - A plasmid vaccine encoding wild type human carcinoembryonic antigen (CEA) fused to a tetanus toxoid T helper epitope, with potential antineoplastic activity. Upon vaccination and subsequent intradermal electroporation, CEA/tetanus toxoid T helper epitope fusion protein-expressing DNA plasmid vaccine may stimulate the immune system to mount a cytotoxic T-lymphocyte (CTL) response against CEA-expressing tumor cells. CEA, a tumor associated antigen, is overexpressed in a variety of cancer cell types. The tetanus toxoid helper peptide epitope, obtained from the bacterial Clostridium tetani toxoid, binds to class II MHC molecules and increases the helper T-cell response thereby inducing an increased and long-term immune response.
  • Cea-muc-1-tricom vaccine cv301 - A cancer prime/boost vaccine-based immunotherapeutic consisting of a prime, which is comprised of a proprietary version of the recombinant vaccinia viral vector, modified vaccinia Ankara-Bavarian Nordic (MVA-BN) and a recombinant fowlpox viral vector, used for the boosts, encoding both the two tumor-associated antigens (TAA), carcinoembryonic antigen (CEA) and mucin-1 (MUC-1), and TRICOM, which is comprised of three immune-enhancing co-stimulatory molecules, B7-1, ICAM-1 and LFA-3, with potential immunostimulatory and antineoplastic activities. The administration of the vaccinia priming dose is followed by multiple boosting doses of the fowlpox vector. CEA-MUC-1-TRICOM Vaccine CV301 may enhance presentation of CEA and MUC-1 to antigen-presenting cells (APCs) and may activate a cytotoxic T-lymphocyte (CTL) response against CEA- and MUC-1-expressing tumor cells. In addition, CV301 upregulates the expression of PD-L1 due to CTL-mediated tumor attack; additionally, when combined with a PD-1 immune checkpoint inhibitor, the antitumor effect may be increased. CEA and MUC-1 are overexpressed in certain cancers.
  • Cea-targeting agent rg6123 - An agent targeting the tumor-associated antigen (TAA) carcinoembryonic antigen (CEA), with potential antineoplastic activity. Upon administration, CEA-targeting agent RG6123 targets and binds to human CEA that is specifically expressed on certain tumor cells. This may, through an as of yet not elucidated mechanism of action, kill CEA-expressing tumor cells. CEA is overexpressed in many cancer cell types.
  • Cebpa-targeting sarna mtl-cebpa liposome - A lipid-based nanoparticle formulation composed of liposomes encapsulating a small oligonucleotide encoding a small activating RNA (saRNA) targeting the CCAAT enhancer binding protein alpha (CEBPA; C/EBP-a) gene, with potential antineoplastic activity. Although the exact mechanism of action through which saRNAs exert their effect(s) is still largely being investigated, it appears that, upon administration, the CEBPA-targeting saRNA MTL-CEBPA liposome targets and binds to a specific DNA regulatory target region, most likely the promoter region, for the CEBPA gene. This restores CEBPA gene transcription, and increases both CEBPA mRNA levels and protein expression. This in turn activates the expression of tumor suppressor genes and may halt proliferation of susceptible tumor cells. Specifically, upregulation of CEBPA in liver cells abrogates liver cancer cell proliferation, thereby prevents liver failure and normalizes liver function. CEBPA, a transcription factor that plays a key role in the regulation of the expression of genes with many functions, including those involved in cellular proliferation, metastasis and normal hepatocyte function, is found in many tissues, including liver cells, adipose tissue and myeloid cells. CEBPA is downregulated in certain types of cancer cells, such as liver cancer cells. saRNA is a short, double-stranded RNA that is structurally related to siRNAs; saRNA is most likely to bind to a target site on the promoter of the CEBPA gene and upregulates its gene expression.
  • Cedazuridine - An orally available synthetic nucleoside analog derived from tetrahydrouridine (THU) and cytidine deaminase inhibitor (CDAi), that can potentially be used to prevent the breakdown of cytidines. Upon oral administration, cedazuridine binds to and inhibits CDA, an enzyme primarily found in the gastrointestinal (GI) tract and liver that catalyzes the deamination of cytidine and cytidine analogs. Given in combination with a cytidine, such as the antineoplastic hypomethylating agent decitabine, it specifically prevents its breakdown and increases its bioavailability and efficacy. In addition, this allows for lower doses of decitabine to be administered, which results in decreased decitabine-associated GI toxicity.
  • Cedazuridine/azacitidine combination agent astx030 - An orally available fixed-dose combination agent containing cedazuridine, a cytidine deaminase (CDA) inhibitor, and the cytidine antimetabolite azacitidine, with potential antineoplastic activity. Upon oral administration of the cedazuridine/azacitidine combination agent ASTX030, cedazuridine binds to and inhibits CDA, an enzyme primarily found in the gastrointestinal (GI) tract and liver that catalyzes the deamination of cytidine and cytidine analogs. This prevents the breakdown of azacitidine, increases its bioavailability and efficacy while decreasing GI toxicity due to the administration of lower doses of azacitidine. Azacitidine exerts its antineoplastic activity through the incorporation of its triphosphate form into DNA, which inhibits DNA methyltransferase (DNMT), thereby blocking DNA methylation and results in hypomethylation of DNA. This interferes with DNA replication and decreases tumor cell growth.
  • Cedefingol - A derivative of sphingosine, with potential antineoplastic activity. As a sphingosine derivative, cedefingol appears to inhibit protein kinase C (PKC), a kinase that plays an important role in tumorigenesis.
  • Cediranib maleate - The maleate salt of an indole ether quinazoline derivative with antineoplastic activities. Competing with adenosine triphosphate, cediranib binds to and inhibits all three vascular endothelial growth factor receptor (VEGFR-1,-2,-3) tyrosine kinases, thereby blocking VEGF-signaling, angiogenesis, and tumor cell growth.
  • Celecoxib - A nonsteroidal anti-inflammatory drug (NSAID) with a diaryl-substituted pyrazole structure. Celecoxib selectively inhibits cyclo-oxygenase-2 activity (COX-2); COX-2 inhibition may result in apoptosis and a reduction in tumor angiogenesis and metastasis.
  • Cell cycle checkpoint/dna repair antagonist ic83 - A proprietary agent with potential antineoplastic activity. IC83 appears to target cell cycle checkpoint/DNA repair enzymes, which are involved in the recognition and repair of damaged DNA and are overexpressed in many types of cancer cells. Inhibition of cell cycle checkpoint/DNA repair enzymes may enhance the cytotoxicity of DNA damaging agents and dissipate tumor cell resistance to chemotherapy and radiation therapy.
  • Cemadotin - A synthetic dolastatin 15 analogue with potential antineoplastic activity. Cemadotin suppresses spindle microtubule dynamics by binding to tubulin, thereby blocking mitosis.
  • Cemadotin hydrochloride - The hydrochloride salt form of cemadotin, a synthetic dolastatin 15 analogue with potential antineoplastic activity. Cemadotin suppresses spindle microtubule dynamics by binding to tubulin, thereby blocking mitosis.
  • Cemiplimab - A human monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed cell death 1 (PD-1, PCD-1) protein, with potential immune checkpoint inhibitory and antineoplastic activity. Upon administration, cemiplimab binds to PD-1, inhibits its binding to the PD-1 ligand programmed cell death-1 ligand 1 (PD-L1), and prevents the activation of its downstream signaling pathways. This may restore immune function through the activation of cytotoxic T-cells. PD-1, a transmembrane protein in the immunoglobulin superfamily expressed on activated T-cells, negatively regulates T-cell activation and effector function when activated by its ligand; it plays an important role in tumor evasion from host immunity.
  • Cenersen - A phosphorothioate oligonucleotide harboring nucleotide sequences complementary to tumor suppressor p53 mRNA. Cenersen hybridizes with p53 mRNA molecules, and induces Rnase H dependent hydrolysis of p53 transcripts in the double stranded section of the hybrids, thereby resulting in loss of p53 production. Loss of p53 activity leads to sensitization of cancer cells to other therapeutics.
  • Cenisertib - A water-soluble, synthetic small molecule with potential antineoplastic activity. Cenisertib selectively binds to and inhibits aurora kinases (AKs), a family of serine-threonine kinases which are important regulators of cell division and proliferation, and which are overexpressed in certain types of cancer. Inhibition of aurora kinases inhibits cell division and proliferation and induces apoptosis in tumor cells overexpressing AKs.
  • Cenp-e inhibitor gsk-923295 - A small-molecule inhibitor of the mitotic kinesin centromere-associated protein E (CENP-E), with potential antineoplastic activity. Upon administration, GSK-923295 binds to and inhibits CENP-E, thereby preventing cell division, inducing cell cycle arrest, and ultimately leading to an inhibition of cell proliferation. CENP-E, a kinetochore-associated mitotic kinesin, plays an essential role in chromosome movement during mitosis and regulates cell-cycle transition from metaphase to anaphase.
  • Ceralasertib - An orally available morpholino-pyrimidine-based inhibitor of ataxia telangiectasia and rad3 related (ATR) kinase, with potential antineoplastic activity. Upon oral administration, Ceralasertib selectively inhibits ATR activity by blocking the downstream phosphorylation of the serine/threonine protein kinase CHK1. This prevents ATR-mediated signaling, and results in the inhibition of DNA damage checkpoint activation, disruption of DNA damage repair, and the induction of tumor cell apoptosis. In addition, AZD6738 sensitizes tumor cells to chemo- and radiotherapy. ATR, a serine/threonine protein kinase upregulated in a variety of cancer cell types, plays a key role in DNA repair, cell cycle progression and survival; it is activated by DNA damage caused during DNA replication-associated stress.
  • Ceramide nanoliposome - A lipid-based nanoparticle formulation composed of the apoptosis-inducing sphingolipid ceramide encapsulated within nanoliposomes, with potential apoptotic and antineoplastic activities. Upon administration, ceramide nanoliposomes accumulate in the tumor environment, due to the unique properties of the tumor vasculature, and easily enter tumor cells. This delivers ceramide inside the tumor cells, where ceramide induces apoptosis. Although the process is not completely understood, ceramide-dependent apoptosis most likely results from the downregulation of nutrient transporter proteins, which prevents cellular access to extracellular nutrients and causes tumor cell starvation. This selectively destroys tumor cells. Ceramide alone is insoluble and has a very short half-life; therefore, the nanoliposome formulation increases its solubility and half-life. Ceramide plays a key role in the regulation of autophagy, apoptosis, survival and proliferation. Serving as a tumor suppressor lipid, the expression of ceramide is inversely correlated with tumor cell growth, survival and metastasis.
  • Cerdulatinib - An orally bioavailable dual inhibitor of spleen tyrosine kinase (Syk) and Janus-associated kinases (JAK), with potential anti-inflammatory and antineoplastic activity. Upon oral administration, cerdulatinib specifically binds to and inhibits the activity of Syk, JAK1, and JAK3 with preferential inhibition of JAK1 and JAK3-dependent cytokine-mediated signaling and functional responses. This negatively affects the downstream JAK-STAT (signal transducer and activator of transcription) pathway, and leads to both reduced inflammation in various animal models and enhanced antiproliferative activity towards non-Hodgkin's lymphoma (NHL) cell lines. Syk is a non-receptor cytoplasmic tyrosine kinase involved in signal transduction in cells of hematopoietic origin including B cells, macrophages, basophils and neutrophils. Abnormal function of Syk has been implicated in several hematopoietic malignancies including NHL and chronic lymphocytic leukemia (CLL). The JAK-STAT pathway plays a key role in the signaling of many cytokines and growth factors and is involved in cellular proliferation, growth, hematopoiesis, and the immune response; JAK kinases may be upregulated in inflammatory diseases, myeloproliferative disorders, and various malignancies.
  • Cereblon e3 ubiquitin ligase modulating agent cc-92480 - A modulator of the E3 ubiquitin ligase complex containing cereblon (CRL4-CRBN E3 ubiquitin ligase), with potential immunomodulating and antineoplastic activities. Upon administration, cereblon E3 ubiquitin ligase modulating agent CC-92480 specifically binds to cereblon (CRBN), thereby affecting the ubiquitin E3 ligase activity, and targeting certain substrate proteins for ubiquitination. This induces proteasome-mediated degradation of certain transcription factors, some of which are transcriptional repressors in T-cells. This leads to modulation of the immune system, including activation of T-lymphocytes, and downregulation of the activity of other proteins, some of which play key roles in the proliferation of certain cancer cell types. CRBN, the substrate recognition component of the CRL4-CRBN E3 ubiquitin ligase complex, plays a key role in the ubiquitination of certain proteins.
  • Cereblon e3 ubiquitin ligase modulating agent cc-99282 - A modulator of the E3 ubiquitin ligase complex containing cereblon (CRL4-CRBN E3 ubiquitin ligase), with potential immunomodulating and antineoplastic activities. Upon administration, cereblon E3 ubiquitin ligase modulating agent CC-99282 specifically binds to cereblon (CRBN), thereby affecting the ubiquitin E3 ligase activity, and targeting certain substrate proteins for ubiquitination. This induces proteasome-mediated degradation of certain transcription factors, some of which are transcriptional repressors in T-cells. This leads to modulation of the immune system, including activation of T-lymphocytes, and downregulation of the activity of other proteins, some of which play key roles in the proliferation of certain cancer cell types. CRBN, the substrate recognition component of the CRL4-CRBN E3 ubiquitin ligase complex, plays a key role in the ubiquitination of certain proteins.
  • Cereblon modulator cc-90009 - A modulator of cereblon (CRBN), which is part of the cullin 4-RING E3 ubiquitin ligase complex (CRL4-CRBN E3 ubiquitin ligase; CUL4-CRBN E3 ubiquitin ligase), with potential immunomodulating and pro-apoptotic activities. Upon administration, CC-90009 specifically binds to CRBN, thereby affecting the activity of the ubiquitin E3 ligase complex. This leads to the ubiquitination of certain substrate proteins and induces the proteasome-mediated degradation of certain transcription factors, including Ikaros (IKZF1) and Aiolos (IKZF3), which are transcriptional repressors in T-cells. This reduces the levels of these transcription factors, and modulates the activity of the immune system, which may include the activation of T-lymphocytes. In addition, this downregulates the expression of other proteins, including interferon regulatory factor 4 (IRF4) and c-myc, which plays a key role in the proliferation of certain cancer cell types. CRBN, the substrate recognition component of the E3 ubiquitin ligase complex, plays a key role in the ubiquitination of certain proteins.
  • Cergutuzumab amunaleukin - A recombinant fusion protein comprised of cergutuzumab, a genetically engineered human immunoglobulin G1 kappa (IgG1k) monoclonal antibody directed against carcinoembryonic antigen (CEA, CEACAM5, CD66e), linked to amunaleukin, an engineered, mutated variant form of interleukin-2 (IL-2v), with potential immunostimulating and antineoplastic activities. Upon administration of cergutuzumab amunaleukin, the cergutuzumab moiety recognizes and binds to CEA, thereby specifically targeting IL-2v to CEA-expressing tumor tissue. Subsequently, the IL-2v moiety stimulates a local immune response, which activates both natural killer (NK) cells and cytotoxic T-cells, and eventually leads to tumor cell killing. CEA is a cell surface protein that is expressed on a wide variety of cancer cells. The mutations found in IL-2v inhibit its binding to IL-2 receptor-alpha (CD25, IL2Ra), which prevents the activation of regulatory T-cells (Tregs); however, IL-2v is able to bind to and induce signaling through IL-2Rbetagamma, which allows the preferential expansion of NK cells and CD8-positive T-cells. The Fc domain of cergutuzumab is modified to prevent Fc-gamma binding and downstream effector functions.
  • Ceritinib - An orally available inhibitor of the receptor tyrosine kinase activity of anaplastic lymphoma kinase (ALK) with antineoplastic activity. Upon administration, ceritinib binds to and inhibits wild-type ALK kinase, ALK fusion proteins and ALK point mutation variants. Inhibition of ALK leads to both the disruption of ALK-mediated signaling and the inhibition of cell growth in ALK-overexpressing tumor cells. ALK belongs to the insulin receptor superfamily and plays an important role in nervous system development. ALK dysregulation and gene rearrangements are associated with a variety of tumor cell types.
  • Cesalin - An antineoplastic protein isolated from the seeds of the plant Caesalpinia gilliesii with antineoplastic activity. Cesalin intercalates into and crosslinks DNA and inhibits the incorporation of the nucleotides uridine and thymidine into DNA, thereby inhibiting DNA and protein synthesis.
  • Cet kras antisense oligonucleotide azd4785 - A proprietary formulation composed of a high affinity antisense oligonucleotide (ASO) that contains 2'-4' constrained ethyl residues (cEt) and targets KRAS (K-RAS) transcripts, with potential antineoplastic activity. Upon intravenous administration, cEt KRAS antisense oligonucleotide AZD4785 targets and binds, with high affinity, to a unique genetic sequence within KRAS messenger RNA (mRNA), thereby inhibiting translation of KRAS protein, including forms containing activating mutations. Inhibition of KRAS protein synthesis prevents KRAS-dependent signaling and inhibits the proliferation of KRAS-driven tumor cells. KRAS, a tumor-associated antigen (TAA), is mutated in a variety of tumor cell types. It plays a key role in tumor cell proliferation and survival and is associated with tumor initiation, metastasis and poor prognosis.
