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Antineoplastic agents jk

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  • Jak inhibitor - Any agent that targets, binds to and inhibits the activity of one or more of the Janus kinase family of enzymes.
  • Jak inhibitor incb047986 - An orally bioavailable inhibitor of Janus-associated kinases (JAK), with potential antineoplastic activity. Upon oral administration, INCB047986 specifically binds to and inhibits the phosphorylation of JAK, which affects JAK-dependent signaling and may lead to an inhibition of cellular proliferation in JAK-overexpressing tumor cells. The JAK-STAT (signal transducer and activator of transcription) 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.
  • Jak1 inhibitor azd4205 - An orally available inhibitor of Janus-associated kinase 1 (JAK1), with potential antineoplastic activity. Upon oral administration, AZD4205 inhibits JAK-dependent signaling and may lead to an inhibition of cellular proliferation in JAK1-overexpressing tumor cells. The JAK-STAT (signal transducer and activator of transcription) signaling pathway is a major mediator of cytokine activity and is often dysregulated in a variety of tumor cell types. Additionally, JAK1 may be a primary driver of STAT3 phosphorylation and signaling, which plays a role in neoplastic transformation, resistance to apoptosis, tumor angiogenesis, metastasis, immune evasion, and treatment resistance.
  • Jak1 inhibitor incb052793 - An orally bioavailable inhibitor of Janus-associated kinase 1 (JAK1), with potential antineoplastic activity. Upon oral administration, INCB052793 specifically binds to and inhibits the phosphorylation of JAK1, which interferes with JAK-dependent signaling and may lead to an inhibition of cellular proliferation in JAK1-overexpressing tumor cells. The JAK-STAT (signal transducer and activator of transcription) signaling pathway is a major mediator of cytokine activity and is often dysregulated in a variety of tumor cell types.
  • Jak2 inhibitor azd1480 - An orally bioavailable inhibitor of Janus-associated kinase 2 (JAK2) with potential antineoplastic activity. JAK2 inhibitor AZD1480 inhibits JAK2 activation, leading to the inhibition of the JAK/STAT (signal transducer and activator of transcription) signaling including activation of STAT3. This may lead to induction of tumor cell apoptosis and a decrease in cellular proliferation. JAK2, often upregulated or mutated in a variety of cancer cells, mediates STAT3 activation and plays a key role in tumor cell proliferation and survival.
  • Jak2 inhibitor bms-911543 - An orally available small molecule targeting a subset of Janus-associated kinase (JAK) with potential antineoplastic activity. JAK2 inhibitor BMS-911543 selectively inhibits JAK2, thereby preventing the JAK/STAT (signal transducer and activator of transcription) signaling cascade, including activation of STAT3. This may lead to an induction of tumor cell apoptosis and a decrease in cellular proliferation. JAK2, often upregulated or mutated in a variety of cancer cells, mediates STAT3 activation and plays a key role in tumor cell proliferation and survival.
  • Jak2 inhibitor xl019 - An orally bioavailable inhibitor of Janus-associated kinase 2 (JAK2) with potential antineoplastic activity. XL019 inhibits the activation of JAK2 as well as the mutated form JAK2V617F, which may result in the inhibition of the JAK-STAT signaling pathway and may induce apoptosis. The JAK2 mutated form JAK2V617F has a valine-to-phenylalanine modification at position 617 and plays a key role in tumor cell proliferation and survival.
  • Jin fu kang - A traditional Chinese herbal medicine derived from the plant Astragalus membranaceus with potential immunopotentiation activity. Jin Fu Kang may stimulate anti-tumor macrophage and natural killer cell activity and may enhance immune recognition of tumor cells by inhibiting the production of T-helper cell type 2 (Th2) cytokines such as interleukin-4 (IL-4) and interleukin-10 (IL-10).
  • Jnk inhibitor cc-401 - A second generation ATP-competitive anthrapyrazolone c-Jun N terminal kinase (JNK) inhibitor with potential antineoplastic activity. Based on the chemistry of SP600125, another anthrapyrazolone inhibitor of JNK, CC-401 competitively binds the ATP binding site of JNK, resulting in inhibition of the phosphorylation of the N-terminal activation domain of transcription factor c-Jun; decreased transcription activity of c-Jun; and a variety of cellular effects including decreased cellular proliferation.
  • Kanglaite - An injectable microemulsion of a purified oil extracted from the seeds of the traditional Chinese medicinal herb Coix lacryma-jobi (Job's tears), with potential antineoplastic activity. Although the exact mechanism of action is unknown, kanglaite exhibits an antineoplastic effect, potentially via interfering with the cell cycle and halting tumor cells in the G2/M phase, which may eventually inhibit mitosis and proliferation of cancer cells.