  • Cetrelimab - A monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed cell death 1 protein (PD-1, PCDC-1), with potential immune checkpoint inhibitory and antineoplastic activity. Upon administration, cetrelimab binds to PD-1, and inhibits the interaction with its ligands, programmed cell death 1 ligand 1 (PD-L1, PD-1L1) and PD-1 ligand 2 (PD-L2, PD-1L2). The inhibition of ligand binding prevents PD-1-mediated signaling and results in both T-cell activation and the induction of T-cell-mediated immune responses against tumor cells. PD-1, an immunoglobulin (Ig) superfamily transmembrane protein and inhibitory receptor, negatively regulates T-cell activation.
  • Cetuximab - A recombinant, chimeric monoclonal antibody directed against the epidermal growth factor (EGFR) with antineoplastic activity. Cetuximab binds to the extracellular domain of the EGFR, thereby preventing the activation and subsequent dimerization of the receptor; the decrease in receptor activation and dimerization may result in an inhibition in signal transduction and anti-proliferative effects. This agent may inhibit EGFR-dependent primary tumor growth and metastasis. EGFR is overexpressed on the cell surfaces of various solid tumors.
  • Cetuximab sarotalocan - A chemical conjugate composed of the dye IR700 linked to cetuximab, a monoclonal antibody directed against the epidermal growth factor receptor (EGFR), with potential antineoplastic activity. Upon injection of cetuximab sarotalocan, the cetuximab moiety targets and binds to EGFR-expressing tumor cells, resulting in the internalization of the conjugate. Upon localized application of near-infrared (NIR) light, the IR700 dye becomes activated, disrupts the cell membrane and selectively kills the EGFR-expressing tumor cells. EGFR, a tyrosine kinase receptor, is overexpressed in a variety of cancers.
  • Cetuximab-loaded ethylcellulose polymeric nanoparticles decorated with octreotide (sy) - A preparation of ethylcellulose polymeric nanoparticles loaded with cetuximab, a recombinant, chimeric monoclonal antibody directed against the epidermal growth factor (EGFR), and decorated with the somatostatin analog, octreotide, with potential antineoplastic activity. Upon oral administration, the octreotide moiety directs the nanoparticles, which remain inert until a pH of 6.8 is reached, to somatostatin receptors (SSTRs), which are present on the cell membranes of many neuroendocrine tumor (NET) cells. At this pH, cetuximab is selectively released from the ethylcellulose polymer. Cetuximab may then bind to the extracellular domain of EGFR-expressing tumor cells, thereby preventing the activation and subsequent dimerization of the receptor. This may inhibit signal transduction and inhibit tumor cell proliferation in EGFR-dependent tumor cells. EGFR, a member of the EGFR receptor tyrosine kinase family, may be overexpressed on the cell surfaces of various tumor types.
  • Cevipabulin - A synthetic, water soluble tubulin-binding agent with potential antineoplastic activity. Cevipabulin appears to bind at the vinca-binding site on tubulin, but seems to act more similar to taxane-site binding agents in that it enhances tubulin polymerization and does not induce tubulin depolymerization. The disruption in microtubule dynamics may eventually inhibit cell division and reduce cellular growth.
  • Cevipabulin fumarate - The fumarate salt of cevipabulin, a synthetic, water soluble tubulin-binding agent with potential antineoplastic activity. Cevipabulin appears to bind at the vinca-binding site on tubulin, but seems to act more similar to taxane-site binding agents in that it enhances tubulin polymerization and does not induce tubulin depolymerization. The disruption in microtubule dynamics may eventually inhibit cell division and reduce cellular growth., a small, water soluble, synthetic tubulin-binding agent with potential antineoplastic activity. Cevipabulin appears to bind at the vinca-binding site on tubulin, but seems to act more similar to taxane-site binding agents in that it enhances tubulin polymerization and does not induce tubulin depolymerization. The disruption in microtubule dynamics may eventually inhibit cell division and may reduce cellular growth.
  • Cevipabulin succinate - The succinate salt form of cevipabulin, a synthetic, water soluble tubulin-binding agent with potential antineoplastic activity. Cevipabulin binds at the vinca-binding site on tubulin, but seems to act more similar to taxane-site binding agents in that it enhances tubulin polymerization and does not induce tubulin depolymerization. This stabilizes tubulin and prevents microtubule disassembly. The disruption in microtubule dynamics may eventually inhibit cell division and reduce cellular growth.
  • Cevostamab - A proprietary recombinant bispecific T-cell engager (BiTE) antibody composed of two single-chain variable fragments (scFv), one directed against the tumor-associated antigen (TAA) Fc receptor-like protein 5 (FCRH5; CD307; FCRL5; IRTA2; BXMAS1) and one that is directed against the CD3 antigen found on T-lymphocytes, with potential immunostimulating and antineoplastic activities. Upon administration of cevostamab, the bispecific antibody binds to both the CD3 antigen on cytotoxic T-lymphocytes (CTLs) and FCRH5 found on FCRH5-expressing tumor cells. This activates and crosslinks CTLs with FCRH5-expressing tumor cells, which results in the CTL-mediated cell death of FCRH5-expressing tumor cells. FCRH5, an immune receptor translocation-associated protein/Fc receptor homolog (IRTA/FCRH) family member and a B-cell lineage marker, is overexpressed on myeloma cells.
  • Cfms tyrosine kinase inhibitor arry-382 - A small molecule and orally available inhibitor of colony-stimulating factor-1 receptor (CSF1R; cFMS) with potential antineoplastic activity. cFMS tyrosine kinase inhibitor ARRY-382 binds to and inhibits the activity of cFMS. By preventing colony-stimulating factor-1 (CSF-1)-cFMS signaling, this agent may inhibit tumor cell proliferation in cFMS-overexpressing tumor cells. cFMS, a tyrosine kinase receptor, is overexpressed in certain tumor cell types and plays an essential role in macrophage differentiation and regulation of cell proliferation.
  • Chaparrin - A quassinoid phytochemical isolated from Simaba cedron and other plant species with potential antineoplastic activity. Chaparrin is a mixture of compounds that includes flavonoids, antioxidants, and nordihydroguaiaretic acid (NDGA). NDGA is an antioxidant and lipoxygenase inhibitor that promotes cell differentiation, induces G1 phase cell-cycle arrest, and causes apoptosis in certain cancer cell lines.
  • Chaparrinone - A quassinoid phytochemical isolated from Ailanthus integrifolia sp. calycina and other plant species with potential antineoplastic activity. Chaparrinone inhibits protein synthesis, has antimalarial properties, and is cytotoxic to some tumor cells.
  • Checkpoint kinase inhibitor azd7762 - A synthetic small molecule inhibitor of checkpoint kinases (Chks) with potential chemosensitizing activity. AZD7762 binds to and inhibits Chks, which may prevent cell cycle arrest and subsequent nucleotide excision repair in DNA-damaged tumor cells, resulting in tumor cell apoptosis. This agent may enhance the cytotoxicity of DNA-damaging agents. Chks are protein kinases that regulate either G1/S or G2/M transitions in the cell cycle. In the presence of DNA damage or incomplete DNA replication, Chks become activated and initiate cell cycle arrest to allow DNA repair or the completion of DNA replication.
  • Checkpoint kinase inhibitor xl844 - A synthetic small-molecule inhibitor of checkpoint kinases 1 and 2 (Chk1 and Chk2) with potential antineoplastic activity. XL844 binds to and inhibits Chks 1 and 2, resulting in inhibition of cell cycle arrest, progressive DNA damage, inhibition of DNA repair, and, ultimately, tumor cell apoptosis. This agent also inhibits vascular endothelial growth factor receptor 1 (VEGFR1) and vascular endothelial growth factor receptor 3 (VEGFR3), important mediators of tumor angiogenesis and lymphogenesis, respectively. In the presence of extensive damage or absence of timely repair, these checkpoint-signaling pathways may also trigger a pathway that effects apoptosis. Normal functions of Chks involve the initiation of cell-cycle arrest and the up-regulation of transcription genes involved with DNA excision repair and dNTP synthesis.
  • Chiauranib - An orally available, small molecule inhibitor of select serine-threonine kinases, including aurora kinase B (aurora B), vascular endothelial growth factor receptors (VEGFRs), stem cell factor receptor (c-KIT), and platelet-derived growth factor receptors (PDGFRs), with potential antineoplastic activity. Upon oral administration, chiauranib binds to and inhibits the activity of aurora B, VEGFRs, c-kit and PDGFRs, which may result in a decrease in the proliferation of tumor cells that overexpress these kinases. These kinases are overexpressed by a variety of cancer cell types.
  • Chimeric costimulatory converting receptor-modified nk-92 cells - A preparation of genetically-modified natural killer (NK) cells derived from the allogeneic NK-92 cell line that are transduced with an as of yet unspecified chimeric costimulatory converting receptor (CCCR) for cancer retargeting purposes, with potential cytolytic, immunomodulating and antineoplastic activities. Upon infusion of the CCCR-modified NK-92 cells, the redirected NK cells recognize and bind to tumor cells. This leads to the secretion and release of perforins, granzymes, cytokines and chemokines, which results in selective tumor cell lysis. The NK-92 cells are derived from a human cytotoxic cell line composed of allogeneic, activated, interleukin-2-(IL-2) dependent-NK cells from a 50-year old male patient with rapidly progressive non-Hodgkin's lymphoma. As NK-92 cells are devoid of killer inhibitory receptors (KIRs; also called killer cell immunoglobulin-like receptors), which are negative regulators of NK cell activity, cancer cells are unable to suppress the cancer cell killing ability of the NK-92 cells.
  • Chimeric humanized anti-cd47 antibody - A humanized, high-chimeric antibody targeting the human cell surface antigen CD47, with potential phagocytosis-inducing and antineoplastic activities. Upon administration, chimeric humanized anti-CD47 antibody selectively binds to CD47 expressed on tumor cells and blocks the interaction of CD47 with signal regulatory protein alpha (SIRPa), a protein expressed on phagocytic cells. This prevents CD47/SIRPa-mediated signaling and abrogates the CD47/SIRPa-mediated inhibition of phagocytosis. This induces pro-phagocytic signaling mediated by the binding of calreticulin (CRT), which is specifically expressed on the surface of tumor cells, to low-density lipoprotein (LDL) receptor-related protein-1 (LRP-1), expressed on macrophages. This results in macrophage activation and the specific phagocytosis of tumor cells. In addition, blocking CD47 signaling activates both an anti-tumor T-lymphocyte immune response and T cell-mediated killing of CD47-expressing tumor cells. CD47, also called integrin-associated protein (IAP), is a tumor-associated antigen (TAA) expressed on normal, healthy hematopoietic stem cells (HSC) and overexpressed on the surface of a variety of cancer cells. Expression of CD47, and its interaction with SIRPa, leads to the inhibition of macrophage activation and protects cancer cells from phagocytosis, which allows cancer cells to proliferate.
  • Chining decoction - A decoction of Liang Ge San, a traditional Chinese herbal medicine, with potential anti-inflammatory and anti-stomatitis activities. Although the complete mechanism of action through which the ChiNing decoction works has yet to be fully elucidated, upon oral administration, the active ingredients may inhibit the inflammatory response, possibly by reducing the levels of pro-inflammatory cytokines, such as interleukin 6 (IL-6) and tumor necrosis factor-alpha (TNFa), in the saliva. This may protect the oral mucosa against these inflammatory mediators, and may reduce and relieve radiation-induced stomatitis and the associated pain.
  • Chk1 inhibitor cct245737 - An orally bioavailable inhibitor of checkpoint kinase 1 (chk1), with potential antineoplastic and chemosensitization activities. Upon oral administration, chk1 inhibitor CCT245737 selectively binds to chk1, thereby preventing chk1 activity and abrogating the repair of damaged DNA. This may lead to an accumulation of damaged DNA, inhibition of cell cycle arrest, and induction of apoptosis. CCT245737 may potentiate the cytotoxicity of DNA-damaging agents and reverse tumor cell resistance to chemotherapeutic agents. Chk1, an adenosine triphosphate (ATP)-dependent serine/threonine kinase overexpressed in a variety of cancer cell types, mediates cell cycle checkpoint control and is essential for DNA repair; it plays a key role in resistance to chemotherapeutic agents by repairing DNA damage.
  • Chk1 inhibitor gdc-0425 - An orally bioavailable inhibitor of checkpoint kinase 1 (chk1), with potential antineoplastic and chemosensitization activities. Upon oral administration, chk1 inhibitor GDC-0425 selectively binds to chk1, thereby preventing activity of chk1 and abrogating the repair of damaged DNA. This may lead to an accumulation of damaged DNA, inhibition of cell cycle arrest, and induction of apoptosis. GDC-0425 may potentiate the cytotoxicity of DNA-damaging agents and reverse tumor cell resistance to chemotherapeutic agents. Chk1, an ATP-dependent serine/threonine kinase, mediates cell cycle checkpoint control, is essential for DNA repair, and plays a key role in resistance to chemotherapeutic agents.
  • Chk1 inhibitor gdc-0575 - A small molecule inhibitor of cell cycle checkpoint kinase 1 (Chk1), with potential chemosensitization activity. Chk1 inhibitor GDC-0575 specifically binds to and inhibits Chk1; this may result in tumor cells bypassing Chk1-dependent cell cycle arrest in the S and G2/M phases, which permits the cells to undergo DNA repair prior to entry into mitosis. Therefore, Chk1 inhibition may sensitize tumor cells to the DNA-damaging effects of certain chemotherapeutic agents. Chk1 is an ATP-dependent serine-threonine kinase that phosphorylates cdc25 phosphatases in response to DNA damage. This results in both inhibitory tyrosine phosphorylation of cyclin-dependent kinase (CDK)-cyclin complexes and cell cycle arrest, which facilitates DNA damage repair.
  • Chk1 inhibitor mk-8776 - An agent targeting cell cycle checkpoint kinase 1 (Chk1) with potential radiosensitization and chemosensitization activities. Chk1 inhibitor MK-8776 specifically binds to and inhibits Chk1, which may result in tumor cells bypassing Chk1-dependent cell cycle arrest in the S and G2/M phases to undergo DNA repair prior to entry into mitosis; tumor cells may thus be sensitized to the DNA-damaging effects of ionizing radiation and alkylating chemotherapeutic agents. Chk1 is an ATP-dependent serine-threonine kinase that in response to DNA damage phosphorylates cdc25 phosphatases, resulting in inhibitory tyrosine phosphorylation of CDK-cyclin complexes and cell cycle arrest.
  • Chk1 inhibitor pf-477736 - A proprietary compound targeting cell cycle checkpoint kinase 1 (chk1) with potential chemopotentiation activity. Chk1 inhibitor PF-477736 inhibits chk1, an ATP-dependent serine-threonine kinase that is a key component in the DNA replication-monitoring S/G2 checkpoint system. By overriding the last checkpoint defense against DNA damaging agent-induced lethal damage, chk1 inhibitor PF-477736 may potentiate the antitumor efficacy of various chemotherapeutic agents against tumor cells with intrinsic checkpoint defects.
  • Chlorambucil - An orally-active antineoplastic aromatic nitrogen mustard. Chlorambucil alkylates and cross-links DNA during all phases of the cell cycle, resulting in disruption of DNA function, cell cycle arrest, and apoptosis.
  • Chlorodihydropyrimidine - A pyrimidine derivative with antitumor activity. Chlorodihydropyrimidine competitively and reversibly inhibits dihydropyrimidine dehydrogenase, a rate-limiting enzyme in the catabolism of fluoropyrimidines thereby blocking the degradation of the fluoropyrimidines.
  • Chloroquine - A 4-aminoquinoline with antimalarial, anti-inflammatory, and potential chemosensitization and radiosensitization activities. Although the mechanism is not well understood, chloroquine is shown to inhibit the parasitic enzyme heme polymerase that converts the toxic heme into non-toxic hemazoin, thereby resulting in the accumulation of toxic heme within the parasite. This agent may also interfere with the biosynthesis of nucleic acids. Chloroquine's potential chemosensitizing and radiosensitizing activities in cancer may be related to its inhibition of autophagy, a cellular mechanism involving lysosomal degradation that minimizes the production of reactive oxygen species (ROS) related to tumor reoxygenation and tumor exposure to chemotherapeutic agents and radiation.
  • Chloroquinoxaline sulfonamide - A chlorinated heterocyclic sulfanilamide with potential antineoplastic activity and potential immunosuppressive activity. Chloroquinoxaline sulfonamide poisons topoisomerase II alpha and topoisomerase II beta, thereby causing double-stranded breaks in DNA, accumulation of unrepaired DNA, and apoptosis. This agent also exhibits lymphotoxicity by inhibiting lymphocyte activation in a cell cycle-specific manner.
  • Chlorotoxin - A neurotoxin with potential anticancer property. Chlorotoxin (CTX) is a 36-amino acid peptide found in the venom of the deathstalker scorpion, and a chloride channel blocker. This toxin binds preferentially to glioma cells via the transmembrane endopeptidase matrix metalloproteinase-2 (MMP-2), and thereby prevents the spread of tumor cells. MMP-2 is specifically up-regulated in gliomas and related cancers, but is not normally expressed in brain.
  • Chlorotoxin (eq)-cd28-cd3zeta-cd19t-expressing car t-lymphocytes - A preparation of genetically modified T-lymphocytes transduced with a lentiviral vector expressing a chimeric antigen receptor (CAR) comprised of a CD28 co-stimulatory signaling domain fused to the zeta chain of the TCR/CD3 complex (CD3zeta), a truncated form of CD19 (CD19t), an immunoglobulin (Ig) G4-Fc (EQ) spacer, and a peptide derived from chlorotoxin (CLTX), with potential imaging and antineoplastic activities. Upon administration, chlorotoxin (EQ)-CD28-CD3zeta-CD19t-expressing CAR T-lymphocytes are re-directed to specific tumor cells in the brain inducing selective toxicity in these tumor cells. CLTX, a 36-amino acid peptide found in the venom of the deathstalker scorpion (Leiurus quinquestriatus) and a chloride channel blocker, preferentially binds to glioma (and other neuroectodermal origin) cells via membrane bound forms of the endopeptidase matrix metalloproteinase-2 (MMP-2). This may direct the T-lymphocytes to and induce selective toxicity in MMP-2-expressing tumor cells. Additionally, binding to MMP-2 on glioma cells may both interfere with transmembrane chloride exchange and inhibit proteolytic extracellular matrix remodeling by MMP-2, which may further limit the spread of these tumor cells. MMP-2 is specifically upregulated in gliomas and related cancers, but is not normally expressed in brain. The CD28 co-stimulatory molecule signaling domain enhances activation and signaling; its inclusion may increase proliferation of T-cells and antitumor activity compared to the inclusion of the CD3 zeta chain alone. IgG4-Fc (EQ) contains two point mutations in its spacer region which prevents recognition of the CAR by Fc receptors (FcRs) without altering the ability of the CAR to mediate antigen-specific lysis. CD19t, which lacks the cytoplasmic signaling tail, provides a non-immunogenic surface marker that allows for accurate measurement, efficient cell tracking and/or imaging of the therapeutic T-cells in vivo following adoptive transfer. Additionally, co-expression of CD19t functions as a "suicide" switch via clinically available antibodies or immunotoxins which can be used to selectively eliminate the genetically modified cells.
  • Chlorozotocin - A glucose-linked chloroethylnitrosourea with potential antineoplastic activity. Chlorozotocin alkylates DNA and proteins, induces the formation of interstrand DNA and DNA-protein crosslinks, and causes DNA strand breakage, thereby damaging DNA and resulting in cell death. This agent has been shown to exhibit antitumor and immunomodulatory effects in cell lines and animal models. Chlorozotocin is a mutagen and is less myelotoxic than other nitrosoureas.
  • Choline kinase alpha inhibitor tcd-717 - A small-molecule inhibitor of choline kinase alpha (CHKA), with potential antineoplastic activity. TCD-717 targets and binds to CHKA, an enzyme that plays a key role in the synthesis of phosphatidylcholine, the major phospholipid in eukaryotic cell membranes. Blockade of this enzyme induces cells to activate a different route for phospholipid production which causes a toxic effect and eventually leads to cell destruction. CHKA, overexpressed in human cancer cells while only minimally expressed in normal cells, appears to play a significant role in cellular proliferation, evasion of apoptosis, increased cell motility and metastasis.
  • Chp-her-2 peptide vaccine - A peptide vaccine, containing nanoparticles of cholesteryl hydrophobized pullulan (CHP) complexed with the tumor-associated antigen HER-2/neu (ErbB-2), with potential antineoplastic activity. Her-2/neu, a member of the epidermal growth factor receptor (EGFR) family of tyrosine kinases, is overexpressed in various tumors, including breast, ovarian, and gastric cancers. Vaccination with CHP-HER-2 peptide vaccine may stimulate the host immune system to mount a humoral as well as a cytotoxic T-cell response against tumor cells expressing the HER-2/neu antigen. This results in an inhibition of tumor cell proliferation and tumor cell death. The self-aggregating CHP, composed of a pullulan backbone and cholesterol branches, forms stable colloidal nanoparticles in water.
  • Chp-ny-eso-1 peptide vaccine imf-001 - A peptide cancer vaccine containing nanoparticles of cholesteryl hydrophobized pullulan (CHP) complexed with the cancer-testis antigen NY-ESO-1 protein, with potential immunostimulating and antineoplastic activities. Upon administration, CHP-NY-ESO-1 peptide vaccine IMF-001 may stimulate the host immune system to mount a humoral and cytotoxic T-cell response against tumor cells expressing NY-ESO-1 antigen, resulting in tumor cell lysis. The self-aggregating CHP, composed of a pullulan backbone and cholesterol branches, forms stable colloidal nanoparticles in water. NY-ESO-1, an antigen found in normal testis, is upregulated in various cancers, including bladder, breast, hepatocellular, melanoma, and prostate cancers.
  • Chromomycin a3 - A glycosidic antineoplastic antibiotic isolated from the bacterium Streptomyces griseus. Chromomycin A3 reversibly binds to guanine-cytosine (G-C) base pairs in the minor groove of DNA, thereby inhibiting RNA synthesis. This agent is used as a fluorescent chromosome dye.
  • Chrysanthemum morifolium/ganoderma lucidum/glycyrrhiza glabra/isatis indigotica/panax pseudoginseng/rabdosia rubescens/scutellaria baicalensis/serona repens supplement - An herbal mixture with potential antineoplastic effects. PC-SPES, an herbal supplement containing extracts from 8 herbs including Chrysanthemum morifolium, Ganoderma lucidum (a root fungus), Glycyrrhiza glabra (Spanish liquorice), Isatis indigotica, Panax pseudoginseng, Rabdosia rubescens, Scutellaria baicalensis, and Serona repens (saw palmetto), with potential antineoplastic and antiproliferative effects, specifically in prostate cancer cells. Its exact pharmacology is not fully understood due to the complexity of the herbal mixture and may involve multiple metabolic pathways. Exposure to PC-SPES in vitro has resulted in a decreased expression of genes encoding cell cycle regulatory proteins as well as an upregulation of genes that modulate apoptosis in both androgen-dependent and androgen-independent cells. The PC in the acronym PC-SPES stands for Prostate Cancer, while SPES is the Latin word for hope.
  • Cibisatamab - An anti-carcinoembryonic antigen (CEA)/anti-CD3 bispecific monoclonal antibody with potential antineoplastic activity. Cibisatamab contains two antigen-recognition sites: one for human CD3, a T-cell surface antigen, and one for human CEA, a tumor-associated antigen that is specifically expressed on certain tumor cells. Upon intravenous administration, cibisatamab binds to both T-cells and CEA-expressing tumor cells, which cross-links the T-cells with the tumor cells. This may result in a potent cytotoxic T-lymphocyte (CTL) response against CEA-expressing tumor cells. CEA is overexpressed in many cancer cell types.
  • Ciclopirox prodrug cpx-pom - A phosphoryloxymethyl (POM) ester-based prodrug of ciclopirox (CPX), a synthetic, broad-spectrum antifungal agent with antibacterial, anti-inflammatory and potential antineoplastic activities. Upon intravenous administration of CPX-POM, the POM moiety is cleaved off by phosphatases and the active metabolite CPX is released. Although its exact anticancer mechanism is not yet fully elucidated, CPX has been shown to inhibit tumor cell proliferation, induce apoptosis, and reduce tumor cell mobility in certain cancer types. CPX inhibits Notch1 activation and inhibits the Notch1-mediated signaling pathway, which is upregulated in many cancer cell types. This inhibits Notch downstream target proteins, inhibits the expression of gamma-secretase complex proteins, and prevents proliferation in susceptible cancer cells. CPX inhibits the iron-containing enzymes, catalase and peroxidase, which facilitate the decomposition of hydrogen peroxide, a reactive oxygen species (ROS) involved in oxidative stress. CPX also inhibits the iron-dependent enzyme ribonucleotide reductase, which is essential in DNA synthesis. CPX downregulates protein expression of cyclin D1 and cyclin E1, as well as their enzymatic counterparts cyclin-dependent kinases 4 and 2 (CDK4 and CDK2), which may inhibit tumor cell proliferation by slowing cell cycle progression from G1/G0 to S phase. Further, CPX may induce apoptosis by downregulating the expression of anti-apoptotic proteins, Bcl-xL and survivin, and increasing cleavage of Bcl-2. Additionally, CPX may inhibit tumor cell proliferation, survival and motility by inhibiting the phosphorylation of p70 S6 kinase 1 (S6K1) and eukaryotic initiation factor 4E binding protein 1 (4E-BP1), two downstream effector molecules of the mammalian target of rapamycin complex 1 (mTORC1). The CPX-POM prodrug improves the solubility of CPX and increases systemic efficacy.
  • Cidan herbal capsule - A capsule-based formulation containing artificial bezoar, Strychni pulveratum (strychnos powder), camphol alcohol (borneol or borneo camphor) and extracts from Zedoary rhizome (Rhizoma curcumae), Pseudobulbus cremastrae seu pleiones (dried pseudobulb of Cremastra appendiculata), Yatantzu (seed of Brucca javanica), beehive, Bombyx mori (Bombyx batryticatus or silkworm), Danshen (dried root of Salvia miltiorrhiza or red sage root), Radix astragali, and Angelica, with potential antineoplastic activity. Upon oral administration of the cidan herbal capsule, the active ingredients in the plant extracts may induce tumor cell apoptosis and reduce tumor cell proliferation.
  • Ciforadenant - A small molecule immune checkpoint inhibitor of the adenosine A2A receptor (ADORA2A) with potential antineoplastic activity. Upon oral administration, ciforadenant binds to adenosine A2A receptors expressed on the surface of immune cells, including T-lymphocytes, natural killer (NK) cells, macrophages and dendritic cells (DCs). This prevents tumor-released adenosine from interacting with the A2A receptors on these key immune surveillance cells, thereby abrogating adenosine-induced immunosuppression in the tumor microenvironment. This may stimulate anti-tumor immune responses, resulting in tumor regression.
  • Cilengitide - A cyclic Arg-Gly-Asp peptide with potential antineoplastic activity. Cilengitide binds to and inhibits the activities of the alpha(v)beta(3) and alpha(v)beta(5) integrins, thereby inhibiting endothelial cell-cell interactions, endothelial cell-matrix interactions, and angiogenesis.
  • Ciltacabtagene autoleucel - A preparation of autologous T-lymphocytes that are transduced, ex vivo, with LCAR-B38M, a lentiviral vector expressing a chimeric antigen receptor (CAR) containing two bispecific anti-B-cell maturation antigen (BCMA) variable fragments of llama heavy-chain murine antibodies fused to the signaling domain of 4-1BB (CD137), with potential immunostimulating and antineoplastic activities. The antigen-binding region of the CAR is a non-scFv structure targeting two distinct regions of BCMA. Upon intravenous administration back into the patient, ciltacabtagene autoleucel are directed to cells expressing BCMA, bind to two different epitopes on BCMA and induce selective toxicity in BCMA-expressing tumor cells. BCMA, a tumor-associated antigen (TAA) and a receptor for both a proliferation-inducing ligand (APRIL) and B-cell activating factor (BAFF), is a member of the tumor necrosis factor receptor superfamily (TNFRSF) and plays a key role in plasma cell survival. BCMA is overexpressed on malignant plasma cells.
  • Cimetidine - A histamine H(2)-receptor antagonist. Enhancing anti-tumor cell-mediated responses, cimetidine blocks histamine's ability to stimulate suppressor T lymphocyte activity and to inhibit natural killer (NK) cell activity and interleukin-2 production. Cimetidine also may inhibit tumor growth by suppressing histamine's growth-factor activity and blocking histamine-induced stimulation of vascular endothelial growth factor (VEGF), a pro-angiogenic growth factor.
  • Cinacalcet hydrochloride - The orally bioavailable hydrochloride salt of the calcimimetic cinacalcet. Cinacalcet increases the sensitivity of calcium-sensing receptors on chief cells in the parathyroid gland to extracellular calcium, thereby reducing parathyroid hormone (PTH) secretion. A reduction in PTH levels inhibits osteoclast activity, which may result in a decrease in cortical bone turnover and bone fibrosis, and normalization of serum calcium and phosphorus levels. In addition, by reducing PTH levels, cinacalcet may reduce PSA levels; PTH appears to raise PSA levels and may increase prostate cancer cell growth.
  • Cinobufagin - A bufadienolide compound extracted from the dried venom secreted by the parotid glands of toads and one of the glycosides in the traditional Chinese medicine ChanSu, with potential antineoplastic activity. Although the mechanism of action of cinobufagin is still under investigation, it has been found to suppress cancer cell proliferation and cause apoptosis in cancer cells via a sequence of apoptotic modulators that include mitochondrial Bax and cytosolic chromosome c, and caspases 3, 8, and 9. Possible upstream mediators of cinobufagin-induced apoptosis include Fas and p53.
  • Cinobufotalin - A bufadienolide isolated from toad venom and utilized in traditional Chinese medicine (TCM) for its cardiotonic, diuretic and hemostatic effects, with potential cytotoxic and antineoplastic activities. Upon administration and although the exact mechanism of action(s) (MoAs) through which this agent exerts its effects have yet to be fully discovered, cinobufotalin causes DNA fragmentation, decreases mitochondrial membrane potential (MMP), increases intracellular calcium (Ca2+) ion concentrations and reactive oxygen species (ROS) production, upregulates Fas protein and activates cytochrome C, various caspases, Bid and Bax. This causes cell cycle arrest, induces apoptosis and inhibits tumor cell growth and survival. In addition, cinobufotalin inhibits the activity of sphingosine kinase 1 (SphK1) and induces pro-apoptotic ceramide production, which further promotes tumor cell apoptosis. Cinobufotalin also induces mitochondrial protein cyclophilin D (Cyp-D)-dependent opening of the mitochondrial permeability transition pore (mPTP), which may contribute to cinobufotalin-induced non-apoptotic death of certain tumor cells.
  • Cinrebafusp alfa - A bivalent, bispecific fusion protein comprised of an anti-human epidermal growth factor receptor (HER2) monoclonal antibody linked to a CD137-targeting anticalin with potential immunostimulatory and antineoplastic activities. Upon administration of cinrebafusp alfa, CD137 clustering is promoted by bridging CD137-positive T-cells with HER2-positive tumor cells, leading to the recruitment of tumor antigen-specific cytotoxic T-lymphocytes (CTLs). This may result in potent CTL-mediated lysis of HER2-expressing tumor cells. HER2 plays a key role in tumor cell proliferation and tumor vascularization. CD137 is a costimulatory immunoreceptor and a member of the tumor necrosis factor receptor superfamily (TNFRSF). Anticalins are synthetic antigen-binding proteins derived from lipocalins. Structurally dissimilar to antibodies, anticalins are able to bind to smaller antigens and exhibit improved tissue penetration.
  • Cintirorgon - An orally bioavailable agonist of retinoic acid-related orphan receptor gamma (RORg), with potential immunomodulatory and antineoplastic activities. Upon oral administration of cintirorgon, this agent selectively binds to the nuclear receptor transcription factor RORg, forming a receptor complex that translocates to the nucleus, and binds to ROR response elements (ROREs), enhancing the function, proliferation and survival of type 17 T-cells, including Th17 (helper T-cells) and Tc17 (cytotoxic T-cells). This may increase the expression of co-stimulatory molecules and decrease the expression of co-inhibitory molecules on T-cells leading to increased production of cytokines and chemokines by T-cells, decreased proliferation of regulatory T-cells (Tregs), and abrogation of tumor-induced immunosuppression. This ultimately induces a T-cell-mediated immune response against cancer cells and leads to a reduction in tumor cell growth. RORg, the nuclear receptor transcription factor that is involved in Th17/Tc17 differentiation, plays a key role in immune activation.
  • Cintredekin besudotox - A recombinant chimeric protein with potent antitumor activity. Cintredekin besudotox is composed of interleukin-13 (IL13), a pleiotropic immunoregulatory cytokine, linked to a mutated form of pseudomonas exotoxin A; this agent targets and kills tumor cells that express the IL13 receptor (IL13R).The IL13 moiety attaches to the IL13R on the tumor cell membrane, facilitating the entry of the exotoxin. The exotoxin moiety induces caspase-mediated apoptosis of tumor cells via a mechanism involving mitochondrial damage; it also catalyzes the transfer of ADP ribose from nicotinamide adenine dinucleotide (NAD) to elongation factor-2 in eukaryotic cells, thereby inactivating elongation factor 2 and inhibiting protein synthesis.
  • Cirmtuzumab - A humanized monoclonal antibody against the extracellular domain of the human receptor tyrosine kinase-like orphan receptor 1 (ROR1), with potential antineoplastic activity. Upon administration, cirmtuzumab binds to ROR1 and blocks ROR1-mediated signaling. This prevents tumor cell proliferation in cancer cells overexpressing ROR1. ROR1, also known as neurotrophic tyrosine kinase, receptor-related 1 (NTRKR1), is normally expressed during embryogenesis. It is overexpressed in certain leukemias and solid tumors, but minimally expressed in healthy cells.
  • Cisplatin - An alkylating-like inorganic platinum agent (cis-diamminedichloroplatinum) with antineoplastic activity. Cisplatin forms highly reactive, charged, platinum complexes which bind to nucleophilic groups such as GC-rich sites in DNA inducing intrastrand and interstrand DNA cross-links, as well as DNA-protein cross-links. These cross-links result in apoptosis and cell growth inhibition.
  • Cisplatin liposomal - A synthetic formulation in which the antineoplastic agent cisplatin is encapsulated in lipids. Cisplatin liposomal consists of small aggregates of cisplatin covered by a single lipid bilayer. Encasement in liposomes improves cisplatin's tumor bioavailability and toxicity profile. Liposomal encapsulation does not affect the pharmacological properties of cisplatin directly. Cisplatin forms highly reactive, charged, platinum complexes which bind to nucleophilic groups such as GC-rich sites in DNA, inducing intrastrand and interstrand DNA cross-links, as well as DNA-protein cross-links. These cross-links result in apoptosis and cell growth inhibition.
  • Cisplatin/vinblastine/cell penetration enhancer formulation int230-6 - A formulation composed of three agents in a fixed ratio: two chemotherapeutic agents, the platinum compound cisplatin and the vinca alkaloid vinblastine, and a proprietary amphiphilic excipient that acts as a penetration enhancer, with potential antineoplastic activity. Upon intra-tumoral (IT) injection of INT230-6, the dispersion/cell penetration enhancer excipient of INT230-6 facilitates dispersion of the two drugs throughout the tumor tissue and enables increased cellular uptake of these agents into tumor cells. Once inside the cell, cisplatin forms highly reactive, charged, platinum complexes which bind to nucleophilic groups such as GC-rich sites in DNA, which results in apoptosis and cell growth inhibition. Vinblastine kills the tumor cells through binding to tubulin and thereby inhibits microtubule formation, resulting in disruption of the mitotic spindle assembly and cell cycle arrest of tumor. In addition, the tumor cell killing leads to recruitment of dendritic cells (DCs) and induces a tumor-specific T-cell-mediated immune response that attacks both the injected tumor and distant tumor lesions. Local administration of both cisplatin and vinblastine, without the diffusion/penetration enhancer, results in to poor diffusion and a lack of cellular uptake of the agents; INT230-6 increases the intracellular concentration of cisplatin and vinblastine, thereby improving efficacy.
  • Cisplatin-e therapeutic implant - An injectable gel comprised of a collagen matrix containing the inorganic platinum (Pt) agent cisplatin and the sympathomimetic agent epinephrine with potential antineoplastic activity. After intratumoral injection, cisplatin forms highly reactive, positively charged, platinum complexes, which covalently bind to nucleophilic groups in DNA, preferably at the N7 position of guanine bases. This induces both intra- and inter-strand DNA cross-links. In addition, cisplatin forms DNA-Pt-protein cross-links. Cross-link formation results in both the induction of apoptosis and cell growth inhibition. Epinephrine, a potent vasoconstrictor, is added to the gel to both enhance the penetration of cisplatin into tumor tissue and reduce its dispersion into the surrounding tissues. Intratumoral injection of cisplatin-E therapeutic implant may increase local chemotherapeutic efficacy, as compared to the systemic administration of cisplatin, while reducing its systemic toxicity.
  • Cis-urocanic acid - A derivative of the amino acid histidine, formed in the mammalian skin from trans-urocanic acid upon ultraviolet radiation, and protodynamic agent, with potential anti-inflammatory and antiproliferative activity. Upon intravesical instillation of cis-urocanic acid (cis-UCA), this agent is protonated at the imidazolyl moiety in the mildly acidic extracellular tumor environment and penetrates into the cancer cell. Once inside the cell and due to the slightly alkaline pH inside the tumor cell, cis-UCA is deprotonated, i.e. the imidazolyl proton is released into the cytosol which eventually raises the intracellular acidity. This acidification impairs many cellular processes, such as metabolic activity, and may lead to cell cycle arrest, an induction of cellular apoptosis and necrotic cell death. In addition, cis-UCA enhances ERK and JNK signaling pathways by inhibiting the activity of serine/threonine and tyrosine phosphatases.
  • Citarinostat - An orally available histone deacetylase (HDAC) inhibitor, with potential antineoplastic activity. Upon oral administration, citarinostat inhibits the activity of HDACs; this results in an accumulation of highly acetylated chromatin histones, the induction of chromatin remodeling and an altered pattern of gene expression. This leads to the inhibition of tumor oncogene transcription, and the selective transcription of tumor suppressor genes, which inhibit tumor cell division and induce tumor cell apoptosis. HDAC, an enzyme upregulated in many tumor types, deacetylates chromatin histone proteins.
  • Citatuzumab bogatox - A fusion protein immunotoxin consisting of a humanized, single-chain monoclonal antibody Fab fragment specific for the epithelial cell adhesion molecule (EpCAM) conjugated with a modified bouganin cytotoxin with potential antineoplastic activity. Citatuzumab bogatox binds to EpCAM, delivering modified bouganin cytotoxin directly to EpCam-positive tumor cells, which may result in the inhibition of tumor cell protein synthesis and tumor cell death. EpCAM, a cell surface protein, is expressed by a variety of tumor cells and is frequently found in head and neck cancers. Bouganin is a plant-derived ribosome-inactivating protein (RIP), a toxic plant N-glycosidase that depurinates the universally conserved alpha-sarcin loop of ribosomal rRNA, inactivating the ribosome and preventing protein synthesis. Compared to unmodified bouganins, modified bouganins may have a reduced propensity to activate human T cells.
  • Cixutumumab - A fully human IgG1 monoclonal antibody directed against the human insulin-like growth factor-1 receptor (IGF-1R) with potential antineoplastic activity. Cixutumumab selectively binds to membrane-bound IGF-1R, thereby preventing the binding of the natural ligand IGF-1 and the subsequent activation of PI3K/AKT signaling pathway. Downregulation of the PI3K/AKT survival pathway may result in the induction of cancer cell apoptosis and may decrease cancer cellular proliferation. IGF-1R, a receptor tyrosine kinase of the insulin receptor superfamily overexpressed by many cancer cell types, stimulates cell proliferation, enables oncogenic transformation, and suppresses apoptosis; IGF-1R signaling has been implicated in tumorigenesis and metastasis.
  • Ck1alpha/cdk7/cdk9 inhibitor btx-a51 - The ditosylated salt of A51, an orally bioavailable inhibitor of casein kinase 1alpha (CK1alpha) and cyclin-dependent kinases 7 and 9 (CDK7 and CDK9), with potential antineoplastic activity. Upon administration, BTX-A51 binds to and inhibits the activity of CK1alpha, CDK7, and CDK9. Blocking the phosphorylation and kinase activity of CK1alpha prevents the enhanced binding of murine double minute X (MDMX) to p53, the formation of CK1alpha and MDM2 complex, and the resulting inhibition of p53. This induces p53-mediated cell cycle arrest, slowing tumor cell proliferation. Blocking the phosphorylation and kinase activity of CDK7 and CDK9 prevents the positive transcription elongation factor b (PTEFb)-mediated activation of RNA polymerase II (RNA Pol II) and leads to the inhibition of gene transcription of various anti-apoptotic proteins. This also induces cell cycle arrest and apoptosis, slowing tumor cell proliferation. CK1alpha, a serine/threonine kinase and a leukemic stem cell target, acts as a tumor suppressor in several cancers through the negative regulation of Wnt/beta-catenin signaling and p53. It negatively regulates p53 by phosphorylating MDMX, thus enhancing binding of MDMX to p53, as well as by forming a complex with MDM2. CDK7, a serine/threonine kinase, plays a role in controlling cell cycle progression, transcriptional regulation, and promotes the expression of key oncogenes such as c-Myc through the phosphorylation of RNA Pol II. CDK9, also a serine/threonine kinase, regulates elongation of transcription through phosphorylation of RNA Pol II at serine 2 (p-Ser2-RNAPII). It is upregulated in various tumor cell types and plays a key role in the regulation of RNA Pol II-mediated transcription of anti-apoptotic proteins. Tumor cells are dependent on anti-apoptotic proteins for their survival.
  • Ck2-targeting synthetic peptide cigb-300 - A synthetic peptide targeting the substrates of casein kinase 2 (CK2), with potential antineoplastic activity. Upon administration and nucleolar localization, CK2-targeting synthetic peptide CIGB-300 binds to phosphoacceptor sites on the CK2 substrates, in particular the oncoprotein nucleophosmin (B23 or NPM1). This blocks the activation of B23 and induces apoptosis, thereby inhibiting tumor cell growth in susceptible tumor cells. CK2, a protein kinase often overexpressed in a variety of cancer cell types, appears to be correlated with malignant transformation, tumor growth and survival. Overexpression of B23 has been correlated with increased cellular growth and proliferation as well as inhibition of differentiation and apoptosis.
  • C-kit inhibitor plx9486 - An orally bioavailable protein tyrosine kinase inhibitor of mutated forms of the tumor-associated antigen mast/stem cell factor receptor c-Kit (SCFR), with potential antineoplastic activity. Upon oral administration, c-Kit inhibitor PLX9486 binds to and inhibits specific c-Kit mutants. This may result in an inhibition of tumor cell proliferation in cancer cell types that overexpress these c-Kit mutations. c-Kit, a transmembrane protein and receptor tyrosine kinase, is overexpressed in solid tumors and hematological malignancies; it plays a key role in the regulation of cell differentiation and proliferation.
  • Cl 246738 - An immunomodulator, 3,6-bis(2-piperidinoethoxy) acridine trihydrochloride, used in a phase I study for possible immunostimulatory effects in colorectal cancer. (NCI)
  • Cladribine - A purine nucleoside antimetabolite analogue. Cladribine triphosphate, a phosphorylated metabolite of cladribine, incorporates into DNA, resulting in single-strand breaks in DNA, depletion of nicotinamide adenine dinucleotide (NAD) and adenosine triphosphate (ATP), and apoptosis. Because this agent is resistant to adenosine deaminase, an enzyme that inactivates some antineoplastic agents, it is selectively toxic to lymphocytes and monocytes which exhibit little deoxynucleotide deaminase activity.
  • Clanfenur - A substituted benzoylphenylurea and an analogue of the pesticide diflubenzuron with potential antineoplastic activity. Unlike most of the anti-cancer drugs causing bone marrow suppression, clanfenur stimulates hematopoiesis both in vivo and in vitro.
  • Clarithromycin - A semisynthetic 14-membered ring macrolide antibiotic. Clarithromycin binds to the 50S ribosomal subunit and inhibits RNA-dependent protein synthesis in susceptible organisms. Clarithromycin has been shown to eradicate gastric MALT (mucosa-associated lymphoid tissue) lymphomas, presumably due to the eradication of tumorigenic Helicobacter pylori infection. This agent also acts as a biological response modulator, possibly inhibiting angiogenesis and tumor growth through alterations in growth factor expression.
  • Class 1/4 histone deacetylase inhibitor oki-179 - An orally bioavailable inhibitor of the histone deacetylase (HDAC) subtypes 1 and 4, with potential antineoplastic activity. Upon administration, class 1/4 HDAC inhibitor OKI-179 targets, binds to and inhibits the activity of HDAC1/4. This results in an accumulation of highly acetylated chromatin histones, the induction of chromatin remodeling and an altered pattern of gene expression. This consequently results in a selective transcription of tumor suppressor genes, tumor suppressor protein-mediated inhibition of tumor cell division and an induction of apoptosis in tumor cells that overexpress HDAC1/4. HDAC, which is upregulated in many tumor cell types, deacetylates chromatin histone proteins and plays a key role in transcriptional regulation and cell cycle progression.
  • Clioquinol - An orally bioavailable, lipophilic, copper-binding, halogenated 8-hydroxyquinoline with antifungal, antiparasitic and potential antitumor activities. Clioquinol forms a stable chelate with copper (copper (II) ions), which inhibits the chymotrypsin-like activity of the proteasome; consequently, ubiquitinated proteins may accumulate in tumor cells, followed by tumor cell apoptosis and the inhibition of tumor angiogenesis. In addition, the clioquinol-copper complex appears to decrease the expression of androgen receptors (AR) in human copper-enriched prostate cancer cells. Serum levels of copper are often elevated in patients with cancer; copper chelation may inhibit copper-dependent endothelial cell proliferation and tumor secretion of angiogenic factors.
  • Clivatuzumab - A humanized monoclonal antibody directed against the pancreatic cancer antigen MUC1, with potential antineoplastic activity. Clivatuzumab binds to tumor cells expressing the MUC1 antigen and prevents MUC1-mediated signaling. MUC1, a mucin antigen, is overexpressed in pancreatic cancer but not in normal, healthy pancreatic cells.
  • Clofarabine - A second generation purine nucleoside analog with antineoplastic activity. Clofarabine is phosphorylated intracellularly to the cytotoxic active 5'-triphosphate metabolite, which inhibits the enzymatic activities of ribonucleotide reductase and DNA polymerase, resulting in inhibition of DNA repair and synthesis of DNA and RNA. This nucleoside analog also disrupts mitochondrial function and membrane integrity, resulting in the release of pre-apoptotic factors, including cytochrome C and apoptotic-inducing factors, which activate apoptosis.
  • Clomesone - The 2-chloroethyl ester of (methylsulfonyl) methanesulfonic acid with potential antineoplastic effects. Acting as a chloroethylating agent, clomesone induces the formation of DNA interstrand crosslinks in some cell lines, and exhibits antitumor activity in some animal models. Alkylating agents exert cytotoxic and, in some cases, chemotherapeutic effects by transferring alkyl groups to DNA, thereby damaging DNA and interfering with DNA synthesis and cell division.
  • Clomiphene - A triphenylethylene nonsteroidal ovulatory stimulant evaluated for antineoplastic activity against breast cancer. Clomiphene has both estrogenic and anti-estrogenic activities that compete with estrogen for binding at estrogen receptor sites in target tissues. This agent causes the release of the pituitary gonadotropins follicle stimulating hormone (FSH) and luteinizing hormone (LH), leading to ovulation.
  • Clomiphene citrate - The citrate salt form of clomiphene, a triphenylethylene nonsteroidal ovulatory stimulant evaluated for antineoplastic activity against breast cancer. Clomiphene has both estrogenic and anti-estrogenic activities that compete with estrogen for binding at estrogen receptor sites in target tissues. This agent causes the release of the pituitary gonadotropins follicle stimulating hormone (FSH) and luteinizing hormone (LH), leading to ovulation.
  • Clostridium novyi-nt spores - Spores of the bacterial strain Clostridium novyi-NT, the attenuated obligate anaerobic C. novyi, with potential immunostimulating, bacteriolytic, and antineoplastic activities. Upon intravenous administration, Clostridium novyi-NT spores germinate exclusively in hypoxic tissue, such as avascular regions of tumors. Germination results in lysis and destruction of surrounding viable tumor cells. Due to their anaerobic nature, C. novyi-NT spores do not proliferate in oxygenated tumor regions. However, this agent may stimulate the immune system to exert a cellular immune response, resulting in additional killing of tumor cells not lysed by the bacteria, including those in the well-oxygenated tumor area.
  • Cmet car-mrna electroporated autologous t lymphocytes - A preparation of autologous T-lymphocytes that have been electroporated with an mRNA encoding a chimeric antigen receptor (CAR) consisting of an anti-human hepatocyte growth factor receptor (HGFR or cMet) scFv (single chain variable fragment) and the zeta chain of the TCR/CD3 complex (CD3-zeta) coupled to the co-stimulatory molecule 4-1BB (CD137), with potential antineoplastic activities. Upon intratumoral administration, cMet CAR-mRNA electroporated autologous T lymphocytes direct T-cells to cMet-expressing tumor cells, which induces a selective toxicity in cMet-expressing tumor cells and causes tumor cell lysis. The 4-1BB co-stimulatory molecule signaling domain enhances activation and signaling after recognition of cMet. The inclusion of the 4-1BB signaling domain may increase the antitumor activity as compared to the inclusion of the CD3-zeta chain alone. The mRNA CAR is expressed for a limited amount of time, which can prevent serious, unforeseen side effects. cMet, a receptor tyrosine kinase overexpressed or mutated in many tumor cell types, plays a key role in cancer cell growth, survival, angiogenesis, invasion, and metastasis.
  • C-met inhibitor abn401 - An orally bioavailable, highly selective inhibitor of the oncoprotein c-Met (hepatocyte growth factor receptor; HGFR), with potential antineoplastic activity. Upon oral administration, ABN401 targets and binds to the c-Met protein, prevents c-Met phosphorylation and disrupts c-Met-dependent signal transduction pathways. This may induce cell death in tumor cells overexpressing c-Met protein or expressing constitutively activated c-Met protein. c-Met protein is overexpressed or mutated in many tumor cell types and plays key roles in tumor cell proliferation, survival, invasion, metastasis, and tumor angiogenesis.
  • C-met inhibitor al2846 - An orally bioavailable small molecule inhibitor of the oncoprotein c-Met (hepatocyte growth factor receptor; HGFR), with potential antineoplastic activity. Upon oral administration AL2846 targets and binds to the c-Met protein, prevents c-Met phosphorylation and disrupts c-Met-dependent signal transduction pathways. This may induce cell death in tumor cells overexpressing c-Met protein or expressing constitutively activated c-Met protein. c-Met protein is overexpressed or mutated in many tumor cell types and plays key roles in tumor cell proliferation, survival, invasion, metastasis, and tumor angiogenesis.
  • C-met inhibitor amg 208 - A selective small-molecule inhibitor of the proto-oncogene c-Met with potential antineoplastic activity. c-Met inhibitor AMG 208 inhibits the ligand-dependent and ligand-independent activation of c-Met, inhibiting its tyrosine kinase activity, which may result in cell growth inhibition in tumors that overexpress c-Met. C-Met encodes the hepatocyte growth factor receptor tyrosine kinase, plays an important role in epithelial cell proliferation and has been shown to be overexpressed in a variety of cancers.
  • C-met inhibitor amg 337 - An orally bioavailable inhibitor of the proto-oncogene c-Met with potential antineoplastic activity. c-Met inhibitor AMG 337 selectively binds to c-Met, thereby disrupting c-Met signal transduction pathways. This may induce cell death in tumor cells overexpressing c-Met protein or expressing constitutively activated c-Met protein. c-Met protein, the product of the proto-oncogene c-Met, is a receptor tyrosine kinase also known as hepatocyte growth factor receptor (HGFR); this protein is overexpressed or mutated in many tumor cell types and plays key roles in tumor cell proliferation, survival, invasion, and metastasis, and tumor angiogenesis.
  • C-met inhibitor gst-hg161 - An orally bioavailable, selective inhibitor of the oncoprotein c-Met (hepatocyte growth factor receptor; HGFR), with potential antineoplastic activity. Upon oral administration, c-Met inhibitor GST-HG161 targets and binds to c-Met protein, thereby disrupting c-Met-dependent signal transduction pathways. This may induce cell death in tumor cells overexpressing c-Met protein. c-Met protein is overexpressed or mutated in many tumor cell types and plays key roles in tumor cell proliferation, survival, invasion, metastasis, and tumor angiogenesis.
  • C-met inhibitor hs-10241 - An orally bioavailable small molecule inhibitor of the oncoprotein c-Met (hepatocyte growth factor receptor; HGFR), with potential antineoplastic activity. Upon oral administration, HS-10241 targets and binds to the c-Met protein, prevents c-Met phosphorylation and disrupts c-Met-dependent signal transduction pathways. This may induce cell death in tumor cells overexpressing c-Met protein or expressing constitutively activated c-Met protein. c-Met protein is overexpressed or mutated in many tumor cell types and plays key roles in tumor cell proliferation, survival, invasion, metastasis, and tumor angiogenesis.
  • C-met inhibitor jnj-38877605 - An orally bioavailable, small-molecule receptor tyrosine kinase inhibitor with potential antineoplastic activity. c-Met inhibitor JNJ-38877605 selectively inhibits c-Met, a receptor tyrosine kinase (RTK) involved in cancer cell survival and invasiveness, and tumor angiogenesis. c-Met is also known as hepatocyte growth factor receptor (HGFR).
  • C-met inhibitor mk2461 - A selective small-molecule inhibitor of the proto-oncogene c-Met with potential antineoplastic activity. c-Met inhibitor MK2461 preferentially inhibits activated c-Met in an ATP-competitive manner, thereby inhibiting its tyrosine kinase activity, which may inhibit c-Met signaling and result in cell growth inhibition in tumors that overexpress c-Met. c-Met, encoding the hepatocyte growth factor receptor (HGFR) tyrosine kinase, plays an important role in tumor cell proliferation and has been shown to be overexpressed or mutated in a variety of cancers.
  • C-met inhibitor mk8033 - An orally bioavailable inhibitor of c-Met, with potential antineoplastic activity. Upon administration, c-Met inhibitor MK8033 binds to and inhibits the autophosphorylation of the c-Met protein, which disrupts c-Met signal transduction pathways and may induce cell death in tumor cells overexpressing or expressing constitutively activated c-Met protein. In addition, MK8033 inhibits Ron (receptor originated from nantes, MST1R). c-Met protein, which is encoded by the proto-oncogene MET, is a receptor tyrosine kinase also known as hepatocyte growth factor receptor (HGFR); this protein is overexpressed or mutated in many tumor cell types and plays key roles in tumor cell proliferation, survival, invasion, and metastasis, and tumor angiogenesis. Ron, a member of the Met family of cell surface receptor tyrosine kinases, is also overexpressed on certain tumor cell types.
  • C-met inhibitor msc2156119j - An orally bioavailable inhibitor of the proto-oncogene c-Met (also known as hepatocyte growth factor receptor (HGFR)) with potential antineoplastic activity. c-Met inhibitor MSC2156119J selectively binds to c-Met, which inhibits c-Met phosphorylation and disrupts c-Met-mediated signal transduction pathways. This may induce cell death in tumor cells overexpressing c-Met protein or expressing constitutively activated c-Met protein. c-Met, a receptor tyrosine kinase overexpressed or mutated in many tumor cell types, plays key roles in tumor cell proliferation, survival, invasion, metastasis, and tumor angiogenesis.
  • Cmv pp65 peptide-pulsed autologous dendritic cell vaccine - A cell-based cancer vaccine composed of autologous dendritic cells (DCs) pulsed with the human cytomegalovirus (CMV) phosphoprotein pp65, with potential immunostimulatory and antineoplastic activities. Upon administration, the CMV pp65 peptide-pulsed autologous DC vaccine exposes the immune system to the CMV pp65 peptide, which may result in a cytotoxic T-lymphocyte (CTL) response against CMV pp65-expressing tumor cells leading to cell lysis. The CMV pp65 protein, also called the 65 kDa lower matrix phosphoprotein, is the primary component of the enveloped subviral particle of CMV and is expressed in certain tumor types, such as glioblastoma.
  • Cmvpp65-a*0201 peptide vaccine - A peptide-based cancer vaccine containing a mutated form of the HLA-A*0201-restricted cytomegaloviral epitope CMVpp65(495-503) with potential immunostimulatory and antitumor activities. Upon subcutaneous administration, CMVpp65-A*0201 peptide vaccine may stimulate a cytotoxic T lymphocyte (CTL) response against CMV-positive cells, resulting in cell lysis. HLA-A*0201 is an MHC class I molecule that presents antigenic peptides to CD8+ T cells; epitope design restricted to epitopes that bind most efficiently to HLA-A*0201 may improve antigenic peptide immunogenicity. CMVpp65, a tegument protein of the herpes virus CMV, is the main viral antigen found in peripheral blood mononuclear cells (PBMCs) after viral infection and may activate cell-mediated immunity.
  • C-myb antisense oligonucleotide g4460 - A 24-base phosphorothiolate antisense oligodeoxynucleotide (ODN) for the proto-oncogene c-myb with potential antineoplastic activity. C-myb antisense oligonucleotide G4460 binds to codon sequences 2 to 9 of c-myb mRNA, inhibiting translation of the transcript. Suppression of c-myb expression with this agent may result in the restoration of normal differentiation pathways, increased antiproliferative effects, and the induction of apoptosis in early progenitor hematopoietic cells and in tumor cells that overexpress c-myb. Tumor-cell overexpression of c-myb blocks differentiation, promotes proliferation, and inhibits apoptosis.
  • Cndo-109-activated allogeneic natural killer cells - A preparation of non-interleukin-2 primed, tumor activated allogeneic natural killer (NK) cells with potential immunostimulating activity. The allogeneic NK cells obtained from a first or second degree relative of the patient are co-incubated with a lysate from the CTV-1 cell line, a minimally differentiated myeloid line derived from an acute myelogenous leukemia patient. Infusion of CNDO-109-activated allogeneic NK cells may be able to lyse and destroy NK-resistant tumor cells and a broad spectrum of tumor cells.
  • Cngrc peptide-tnf alpha conjugate - A cytokine-peptide conjugate composed of the cytokine tumor necrosis factor alpha (TNF-alpha) chemically linked to the peptide CNGRC. The peptide moiety CNGRC, a ligand for the membrane-bound metalloprotease CD13, binds to endothelial cells of the angiogenic vasculature that express CD13 (also known as aminopeptidase N); subsequently, the TNF-alpha moiety induces apoptosis in endothelial cells expressing CD13, thereby inhibiting tumor-associated angiogenesis. (NCI05)
  • Cobimetinib - An orally bioavailable small-molecule inhibitor of mitogen-activated protein kinase kinase 1 (MAP2K1 or MEK1), with potential antineoplastic activity. Cobimetinib specifically binds to and inhibits the catalytic activity of MEK1, resulting in inhibition of extracellular signal-related kinase 2 (ERK2) phosphorylation and activation and decreased tumor cell proliferation. Preclinical studies have demonstrated that this agent is effective in inhibiting the growth of tumor cells bearing a B-RAF mutation, which has been found to be associated with many tumor types. A threonine-tyrosine kinase and a key component of the RAS/RAF/MEK/ERK signaling pathway that is frequently activated in human tumors, MEK1 is required for the transmission of growth-promoting signals from numerous receptor tyrosine kinases.
  • Cobolimab - A monoclonal antibody against the inhibitory T-cell receptor, T-cell immunoglobulin and mucin domain-containing protein 3 (TIM-3; TIM3; hepatitis A virus cellular receptor 2; HAVCR2), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, cobolimab binds to TIM-3 expressed on certain T-cells, including tumor infiltrating lymphocytes (TILs). This abrogates T-cell inhibition, activates antigen-specific T-lymphocytes and enhances cytotoxic T-cell-mediated tumor cell lysis, which results in a reduction in tumor growth. TIM-3, a transmembrane protein and immune checkpoint receptor, is associated with tumor-mediated immune suppression.
  • Cobomarsen - A locked nucleic acid (LNA)-based oligonucleotide inhibitor of microRNA (miRNA) 155 (miR-155), with potential antineoplastic activity. Upon administration, cobomarsen targets, binds to and inhibits miR-155. This silences miR-155 and prevents the translation of certain tumor promoting genes, which leads to the induction of cancer cell apoptosis and the inhibition of tumor cell growth. miR-155, an oncogenic single-stranded, non-coding RNA that is critical to the regulation of gene expression, is overexpressed in certain tumor cell types. Up-regulation of miR-155 plays a key role in increased tumor cell proliferation and survival. The LNA is an RNA analog in which the ribose ring is locked in a particular confirmation that increases stability. Compared to the unmodified oligonucleotide, the LNA-modified oligonucleotide shows increased affinity for its target miR-155.
  • Codrituzumab - A humanized monoclonal antibody directed against the cell surface oncofetal protein glypican-3 (GPC3) with potential antineoplastic activity. Anti-GPC3 monoclonal antibody GC33 binds to GPC3 and triggers a host immune response against GPC3-expressing tumor cells, which may result in tumor cell death. GPC3, a heparin sulfate proteoglycan, is frequently upregulated in hepatocellular carcinoma and mesoderm-derived organs such as the liver, lungs, and kidney.
  • Coenzyme q10 - A naturally occurring benzoquinone important in electron transport in mitochondrial membranes. Coenzyme Q10 functions as an endogenous antioxidant; deficiencies of this enzyme have been observed in patients with many different types of cancer and limited studies have suggested that coenzyme Q10 may induce tumor regression in patients with breast cancer. This agent may have immunostimulatory effects.
  • Cofetuzumab pelidotin - An antibody-drug conjugate (ADC) composed of a humanized monoclonal antibody against human inactive tyrosine-protein kinase 7 (PTK7) linked, via a cleavable valine-citrulline linker, to an analog of the auristatin microtubule inhibitor dolastatin 10, auristatin-0101, with potential antineoplastic activity. Upon administration, cofetuzumab pelidotin targets and binds to PTK7 expressed on tumor cells. Upon binding, internalization and cleavage, auristatin-0101 binds to tubulin and inhibits its polymerization, resulting in G2/M phase arrest and apoptosis of PTK7-expressing tumor cells. PTK7, a tumor-associated antigen (TAA), is overexpressed on a variety of cancer cells.
  • Colchicine-site binding agent abt-751 - An orally bioavailable antimitotic sulfonamide. ABT- 751 binds to the colchicine-binding site on beta-tubulin and inhibits the polymerization of microtubules, thereby preventing tumor cell replication. This agent also disrupts tumor neovascularization, reducing tumor blood flow and so inducing a cytotoxic effect.
  • Cold contaminant-free iobenguane i-131 - An I 131 radioiodinated synthetic analogue of the neurotransmitter norepinephrine, manufactured with a proprietary process, with radioisotopic and potential antineoplastic activities. Cold contaminant-free iobenguane I 131 (MIBG) localizes to adrenergic tissue and may be used to image or eradicate tumor cells that accumulate and metabolize norepinephrine. This agent is manufactured using a technology that avoids the production of unwanted "cold contaminants" (i.e., carrier molecules), which may cause undesirable side effects and compete with MIBG for binding on target receptor sites.
  • Colloidal gold-bound tumor necrosis factor - A nanoparticle delivery system for recombinant human tumor necrosis factor (TNF) consisting of recombinant TNF bound to pegylated colloidal gold nanoparticles with potential antineoplastic activity. Upon intravenous administration, colloidal gold-bound recombinant human TNF travels through the bloodstream, avoiding immune detection and uptake by the reticuloendothelial system because of nanoparticle pegylation. Due to their size, the colloidal gold nanoparticles exit the circulatory system only at hyperpermeable tumor neovasculature sites; TNF then binds to and activates tumor cell TNF receptors, which may result in an increase in tumor cell apoptosis and a reduction in tumor cell proliferation. Compared to the administration of unbound TNF, colloidal gold-bound TNF may improve the efficacy and safety of TNF administration by delivering TNF specifically to tumor tissue.
  • Colorectal cancer peptide vaccine polypepi1018 - A peptide cancer vaccine consisting of a combination of six synthetic polypeptides directed against cancer testis antigens (CTAs) frequently expressed in colorectal cancers, with potential antineoplastic and immunostimulatory activities. Colorectal cancer peptide vaccine PolyPEPI1018 potentially elicits a cytotoxic T-lymphocyte response against colorectal tumors expressing the CTAs associated with the vaccine, which may result in a reduction in tumor cell proliferation.
  • Colorectal tumor-associated peptides vaccine ima910 - A synthetic tumor-associated peptide (TUMAP)-based cancer vaccine directed against colorectal cancer with potential immunostimulatory and antineoplastic activities. Synthetic colorectal tumor-associated peptides vaccine IMA910 contains 13 different synthetic TUMAPs, each of which represents a tumor associated antigen (TAA) specific for colorectal cancer. Upon administration, this agent may elicit a cytotoxic T-lymphocyte (CTL) response against colorectal tumors expressing these TAAs, which may result in a reduction in colorectal tumor cell proliferation.
  • Coltuximab ravtansine - An immunoconjugate consisting of an anti-CD19 monoclonal antibody conjugated to the maytansinoid DM4, a derivative of the cytotoxic agent maytansine (DM1), with potential antineoplastic activity. Coltuximab ravtansine targets the cell surface antigen CD19, found on a number of B-cell-derived cancers. Upon antibody/antigen binding and internalization, the immunoconjugate releases DM4, which binds to tubulin and disrupts microtubule assembly/disassembly dynamics, resulting in inhibition of cell division and cell growth of CD19-expressing tumor cells.
  • Combretastatin - A stilbenoid phenol, originally isolated from the bark of the African bush willow tree Combretum caffrum, with vascular disrupting and antineoplastic activities. Combretastatin targets and binds to the colchicine-binding site of tubulin, thereby impairs the polymerization of tubulin dimers and prevents the formation of microtubules in the endothelial cells of tumor. As a result, this may eventually lead to a destruction of the tumor vasculature, disruption of tumor blood flow and tumor cell necrosis.
  • Combretastatin a-1 - A stilbenoid originally isolated from the plant Combretum caffrum, with vascular-disrupting and antineoplastic activities. Upon administration, combretastatin A1 (CA1) promotes rapid microtubule depolymerization; endothelial cell mitotic arrest and apoptosis; destruction of the tumor vasculature; disruption of tumor blood flow; and tumor cell necrosis. In addition, orthoquinone intermediates, metabolized from combretastatin A1 by oxidative enzymes found to be elevated in some tumor types, may bind to tumor cell thiol-specific antioxidant proteins and DNA, and stimulate oxidative stress by enhancing superoxide/hydrogen peroxide production.
  • Combretastatin a1 diphosphate - The diphosphate prodrug of the stilbenoid combretastatin A1, originally isolated from the plant Combretum caffrum, with vascular-disrupting and antineoplastic activities. Upon administration, combretastatin A1 diphosphate (CA1P) is dephosphorylated to the active metabolite combretastatin A1 (CA1), which promotes rapid microtubule depolymerization; endothelial cell mitotic arrest and apoptosis, destruction of the tumor vasculature, disruption of tumor blood flow and tumor cell necrosis may ensue. In addition, orthoquinone intermediates, metabolized from combretastatin A1 by oxidative enzymes found to be elevated in some tumor types, may bind to tumor cell thiol-specific antioxidant proteins and DNA, and stimulate oxidative stress by enhancing superoxide/hydrogen peroxide production. CA1 binds to tubulin at the same site as colchicine but with higher affinity.
  • Commensal bacterial strain formulation ve800 - An orally bioavailable formulation composed of eleven alive, distinct nonpathogenic, nontoxigenic, human commensal bacterial strains, isolated from healthy human donor feces, with potential immunostimulating and antineoplastic activities. Upon administration of the commensal bacterial strain formulation VE800, the bacterial strains induce an interferon-gamma (IFN-g)-producing CD8-positive T-cell-mediated immune response in the intestines. This may activate an IFN-g-expressing CD8+ T-cell -mediated anti-cancer immune response and may eradicate tumor cells.
  • Compound kushen injection - A traditional Chinese medicine (TCM) formulation composed of compound Kushen injection (CKI) containing aqueous extracts from the roots of Kushen (Radix Sophorae Flavescentis) and Baituling (Rhizoma smilacis Glabrae), with potential antineoplastic and immunomodulating activities. CKI contains numerous chemicals including alkaloids, such as matrine and oxymatrine, flavonoids, alkylxanthones, quinones, triterpene glycosides, fatty acids, and essential oils. Although the exact mechanism(s) of action through which CKI exerts its effects has yet to be fully elucidated, CKI is able to interfere with the activation of various signal transduction pathways, such as the Wnt/beta-catenin signaling pathway, inhibit nuclear factor-kappa B (NF-KB) activation, and block the activity of multiple receptor tyrosine kinases, such as epidermal growth factor receptor (EGFR) and vascular endothelial growth factor receptor (VEGFR). CKI induces apoptosis in and inhibits proliferation, migration, invasion and adhesion of tumor cells. CKI also modulates the production of inflammatory mediators.
  • Conatumumab - A fully human monoclonal agonist antibody directed against the extracellular domain of human TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) receptor 2 (TR-2) with potential antineoplastic activity. Conatumumab mimics the activity of native TRAIL, binding to and activating TR-2, thereby activating caspase cascades and inducing tumor cell apoptosis. TR-2 is expressed by a variety of solid tumors and cancers of hematopoietic origin.
  • Conbercept - A recombinant, soluble, vascular endothelial growth factor receptor (VEGFR) protein composed of the second immunoglobulin (Ig) domain of VEGFR-1, the third and fourth Ig domains of VEGFR-2, and the constant region (Fc) of human immunoglobulin G1 (IgG1) with potential anti-angiogenic activities. Upon intravitreal injection, conbercept, functioning as a soluble decoy receptor, binds with high affinity to all VEGF-A isoforms, VEGF-B, as well as placenta growth factor (PlGF)-1 and PlGF-2. This prevents the binding of these growth factors to their endogenous receptors, potentially inhibiting angiogenesis and tumor cell growth.
  • Concentrated lingzhi mushroom extract - A nutritional supplement and traditional Chinese medicine (TCM) composed of a highly concentrated extract of the fruiting body of the red reishi mushroom Ganoderma lucidum (G. lucidum; lingzhi), with potential immunomodulating activities. Upon administration, the concentrated lingzhi mushroom extract may support the body's immune function and may support the immune system to eliminate tumor cells. The lingzhi mushroom extract contains high amounts of G. lucidum polysaccharides and G. lucidum triterpenoids (GLTs).
  • Conditionally active biologic anti-axl antibody-drug conjugate ba3011 - An antibody-drug conjugate (ADC) composed of a conditionally active biologic (CAB) antibody against AXL receptor tyrosine kinase (AXL; UFO) conjugated to an as of yet undisclosed cytotoxic agent, with potential antineoplastic activity. Upon administration of CAB-AXL-ADC BA3011, the anti-AXL antibody becomes activated through an as of yet not fully elucidated process only under the unique microphysical conditions that are present in the tumor microenvironment (TME) as a result of the glycolytic metabolism of cancer cells, and not in the microenvironment of normal, healthy tissues. Upon selective binding to AXL-expressing tumor cells and internalization, the cytotoxic agent kills the tumor cells through an as of yet undisclosed mechanism of action (MoA). AXL, a member of the TAM (TYRO3, AXL and MER) family of receptor tyrosine kinases normally expressed on many normal, healthy cells and overexpressed by many tumor cell types, plays a key role in tumor cell proliferation, survival, invasion and metastasis; its expression is associated with drug resistance and poor prognosis. The CAB antibody allows for efficient and reversible binding to AXL-expressing tumor cells under conditions that are present only in the TME, thereby maximizing efficacy while minimizing toxicity by avoiding activation and thus binding of the antibody to normal, healthy AXL-expressing cells under normal conditions.
  • Conditionally replicative adenovirus 5/3-delta24 - A replication competent, oncolytic adenovirus serotype 5 (Ad5) with its knob domain of fiber protein substituted by that of the serotype 3 (Ad5/3-delta24), with potential oncolytic activity. Upon administration, oncolytic adenovirus Ad5/3-delta24 binds to specific Ad3 receptors that are highly expressed on certain tumor cells. This results in the replication of oncolytic adenovirus Ad5/3-delta24 in tumor cells and induces tumor cell lysis which may potentially result in the activation of a systemic immune response against tumor-associated antigens. The Ad5/3-delta24 has a 24 base pair deletion in constant region 2 of the E1A gene which allows for selective replication in cells that are defective in the retinoblastoma gene (Rb) or cyclin-dependent kinase inhibitor-2A (CDKN2A or p16INK4a). As most tumor cells are defective in the Rb/p16 pathway, this virus selectively replicates in these cells. The replacement of the Ad5 fiber knob, which mediates viral-cell receptor binding, allows for a Coxsackie-adenovirus receptor (CAR)-independent infection of tumor cells; CAR expression is often deficient on cancer cells.
  • Contusugene ladenovec - A replication-defective adenoviral-CMV vector that encodes a wild-type p53 gene. Contusugene ladenovec induces tumor cells that have been transfected with the vector to produce wild-type p53, a tumor suppressor gene that is deleted or mutated in a significant number of cancers. In transfected tumor cells, the wild-type p-53 gene product exerts an antitumor effect by blocking cell cycle progression at the G1/S regulation point, activating DNA repair proteins in the presence of DNA damage, and initiating apoptosis when DNA damage is irreparable.
  • Copanlisib - A phosphoinositide 3-kinase (PI3K) inhibitor with potential antineoplastic activity. Copanlisib inhibits the activation of the PI3K signaling pathway, which may result in inhibition of tumor cell growth and survival in susceptible tumor cell populations. Activation of the PI3K signaling pathway is frequently associated with tumorigenesis and dysregulated PI3K signaling may contribute to tumor resistance to a variety of antineoplastic agents.
  • Copper cu 64-atsm - A radioconjugate consisting of a lipophilic copper(II)bis(thiosemicarbazone) labeled with the positron- and beta-emitting isotope (64)Cu with hypoxia-selective and antineoplastic activities. With a high membrane permeability and redox potential, copper Cu 64-ATSM is preferentially taken up by hypoxic cells compared to normoxic cells; the extent of retention in tissue is inversely related to the state of tissue oxygenation allowing the quantitation of tissue hypoxia by positron emission tomography (PET). In addition, the radioactive copper moiety of this agent may deliver a selective cytotoxic dose of beta radiation to hypoxic tumor cells.
  • Copper cu 67 tyr3-octreotate - A radioconjugate consisting of the tyrosine-containing somatostatin analog Tyr3-octreotate (TATE) conjugated with the bifunctional chelator 5-(8-methyl-3,6,10,13,16,19-hexaaza-bicyclo[6.6.6]icosan-1-ylamino)-5-oxopentanoic acid (MeCOSar) and radiolabeled with the beta-emitting radioisotope copper Cu 67, with potential antineoplastic activity. Upon administration, copper Cu 67 Tyr3-octreotate binds to somatostatin receptors (SSTRs), with high affinity to type 2 SSTR, present on the cell membranes of many types of neuroendocrine tumor (NET) cells. Upon binding and internalization, this radioconjugate specifically delivers a cytotoxic dose of beta radiation to SSTR-positive cells. TATE is an octreotide derivative in which phenylalanine at position 3 is substituted by tyrosine and position 8 threoninol is replaced with threonine. SSTRs have been shown to be present in large numbers on NET and their metastases, while most other normal tissues express low levels of SSTRs.
  • Copper gluconate - The orally bioavailable copper salt of D-gluconic acid. In addition to its roles as an enzyme cofactor for cytochrome C oxidase and superoxide dismutase, copper forms complexes with the thiocarbamate disulfiram (DSF) forming DSF-copper complexes, which enhances the DSF-mediated inhibition of the 26S proteasome; proteasome inhibition may result in inhibition of cellular protein degradation, cessation of cell cycle progression, inhibition of cellular proliferation, and the induction of apoptosis in susceptible tumor cell populations.
  • Cord blood derived car t-cells - A preparation of umbilical cord blood (CB)-derived T-lymphocytes that are genetically engineered to express a chimeric antigen receptor (CAR) that targets an as of yet unidentified tumor-associated antigen (TAA), with potential immunomodulatory and antineoplastic activities. Upon administration of the cord blood derived CAR T-cells, the T-cells target, bind to and induce selective cytotoxicity in tumor cells expressing the TAA.
  • Cord blood-derived expanded allogeneic natural killer cells - A preparation of human umbilical cord blood (UCB)-derived and ex vivo-expanded allogeneic natural killer (NK) cells, with immunomodulating and cytotoxic activities. Upon infusion of the cord blood-derived expanded allogeneic NK cells, these cells recognize and bind to tumor cells, and secrete perforins, granzymes, and cytokines, which cause cancer cell lysis.
  • Cord blood-derived expanded natural killer cells pnk-007 - A population of allogeneic lytic natural killer (NK) cells derived from human umbilical cord blood (UCB), with potential cytotoxic activity. Hematopoietic stem cells (HSC) are isolated from human UCB; this is followed by ex vivo differentiation into mature, highly lytic, NK cells, and expansion. Upon administration, the CB-derived expanded NK cells PNK-007 may lyse cancer cells.
  • Cordycepin - A purine nucleoside antimetabolite and antibiotic isolated from the fungus Cordyceps militaris with potential antineoplastic, antioxidant, and anti-inflammatory activities. Cordycepin is an inhibitor of polyadenylation, activates AMP-activated protein kinase (AMPK) and reduces mammalian target of rapamycin (mTOR) signaling, which may result in both the induction of tumor cell apoptosis and a decrease in tumor cell proliferation. mTOR, a serine/threonine kinase belonging to the phosphatidylinositol 3-kinase (PI3K)-related kinase (PIKK) family, plays an important role in the PI3K/AKT/mTOR signaling pathway that regulates cell growth and proliferation, and its expression or activity is frequently dysregulated in human cancers.
  • Cordycepin triphosphate - The triphosphate salt of cordycepin, a purine nucleoside antimetabolite and antibiotic isolated from the fungus Cordyceps militaris with potential antineoplastic, antioxidant, and anti-inflammatory activities. Cordycepin is an inhibitor of polyadenylation, activates AMP-activated protein kinase (AMPK), and reduces mammalian target of rapamycin (mTOR) signaling, which may result in both the induction of tumor cell apoptosis and a decrease in tumor cell proliferation. mTOR, a serine/threonine kinase belonging to the phosphatidylinositol 3-kinase (PI3K)-related kinase (PIKK) family, plays an important role in the PI3K/AKT/mTOR signaling pathway that regulates cell growth and proliferation, and its expression or activity is frequently dysregulated in human cancers.
  • Coriolus versicolor extract - An extract derived from the mushroom Coriolus versicolor, containing polysaccharide K (PSK) and polysaccharide-peptide (PSP), with potential immunomodulating and antineoplastic activities. Coriolus versicolor extract has been shown to stimulate the production of lymphocytes and cytokines, such as interferons and interleukins, and may exhibit antioxidant activities. However, the precise mechanism of action(s) of this agent is unknown.
  • Corticorelin acetate - The acetate salt form of coticorelin, a synthetic peptide of neurohormone corticotropin-releasing factor (CRF), with potential antitumor and antiangiogenesis activities. Upon administration, corticorelin stimulates adrenocorticotropic hormone (ACTH) secretion from the anterior pituitary gland. In turn, ACTH stimulates cortisol production from the adrenal cortex and is regulated by a negative feedback mechanism. Corticorelin appears to inhibit swelling around brain tumors through reduction in vascular leakage and maintenance of endothelial cell integrity. This agent potentially suppresses vascularization and tumor cell growth through reduction of vascular endothelial growth factor (VEGF) that appears to be via activation of corticotrophin-releasing factor receptor 2 (CRFR2), a G protein-coupled receptor.
  • Cortisone acetate - The acetate salt form of cortisone, a synthetic or semisynthetic analog of the naturally occurring cortisone hormone produced by the adrenal glands with anti-inflammatory and immunomodulating properties. Cortisone acetate diffuses through the cell membrane and binds to nuclear glucocorticoid receptors. The receptor-ligand complex binds to promotor regions of certain genes and initiates RNA transcription. This results in an induction of synthesis of certain anti-inflammatory proteins while inhibiting the synthesis of certain inflammatory mediators.
  • Cosibelimab - An immunoglobulin G1 (IgG1), human monoclonal antibody directed against the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, cosibelimab specifically targets and binds to PD-L1, blocking its binding to and activation of its receptor programmed cell death protein 1 (PD-1; PDCD1; CD279; programmed death-1). This reverses T-cell inactivation caused by PD-1/PD-L1 signaling and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1 on T-cells suppresses the immune system and results in immune evasion. PD-1, a transmembrane protein belonging to the immunoglobulin superfamily expressed on activated T-cells, is a negative regulator of the immune system that limits the expansion and survival of CD8-positive T-cells.
  • Cositecan - A synthetic silicon-containing agent related to camptothecin with antineoplastic properties. Cositecan stabilizes the cleavable complex between topoisomerase I and DNA, resulting in DNA breaks and consequently triggering apoptosis. Because it is lipophilic, cositecan exhibits enhanced tissue penetration and bio-availability compared to water-soluble camptothecins.
  • Coxsackievirus v937 - A preparation of naturally occurring, oncolytic enterovirus, with potential antineoplastic activity. Upon administration, coxsackievirus V937 targets and binds to intracellular adhesion molecule 1 (ICAM-1) and decay acceleration factor (DAF), both cell surface molecules that are overexpressed on certain malignant cells. After entering the cells, coxsackievirus V937 replicates in these cancer cells, thereby causing cancer cell lysis. This results in a reduction of tumor cell growth.
  • Cpg oligodeoxynucleotide gnkg168 - A synthetic, 21-mer, unmethylated CpG motif-based oligodeoxynucleotide (ODN), with immunostimulatory activity. CpG oligodeoxynucleotide GNKG168 binds to and activates Toll-like receptor 9 (TLR9) and is taken up into cells by endocytosis; once internalized, it may activate numerous signaling transduction pathways resulting in the release of multiple cytokines, such as immunoglobulins (Igs), interferons (IFNs), interleukins (ILs) and tumor necrosis factor (TNF). Through activation of TLR9, this ODN can directly stimulate B-lymphocytes, dendritic and natural killer (NK) cells, resulting in an increase in innate immunity and antibody-dependent cellular cytotoxicity (ADCC). In addition, through the release of IL-12 and IFN, this agent may induce a preferential shift to the T-helper 1(Th1) phenotype resulting in enhanced CD8+ T cell-mediated antitumor cytotoxicity.
  • C-raf antisense oligonucleotide isis 5132 - A synthetic, 20-base antisense oligodeoxynucleotide that hybridizes to c-raf kinase messenger RNA. ISIS 5132 has been shown to specifically suppress Raf-1 expression both in vitro and in vivo. Raf-1 serine/threonine kinase functions as a critical effector of Ras-mediated signal transduction; constitutive activation of this pathway directly contributes to malignant transformation.
  • Crenolanib - An orally bioavailable benzimidazole targeting the platelet-derived growth factor receptor (PDGFR) subtypes alpha and beta and FMS-related tyrosine kinase 3 (Flt3), with potential antineoplastic activity. Upon oral administration, crenolanib binds to and inhibits both wild-type and mutated forms of PDGFR and Flt3, which may result in the inhibition of PDGFR- and Flt3-related signal transduction pathways. This results in inhibition of tumor angiogenesis and tumor cell proliferation in PDGFR and/or Flt3 overexpressing tumor cells. PDGFR and Flt3, class III receptor tyrosine kinases, are upregulated or mutated in many tumor cell types.
  • Crenolanib besylate - The besylate salt form of crenolanib, an orally bioavailable benzimidazole targeting the platelet-derived growth factor receptor (PDGFR) subtypes alpha and beta and FMS-related tyrosine kinase 3 (Flt3), with potential antineoplastic activity. Upon oral administration, crenolanib binds to and inhibits both wild-type and mutated forms of PDGFR and Flt3, which may result in the inhibition of PDGFR- and Flt3-related signal transduction pathways. This results in inhibition of tumor angiogenesis and tumor cell proliferation in PDGFR and/or Flt3 overexpressing tumor cells. PDGFR and Flt3, class III receptor tyrosine kinases, are upregulated or mutated in many tumor cell types.
  • Crispr-cas9-mediated pd-1 and tcr gene-deleted anti-mesothelin car t-cells - A preparation of human T-lymphocytes transduced with a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) mesothelin and gene-edited with the clustered regularly interspaced short palindromic repeats (CRISPR)-Cas9 nuclease complex to eliminate endogenous TCR and programmed death 1 (PD-1; PDCD1; CD279; programmed cell death-1) expression, with potential immunostimulating and antineoplastic activities. The CRISPR guide RNA (gRNA) specifically targets and binds to complementary sites on TCRalpha, TCRbeta and PD-1. In turn, Cas9 cleaves these specific DNA sites, thereby disrupting transcription. Upon isolation, transduction, electroporation with TCRalpha, TCRbeta and PD-1 gRNAs, which are complexed to Cas9 RNA to disrupt expression of endogenous TCRalpha, TCRbeta and PD-1, expansion ex vivo, and introduction into the patient, the CRISPR-Cas9-mediated PD-1 and TCR gene-deleted anti-mesothelin CAR T-cells recognize and bind to mesothelin-overexpressing tumor cells. This may result in a specific cytotoxic T-lymphocyte (CTL)-mediated killing of mesothelin-positive tumor cells. PD-1, an immune checkpoint receptor expressed on T-cells, plays a key role in tumor immune evasion by binding to its ligand programmed death ligand 1 (PD-L1; cluster of differentiation 274; CD274; programmed cell death-1 ligand 1) expressed on tumor cells. By removing PD-1 from T-cells, PD-1-mediated signaling is halted which may decrease T-cell exhaustion and may enhance T-cell activity against the mesothelin-expressing tumor cells. Removal of endogenous TCR reduces TCR competition for expression, increases the persistence and function of the expressed transgenic TCR, enhances resistance to T-cell exhaustion and increases T-cell activity. Mesothelin is upregulated on a variety of tumor cell types.
  • Crizotinib - An orally available aminopyridine-based inhibitor of the receptor tyrosine kinase anaplastic lymphoma kinase (ALK) and the c-Met/hepatocyte growth factor receptor (HGFR) with antineoplastic activity. Crizotinib, in an ATP-competitive manner, binds to and inhibits ALK kinase and ALK fusion proteins. In addition, crizotinib inhibits c-Met kinase, and disrupts the c-Met signaling pathway. Altogether, this agent inhibits tumor cell growth. ALK belongs to the insulin receptor superfamily and plays an important role in nervous system development. ALK dysregulation and gene rearrangements are associated with a series of tumors.
  • Crolibulin - A small molecule tubulin polymerization inhibitor with potential antineoplastic activity. Microtubulin inhibitor EPC2407 binds to the colchicine-binding site on beta-tubulin and inhibits the polymerization of tubulin into microtubules, which may result in cell cycle arrest, the induction of apoptosis, and the inhibition of tumor cell proliferation. As a vascular disruption agent (VDA), this agent also disrupts tumor neovascularization, which may result in a reduction in tumor blood flow and tumor hypoxia and ischemic necrosis.
  • Cryptophycin - The cryptophycins are a family of 16-membered macrolide antimitotic agents isolated from the cyanobacteria Nostoc sp. The mechanism of anticancer activity of the cryptophycins has been associated with their destabilization of microtubules and induction of bcl-2 phosphorylation leading to apoptosis. Cryptophycins demonstrated activity against the wide spectrum of solid tumors including those that overexpress the multidrug resistance efflux pump P-glycoprotein. (NCI)
  • Cryptophycin 52 - A member of the cryptophycin family of antitumor agents that binds to microtubules, inducing growth arrest and apoptosis in solid tumors. (NCI)
  • Crystalline genistein formulation axp107-11 - An orally available crystalline formulation of genistein, a soy-derived isoflavone and phytoestrogen with potential antineoplastic, chemosensitizing, and antioxidant activities. Similar to genistein, crystalline genistein formulation AXP107-11 increases expression of phosphatase and tensin homolog (PTEN), which deactivates protein kinase Akt and mitogen-activated protein kinases (MAPK1 and 3; ERK2 and 1), thereby disrupting PI3K/Akt signal transduction and inducing apoptosis. This agent also induces antioxidant enzymes through AMP-activated protein kinase (AMPK) activation, inhibits NF-kB activation and decreases inflammation response, thereby sensitizing tumors to chemotherapy. Compared to genistein itself, this crystalline formulation shows improved solubility and bioavailability.
  • Csf1r inhibitor absk021 - An orally bioavailable inhibitor of colony stimulating factor 1 receptor (CSF1R; CSF-1R; CD115; M-CSFR), with potential immunomodulatory and antineoplastic activities. Upon administration, CSF1R inhibitor ABSK021 targets and binds to CSF1R, thereby blocking CSF1R activation and CSF1R-mediated signaling. This inhibits the activities of tumor-associated macrophages (TAMs) and myeloid-derived suppressor cells (MDSCs), and prevents immune suppression in the tumor microenvironment (TME). This enhances antitumor T-cell immune responses and inhibits the proliferation of tumor cells. CSF1R, also known as macrophage colony-stimulating factor receptor (M-CSFR) and CD115 (cluster of differentiation 115), is a cell-surface receptor that plays major roles in tumor cell proliferation and metastasis.
  • Csf-1r inhibitor blz945 - An orally bioavailable inhibitor of colony stimulating factor 1 receptor (CSF-1R; CSF1R), with potential antineoplastic activity. CSF1R inhibitor BLZ945 selectively binds to CSF1R expressed on tumor-associated macrophages (TAMs), blocks the activity of CSF1R, and inhibits CSF1R-mediated signal transduction pathways. This inhibits the activity and proliferation of TAMs, and reprograms the immunosuppressive nature of existing TAMs. Altogether, this reduces TAM-mediated immune suppression in the tumor microenvironment, re-activates the immune system, and improves anti-tumor cell responses mediated by T-cells. CSF1R, also known as macrophage colony-stimulating factor receptor (M-CSFR) and CD115 (cluster of differentiation 115), is a cell-surface receptor for its ligand, colony stimulating factor 1 (CSF1); this receptor is overexpressed by TAMs in the tumor microenvironment, and plays a major role in both immune suppression and the induction of tumor cell proliferation.
  • Csf1r inhibitor dcc-3014 - An orally bioavailable inhibitor of the tyrosine kinase receptor colony stimulating factor 1 receptor (CSF1R; CSF-1R; C-FMS; CD115; M-CSFR), with potential antineoplastic, macrophage checkpoint-inhibitory and immunomodulating activities. Upon administration, CSF1R inhibitor DCC-3014 targets and binds to CSF1R expressed on monocytes, macrophages, and osteoclasts and inhibits the binding of the CSF1R ligands colony-stimulating factor-1 (CSF-1) and interleukin-34 (IL-34), to CSF1R. This prevents CSF1R activation and CSF1R-mediated signaling in these cells. This blocks the production of inflammatory mediators by macrophages and monocytes and reduces inflammation. By blocking the recruitment to the tumor microenvironment and activity of CSF1R-dependent tumor-associated macrophages (TAMs), DCC-3014 inhibits the immunomodulating activity by macrophages and enhances T-cell infiltration and antitumor T-cell immune responses, which inhibits the proliferation of tumor cells. TAMs play key roles in the tumor microenvironment and allow for immune suppression; TAMs promote inflammation, tumor cell proliferation, angiogenesis, invasiveness and survival.
  • Csf1r inhibitor plx73086 - An inhibitor of colony stimulating factor 1 receptor (CSF1R; CSF-1R), with potential antineoplastic activity. Upon administration, CSF1R inhibitor PLX73086 targets and binds to CSF1R, thereby blocking CSF1R activation and CSF1R-mediated signaling. This inhibits the activity of tumor-associated macrophages (TAMs) in the tumor tissue and prevents TAM-related tumor cell growth. CSF1R, also known as macrophage colony-stimulating factor receptor (M-CSFR) and CD115 (cluster of differentiation 115), is a cell-surface receptor for its ligand colony stimulating factor 1 (CSF1) and plays major roles in tumor cell proliferation and metastasis.
  • Ct2584 hms - A lipid metabolism modulator which may inhibit angiogenesis, thereby possibly having antitumor activity. (NCI)
  • Ctla-4-directed probody bms-986249 - A probody composed of ipilimumab, a recombinant human immunoglobulin (Ig) G1 monoclonal antibody directed against the human T-cell receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; CTLA-4), linked to a proprietary masking peptide that covers the active antigen-binding site of the antibody through a protease-cleavable linker, with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration of CTLA-4-directed probody BMS-986249, the masking peptide is cleaved by tumor-associated proteases upon extravasation into the tumor microenvironment (TME). Protease-mediated removal of the linker enables binding of the unmasked monoclonal antibody moiety to CTLA-4, which is expressed on certain T-cells. This inhibits the CTLA4-mediated downregulation of T-cell activation, and leads to both activation of tumor infiltrating T-effector cells and a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells. CTLA4, an inhibitory receptor and member of the immunoglobulin superfamily expressed on activated effector T-cells (Teffs) and regulatory T-cells (Tregs), plays a key role in the inhibition of T-cell activity and downregulation of the immune system. The peptide masking of BMS-986249 minimizes binding to CTLA-4 in normal tissues and may reduce systemic toxicity, when compared to ipilimumab. Tumor-associated proteases are present in high concentrations and aberrantly activated in the TME.
  • Curcumin - A phytopolylphenol pigment isolated from the plant Curcuma longa, commonly known as turmeric, with a variety of pharmacologic properties. Curcumin blocks the formation of reactive-oxygen species, possesses anti-inflammatory properties as a result of inhibition of cyclooxygenases (COX) and other enzymes involved in inflammation; and disrupts cell signal transduction by various mechanisms including inhibition of protein kinase C. These effects may play a role in the agent's observed antineoplastic properties, which include inhibition of tumor cell proliferation and suppression of chemically induced carcinogenesis and tumor growth in animal models of cancer.
  • Curcumin/doxorubicin-encapsulating nanoparticle imx-110 - A water-soluble, nano-sized formulation composed of nanoparticles encapsulating the poorly water-soluble curcumin, a signal transducer and activator of transcription 3 (Stat3), nuclear factor Kappa B (NF-kB) and poly-tyrosine kinase inhibitor (TKI), and the antineoplastic anthracycline antibiotic doxorubicin, with potential antineoplastic activity. Upon administration of the curcumin/doxorubicin-encapsulating nanoparticle IMX-110, the curcumin moiety targets and inhibits the activation of STAT3 and NF-kB and prevents STAT3- and NF-kB-mediated signaling pathways, both of which are activated in a variety of human cancers and plays a key role in neoplastic transformation, uncontrolled tumor cell proliferation, tumor resistance to apoptosis, metastasis and immune evasion. The doxorubicin moiety intercalates into DNA and interferes with topoisomerase II activity. This inhibits DNA replication and RNA synthesis, leading to tumor cell growth inhibition and apoptosis. This agent also interacts with cell membrane lipids causing lipid peroxidation. Delivery of doxorubicin in nanoparticles may improve drug penetration into tumors and curcumin, by inhibiting NFkB and STAT3 activity, may circumvent the tumor cells multidrug resistance mechanisms and may therefore be effective in chemoresistant tumor cells. Chemotherapeutic agents, such as doxorubicin, upregulate the expression of NF-kB in tumor cells which generates chemotherapy-resistant tumor cells.
  • Cusatuzumab - A defucosylated, humanized IgG1 monoclonal antibody directed against the extracellular domain of the human CD70 molecule with potential antineoplastic activity. Upon administration, cusatuzumab selectively binds to, and neutralizes the activity of CD70, which may also induce an antibody-dependent cellular cytotoxicity (ADCC) response against CD70-expressing tumor cells. CD70, the ligand for the costimulatory receptor CD27 and a member of the tumor necrosis factor (TNF) family, is found on a number of solid and hematological tumors. Its overexpression may play an important role in evasion of immune surveillance.
  • Custirsen sodium - The eicosasodium salt of a mixed-backbone antisense oligodeoxynucleotide with chemosensitizing properties. Custirsen inhibits testosterone-repressed prostate message-2 (TRPM-2). Administration of custirsen abrogates the anti-apoptotic effect of TRPM-2, thereby sensitizing cells to chemotherapy and resulting in tumor cell death. TRPM-2 is an anti-apoptotic clusterin that is overexpressed by prostate cancer cells and is associated with chemoresistance.
  • C-visa bikdd:liposome - A formulation composed of DOTAP:cholesterol liposome nanoparticles complexed with the plasmid C-VISA BiKDD, with potential antineoplastic activity. C-VISA BikDD: liposome consists of a pancreatic-cancer-specific expression vector VISA (VP16-GAL4-WPRE integrated systemic amplifier) and a pancreatic-cancer-specific promoter CCKAR (cholecystokinin type A receptor) (CCKAR-VISA or C-VISA) which drives expression of the gene BikDD, a mutant form of the potent proapoptotic gene Bik (Bcl-2 interacting killer). Upon administration and transduction into pancreatic tumor cells, expression of BikDD by C-VISA BikDD:liposome may induce pancreatic tumor cell apoptosis and suppress pancreatic tumor cell proliferation. BikDD binds with greater affinity to anti-apoptotic proteins bcl-2, bcl-xl, bcl-w and Mcl-1 and is more potent than wild-type Bik. DOTAP:cholesterol liposome is composed of cationic lipid dioleoyl-trimethylammonium propane (DOTAP) and cholesterol at molar ratio of 1:1.
  • Cxc chemokine receptor 2 antagonist azd5069 - An orally bioavailable, selective and reversible antagonist of CXC chemokine receptor 2 (CXCR2), with potential anti-inflammatory and antineoplastic activities. Upon administration, CXC chemokine receptor 2 antagonist AZD5069 directly binds to CXCR2 and inhibits its activation. This inhibits CXCR2-mediated signaling and may inhibit tumor cell proliferation in CXCR2-overexpressing tumor cells. In addition, AZD5069 reduces both neutrophil recruitment and migration from the systemic circulation into sites of inflammation, including the lung mucosa; it may also prevent neutrophil migration from the bone marrow. This results in the reduction of inflammation, mucus production, and neutrophil proteinase-mediated tissue destruction in the lung. CXCR2, a G protein-coupled receptor protein also known as IL-8 receptor B (IL-8RB), is upregulated in a variety of tumor cell types and plays a key role in tumor cell proliferation and progression; it is known to be elevated in several inflammatory diseases, such as chronic obstructive pulmonary disease (COPD), asthma and fibrotic pulmonary disorders.
  • Cxcr1/2 inhibitor sx-682 - An orally bioavailable, selective and reversible antagonist of C-X-C motif chemokine receptors 1 (CXCR1) and 2 (CXCR2), with potential anti-inflammatory and antineoplastic activities. Upon administration CXCR1/2 inhibitor SX-682 selectively and allosterically binds to CXCR 1 and 2 and inhibits their activation by tumor-secreted chemokines. This inhibits CXCR1/2-mediated signaling, reduces both recruitment and migration of immunosuppressive myeloid-derived suppressor cells (MDSCs) and neutrophils in the tumor microenvironment (TME), inhibits inflammatory processes and abrogates the immunosuppressive-induced nature of the TME. This allows effector cells, such as natural killer (NK) cells and cytotoxic T-lymphocytes (CTLs), to kill and eliminate cancer cells. This inhibits tumor cell migration, metastasis, angiogenesis and tumor cell proliferation. CXCR1 and 2, G protein-coupled receptor proteins located on myeloid cells and certain tumor cells, play key roles in the immunosuppressive nature of the TME, tumor metastasis, therapy-resistance and myeloid cell suppression. They play a key role in inflammation and their expression is elevated in several inflammatory-driven diseases.
  • Cxcr2 antagonist qbm076 - An orally available small molecule antagonist of the G protein-coupled receptor, C-X-C motif chemokine receptor 2 (CXCR2), with potential immunomodulating and antineoplastic activities. Upon administration, QBM076 binds to and inhibits the activation of CXCR2, resulting in reduced neutrophil recruitment, myeloid-derived suppressor cell (MDSC) accumulation, and may potentially slow tumorigenesis and metastatic processes. CXCR2 is upregulated in a variety of cancer types, predominately in neutrophils/MDSCs rather than tumor cells, and is thought to contribute to tumor cell proliferation, invasion, and metastasis.
  • Cxcr2-transduced autologous tumor infiltrating lymphocytes - A preparation of autologous tumor infiltrating lymphocytes (TILs) that are transduced, ex vivo, with a retroviral vector encoding a gene for CXC chemokine receptor 2 (CXCR2), with potential antineoplastic activity. Upon administration of the CXCR2-transduced autologous TILs, the CXCR2-expressing T-cells selectively migrate toward tumor cells expressing CXCR2 ligands, which leads to tumor cell killing. CXCR2 expression allows for optimal TIL migration towards tumor cells and enhances the TILs anti-tumor activity. This leads to a reduction in both tumor cell proliferation and survival. CXCR2, a transmembrane protein also known as IL-8 receptor B (IL-8RB), plays a key role in inflammation and cancer progression. Certain CXCR2 ligands, such as CXCL1 and CXCL8 (IL-8), are expressed by tumor cells.
  • Cxcr4 antagonist usl311 - An orally bioavailable inhibitor of C-X-C chemokine receptor type 4 (CXCR4), with potential antineoplastic activity. Upon administration, USL311 binds to CXCR4, thereby preventing the binding of stromal-cell derived factor-1 (SDF-1 or CXCL12) to CXCR4 and inhibiting CXCR4 activation, which may result in decreased proliferation and migration of CXCR4-expressing tumor cells. CXCR4, a chemokine receptor belonging to the G protein-coupled receptor (GPCR) family, plays an important role in chemotaxis and angiogenesis, and is upregulated in several tumor cell types.
  • Cxcr4 inhibitor q-122 - An orally bioavailable inhibitor of CXCR4 with potential antineoplastic and antiviral activities. CXCR4 inhibitor MSX-122 binds to the chemokine receptor CXCR4, preventing the binding of stromal derived factor-1 (SDF-1) to the CXCR4 receptor and receptor activation, which may result in decreased tumor cell proliferation and migration. CXCR4, a chemokine receptor belonging to the GPCR (G protein-coupled receptor) gene family, plays an important role in chemotaxis and angiogenesis and is upregulated in several tumor cell types; it is also a co-receptor for HIV entry into T cells.
  • Cxcr4 peptide antagonist ly2510924 - An inhibitor of CXC chemokine receptor 4 (CXCR4), with potential antineoplastic activity. Upon subcutaneous administration, CXCR4 inhibitor LY2510924 binds to the chemokine receptor CXCR4, thereby preventing CXCR4 binding to its ligand, stromal derived factor-1 (SDF-1), and subsequent receptor activation. This may result in decreased tumor cell proliferation and migration. CXCR4, a chemokine receptor belonging to the G protein-coupled receptor (GPCR) gene family, plays an important role in chemotaxis and angiogenesis and is upregulated in several tumor cell types.
  • Cxcr4/e-selectin antagonist gmi-1359 - An antagonist of both the C-X-C chemokine receptor type 4 (CXCR4) and E-selectin (CD62E), with potential antineoplastic activity. Upon administration, CXCR4/E-selectin antagonist GMI-1359 binds to both CXCR4 and E-selectin expressed on endothelial cells. The binding to CXCR4 prevents the binding of stromal-cell derived factor-1 (SDF-1; CXCL12) to CXCR4 and inhibits CXCR4 activation, which may result in decreased proliferation and migration of CXCR4-expressing tumor cells. The binding to E-selectin expressed on endothelial cells prevents their interaction with E-selectin ligand-expressing cancer cells. This may prevent tumor cell activation, migration and metastasis. CXCR4, a chemokine receptor belonging to the G protein-coupled receptor (GPCR) family, plays an important role in chemotaxis and angiogenesis, and is upregulated in several tumor cell types. E-selectin is a cell adhesion molecule involved in cell rolling, signaling and chemotaxis. Its overexpression has been associated with tumor angiogenesis and metastasis in several cancers.
  • Cyclin b1 peptide-pulsed autologous dendritic cell vaccine - A cell-based cancer vaccine comprised of autologous dendritic cells (DCs) pulsed with cyclin B1 peptide, with potential immunostimulatory and antineoplastic activities. Upon administration, cyclin B1 peptide-pulsed autologous dendritic cell vaccine may stimulate anti-tumoral cytotoxic T lymphocyte (CTL) and anti-cyclin B1 antibody responses against cyclin B1-expressing cancer cells, resulting in tumor cell lysis. Cyclin B1, a key regulator of the cell cycle and cell division, is overexpressed in a variety of cancer cells.
  • Cyclin-dependent kinase 8/19 inhibitor bcd 115 - An orally bioavailable inhibitor of cyclin dependent kinases 8 and 19 (CDK8/19), with potential antineoplastic and chemoprotective activities. Upon oral administration, CDK8/19 inhibitor BCD 115 binds to and inhibits the activity of CDK8/19, which prevents activation of CDK8/19-mediated oncogenic signaling pathways, blocks selective transcription of certain tumor promoting genes, and inhibits proliferation of CDK8/19-overexpressing tumor cells. CDKs are serine/threonine kinases involved in the regulation of the cell cycle and may be overexpressed in certain cancer cell types. CDK8 plays a key role in transcription regulation and is an important oncogenic driver in a variety of cancer cell types.
  • Cyclin-dependent kinase inhibitor pf-06873600 - An orally bioavailable, cyclin dependent kinase (CDK) inhibitor, with potential antineoplastic activity. Upon administration, PF-06873600 selectively targets, binds to and inhibits the activity of CDKs. Inhibition of these kinases leads to cell cycle arrest, an induction of apoptosis, and inhibition of tumor cell proliferation. CDKs are ATP-dependent serine/threonine kinases that are important regulators of cell cycle progression and proliferation and are frequently overexpressed in tumor cells.
  • Cyclodextrin-based polymer-camptothecin crlx101 - A formulation of camptothecin, an alkaloid isolated from the Chinese tree Camptotheca acuminata, conjugated with to a hydrophilic, cyclodextrin-based linear polymer with potential antineoplastic activity. Upon intravenous administration, camptothecin is slowly released from the formulation at the tumor site and taken up by tumor cells. During the S phase of the cell cycle, camptothecin selectively stabilizes topoisomerase I-DNA covalent complexes, thereby inhibiting religation of topoisomerase I-mediated single-strand DNA breaks and producing potentially lethal double-strand DNA breaks when encountered by the DNA replication machinery. Compared to camptothecin alone, the cyclodextrin-based polymer formulation has a prolonged half life and greatly improves the biodistribution of camptothecin resulting in an accumulation of camptothecin at the tumor site, which enhances tumor exposure while greatly reducing toxic side effects. In addition, cyclodextrin-based polymer-camptothecin may be able to overcome certain kinds of multidrug resistance.
  • Cyclodisone - A cyclic sulfonate ester with potential antineoplastic activity. As an alkylating agent, clyclodisone induces the formation of DNA interstrand crosslinks, DNA strand breaks, and alkali-labile lesions in the DNA of some tumor cell lines. Alkylating agents exert cytotoxic and chemotherapeutic effects by transferring alkyl groups to DNA, thereby damaging DNA and interfering with DNA synthesis and cell division.
  • Cycloleucine - A non-metabolizable synthetic amino acid, formed through the cyclization of the amino acid leucine, with immunosuppressive, antineoplastic, and cytostatic activities. Cycloleucine competitively inhibits the enzyme methionine adenosyltransferase, resulting in the inhibition of S-adenosylmethionine (SAM) synthesis from methionine and ATP, and subsequent nucleic acid methylation and polyamine production; RNA, and perhaps to a lesser extent, DNA biosyntheses and cell cycle progression are finally disrupted. This agent is also a competitive inhibitor at the glycine modulatory site of the N-methyl-D-aspartate (NMDA) receptor.
  • Cyclopentenyl cytosine - A pro-drug carbocyclic analogue of cytidine with antineoplastic and antiviral activities. Cyclopentenyl cytosine (CPEC) is converted to the active metabolite cyclopentenyl cytosine 5'-triphosphate (CPEC-TP); CPEC-TP competitively inhibits cytidine triphosphate (CTP) synthase, thereby depleting intracellular cytidine pools and inhibiting DNA and RNA synthesis. This agent may also induce differentiation of some tumor cell types. The antiviral activity of this agent is broad-spectrum.
  • Cyclophosphamide - A synthetic alkylating agent chemically related to the nitrogen mustards with antineoplastic and immunosuppressive activities. In the liver, cyclophosphamide is converted to the active metabolites aldophosphamide and phosphoramide mustard, which bind to DNA, thereby inhibiting DNA replication and initiating cell death.
  • Cyclophosphamide anhydrous - The anhydrous form of cyclophosphamide, a synthetic nitrogen mustard alkylating agent, with antineoplastic and immunosuppressive activities. In the liver, cyclophosphamide is converted to active metabolites including phosphoramide mustard, which binds to and crosslinks DNA and RNA, thereby inhibiting DNA replication and protein synthesis. This agent, at low doses, is also a potent immunosuppressant primarily by depleting T-regulatory cells.
  • Cyl-02 plasmid dna - A gene transfer preparation of a plasmid DNA encoding mouse somatostatin receptor subtype 2 (sst2) and a fusion protein of human deoxycytidine kinase (DCK) and uridine monophosphate kinase (UMK), complexed to a synthetic polycationic carrier, polyethylenimine, with antineoplastic adjuvant application. Upon administration, CYL-02 plasmid DNA expresses DCK::UMK fusion protein that converts gemcitabine into its toxic phosphorylated metabolite. Expression of sst2 protein by this agent could induce both antioncogenic and local antitumor bystander effects. A loss of sst2 gene expression often is found in pancreatic and colorectal cancers, and is the receptor for somatostatin which negatively regulates a number of processes such as epithelial cell proliferation. Combination effects of these gene products allows for less chemotherapy to cause tumor cell lysis in not only the original tumor, but in distant tumors as well.
  • Cyp11a1 inhibitor odm-208 - An orally bioavailable, non-steroidal, selective inhibitor of the enzyme cytochrome 450 side-chain cleavage (scc) (CYP11A1), with potential antineoplastic activity. Upon oral administration, CYP11A1 inhibitor ODM-208 targets, binds to and inhibits the activity of CYP11A1. This prevents the synthesis of all steroid hormones and their precursors. This may inhibit proliferation of hormone-positive tumor cells. CYP11A1, a mitochondrial enzyme, catalyzes the conversion of cholesterol to pregnenolone (Preg), which is the first rate-liming step in steroid hormone biosynthesis.
  • Cyp11a1 inhibitor odm-209 - An orally bioavailable inhibitor of the enzyme cytochrome 450 side-chain cleavage (scc)(CYP11A1), with potential antineoplastic activity. Upon oral administration, CYP11A1 inhibitor ODM-209 targets, binds to and inhibits the activity of CYP11A1. This prevents the synthesis of all steroid hormones and their precursors. This may inhibit the proliferation of hormone-positive tumor cells. CYP11A1, a mitochondrial enzyme, catalyzes the conversion of cholesterol to pregnenolone (Preg), which is the first rate-limiting step in steroid hormone biosynthesis.
  • Cyp17 lyase inhibitor asn001 - An orally available non-steroidal, lyase-selective inhibitor of the steroid 17-alpha-hydroxylase/C17,20 lyase (CYP17A1 or CYP17), with potential anti-androgenic and antineoplastic activities. Upon oral administration, CYP17 lyase inhibitor ASN001 selectively binds to and inhibits the lyase activity of CYP17A1 in both the testes and adrenal glands, resulting in a significant reduction in androgen production to castrate-range levels. This may both decrease androgen-dependent growth signaling and inhibit the proliferation of androgen-dependent tumor cells. The cytochrome P450 enzyme CYP17A1, which is localized to the endoplasmic reticulum, exhibits both 17alpha-hydroxylase and 17,20-lyase activities; it plays a key role in the steroidogenic pathway. The selective inhibition of CYP17A1 lyase activity by ASN001 prevents the increased synthesis of mineralocorticoids that is normally seen with non-selective CYP17 inhibitors, which also inhibit the 17-alpha-hydroxylase activity of CYP17A1.
  • Cyp17/androgen receptor inhibitor odm 204 - An orally available inhibitor of both the steroid 17-alpha-hydroxylase/C17,20 lyase (CYP17A1 or CYP17) and androgen receptor (AR), with potential anti-androgen and antineoplastic activities. Upon oral administration, CYP17/AR inhibitor ODM 204 selectively inhibits the enzymatic activity of CYP17A1 in both the testes and adrenal glands, thereby inhibiting androgen production. This may both decrease androgen-dependent growth signaling and inhibit the proliferation of androgen-dependent tumor cells. In addition, ODM 204 binds to ARs in target tissues and inhibits androgen-induced receptor activation and AR nuclear translocation, which prevents the binding to and transcription of AR-responsive genes. This leads to an inhibition of growth in AR-expressing prostate cancer cells. The cytochrome P450 enzyme CYP17A1, which is localized to the endoplasmic reticulum, exhibits both 17alpha-hydroxylase and 17,20-lyase activities.
  • Cyp17/cyp11b2 inhibitor lae001 - An orally bioavailable, non-steroidal, potent, reversible, dual inhibitor of cytochrome P450 17 (CYP17 or CYP17A1) and CYP11B2, with potential antiandrogen and antineoplastic activities. Upon oral administration, LAE001 inhibits the enzymatic activity of CYP17A1 in both the testes and adrenal glands, thereby inhibiting androgen production. This may decrease androgen-dependent growth signaling and may inhibit cell proliferation of androgen-dependent tumor cells. LAE001 also inhibits the enzymatic activity of CYP11B2, thereby inhibiting aldosterone production. This may reduce the elevated aldosterone levels resulting from CYP17 inhibition and androgen deprivation, leading to a reduction in mineralocorticoid side effects including cardiovascular complications. The cytochrome P450 enzyme CYP17A1, localized to the endoplasmic reticulum, exhibits both 17alpha-hydroxylase and 17,20-lyase activities, and plays a key role in the steroidogenic pathway that produces steroidal hormones. The cytochrome P450 enzyme CYP11B2, aldosterone synthase, is an enzyme that plays a key role in aldosterone biosynthesis.
  • Cyproterone - A synthetic steroidal anti-androgen with antineoplastic activity. Cyproterone, in its acetate form, binds the androgen receptor (AR), thereby preventing androgen-induced receptor activation and inhibiting the growth of testosterone-sensitive tumor cells. This agent also exerts progesterogenic activity, resulting in a reduction in testicular androgen secretion and total androgen blockade.
  • Cyproterone acetate - The acetate salt of a synthetic steroidal antiandrogen with weak progestational and antineoplastic activities. Cyproterone binds the androgen receptor (AR), thereby preventing androgen-induced receptor activation in target tissues and inhibiting the growth of testosterone-sensitive tumor cells. This agent also exerts progestational agonist properties at the level of the pituitary that reduce luteinizing hormone (LH), resulting in reductions in testicular androgen secretion and serum testosterone levels. Treatment with cyproterone alone results in incomplete suppression of serum testosterone levels.
  • Cytarabine - An antimetabolite analogue of cytidine with a modified sugar moiety (arabinose instead of ribose). Cytarabine is converted to the triphosphate form within the cell and then competes with cytidine for incorporation into DNA. Because the arabinose sugar sterically hinders the rotation of the molecule within DNA, DNA replication ceases, specifically during the S phase of the cell cycle. This agent also inhibits DNA polymerase, resulting in a decrease in DNA replication and repair.
  • Cytarabine monophosphate prodrug mb07133 - A prodrug of the monophosphate (MP) form of the antimetabolite cytarabine (araCMP), an analogue of cytidine with a modified sugar moiety (arabinose instead of ribose), with potential antineoplastic activity. Upon administration of the cytarabine MP prodrug MB07133, the targeting moiety of this agent specifically delivers the cytarabine moiety to the liver. In turn, araCMP is selectively converted to araC triphosphate (araCTP) by a liver kinase, where it binds to and competes with cytidine for incorporation into DNA, thereby inhibiting DNA polymerase, and DNA synthesis. This leads to the inhibition of tumor cell proliferation and destruction of liver cancer cells. The liver is not able to convert araC into araCMP; araCMP is not converted into araCTP in tissues other than the liver. This enhances efficacy and minimizes systemic toxicity.
  • Cytochlor - A radio-sensitizing pyrimidine nucleoside with potential antineoplastic activity. Cytochlor is metabolized first to a phosphate derivative, CldCMP, by the enzyme deoxycytidine kinase and then to the active uracyl derivative, CldUMP, by the enzyme dCMP deaminase; deoxycytidine kinase and dCMP deaminase have been found in abnormally high concentrations in most cancers. CldUMP, the active metabolite, incorporates into DNA and, upon exposure to radiation, induces the formation of uracil radicals and double-strand DNA breaks.
  • Cytokine-based biologic agent irx-2 - A cell-free mixture comprised of a variety of naturally-derived cytokines obtained from normal, unrelated donor lymphocytes with potential immunostimulatory activity. The cytokines in IRX-2, including interleukin (IL)-1, -2, -6, -8, -10, -12, tumor necrosis factor alpha (TNF-a), interferon-gamma (IFN-g) and colony stimulating factors (CSFs), play vital roles in regulating cellular immunity and may synergistically stimulate a cellular immune response against tumor cells.
  • Cytokine-induced killer cells - A preparation of autologous lymphocytes with potential immunopotentiating and antineoplastic activities. Cytokine-induced killer (CIK) cells are CD3- and CD56-positive, non-major histocompatibility complex (MHC)-restricted, natural killer (NK)-like T lymphocytes, generated ex-vivo by incubation of peripheral blood lymphocytes (PBLs) with anti-CD3 monoclonal antibody, interleukin (IL)-2, IL-1, and interferon gamma (IFN-gamma) and then expanded. When reintroduced back to patients after autologous stem cell transplantation, CIK cells may recognize and kill tumor cells associated with minimal residual disease (MRD). CIK cells may have enhanced cytotoxic activity compared to lymphokine-activated killer (LAK) cells.

Alphabetic list of antineoplastic agents - 0-9 - A1 - A2 - A3 - A4 - A5 -A6 - B - C - D - E - F - G - H - I - JK - L - M - NO - PQ - R - S - T - UVW - XYZ

Antineoplastic agents c is part of WikiMD's Physician reviewed^ articles available 4free, 4all, 4ever!
Medicine: Health - Encyclopedia‏‎‏‎ - Topics‏‎ -‏‎ Diseases‏‎ - Cancer - Rare diseases - Random Page Navigation: Drugs - Wellness - Obesity‏‎ - Diet - Ketogenic diet - W8MD weight loss diet - Editors: Recently Edited Pages - Alphabetical Order - Sponsors - USMLE The content on or accessible through WikiMD is for informational purposes only. WikiMD is not a substitute for professional medical advice. ^See full Disclaimers
W8MD weight loss logo

Ad. Tired of being overweight?. W8MD's physician weight loss program can HELP*
Special: W8MD's tele-weight loss consultations only $99.99. Call 718-946-5500. Limited acceptance.