  • Kanitinib - A tyrosine kinase inhibitor targeting the oncoprotein c-Met (hepatocyte growth factor receptor; HGFR; MET) and vascular endothelial growth factor receptor 2 (VEGFR2), with potential anti-angiogenic and antineoplastic activities. Upon oral administration, kanitinib targets and binds to c-Met and VEGFR2, thereby disrupting c-Met- and VEGFR2-dependent signal transduction pathways. This may induce cell death in tumor cells overexpressing c-Met and/or VEGFR2 protein. c-Met and VEGFR2 are both overexpressed in many tumor cell types and play key roles in tumor cell proliferation, survival, invasion, metastasis, and tumor angiogenesis.
  • Ketoconazole - A synthetic derivative of phenylpiperazine with broad antifungal properties and potential antineoplastic activity. Ketoconazole inhibits sterol 14-a-dimethylase, a microsomal cytochrome P450-dependent enzyme, thereby disrupting synthesis of ergosterol, an important component of the fungal cell wall.
  • Ketotrexate - A folic acid antagonist and mammalian dihydrofolate reductase inhibitor with antineoplastic activity. Ketotrexate inhibits dihydrofolate reductase, an enzyme that reduces dihydrofolic acid to tetrahydrofolic acid which is essential for the synthesis of purine nucleotides and thymidylate. By depleting tetrahydrofolic acid availability, DNA synthesis is halted.
  • Klh/ny-eso-1/mart-1 peptide-pulsed dendritic cell vaccine - A cell-based cancer vaccine composed dendritic cells (DC) that were matured in the presence of a synthetic complex comprised of polyinosinic-polycytidylic acid, poly-L-lysine double-stranded RNA, and carboxymethylcellulose (poly-ICLC), and then pulsed with peptides derived from the tumor-associated antigens (TAAs) cancer/testis antigen NY-ESO-1 and melanoma antigen recognized by T-cells (MART-1/Melan-A), which are linked to the immunostimulant and carrier protein keyhole limpet hemocyanin (KLH), with potential immunostimulatory and antineoplastic activities. Upon intradermal administration, the KLH/NY-ESO-1/MART-1 peptide-pulsed DC vaccine stimulates the immune system to mount an anti-tumor cytotoxic T-lymphocyte (CTL) response against NY-ESO-1/MART-1-expressing tumor cells, which may result in tumor cell lysis. NY-ESO-1 is expressed both in normal testes and on the surfaces of various tumor cells. MART-1 is expressed by melanoma cells. The adjuvant poly-ICLC, a ligand for toll-like receptor-3 (TLR-3), induces the release of cytokines that may help boost the immune response against the TAAs. KLH boosts the immune response against the TAA-expressing tumor cells.
  • Klh-lymphoma ig vaccine - A chimeric lymphoma vaccine generated by combining the recipient's Ig idiotype (Id) protein with keyhole limpet hemocyanin (KLH), an immune stimulant, with potential antineoplastic activity. Vaccination with KLH-Lymphoma Ig Vaccine may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against lymphoma cells, resulting in decreased tumor growth.
  • Kras g12c inhibitor gdc-6036 - An orally available inhibitor of the oncogenic KRAS substitution mutation, G12C, with potential antineoplastic activity. Upon oral administration, KRAS G12C inhibitor GDC-6036 selectively targets the KRAS G12C mutant and inhibits KRAS G12C mutant-dependent signaling. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.
  • Kras g12c inhibitor ly3499446 - An orally available inhibitor of the oncogenic KRAS substitution mutation, G12C, with potential antineoplastic activity. Upon oral administration, LY3499446 targets and covalently binds to cytosine 12 within the switch II pocket of GDP-bound KRAS G12C, thereby inhibiting mutant KRAS-dependent signaling. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.
  • Kras g12c inhibitor mrtx849 - An orally available, small molecule inhibitor that targets the oncogenic KRAS substitution mutation, G12C, with potential antineoplastic activity. Upon oral administration MRTX849 covalently binds to cytosine 12 within the switch II pocket of GDP-bound KRAS G12C, thereby inhibiting mutant KRAS-dependent signaling. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.
  • Krasg12c inhibitor jnj-74699157 - An orally available, small molecule inhibitor of the oncogenic Kirsten rat sarcoma virus homolog KRAS glycine-to-cysteine substitution mutation, G12C, with potential antineoplastic activity. Upon oral administration JNJ-74699157 targets and binds to cytosine 12 within the switch II pocket of GDP-bound KRAS G12C, thereby inhibiting mutant KRAS-dependent signaling. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.
  • Kras-mapk signaling pathway inhibitor jab-3312 - An orally bioavailable inhibitor of the KRAS-mitogen-activated protein kinase (MAPK) signaling pathway, with potential antineoplastic activity. Upon oral administration, JAB-3312 blocks signaling through the KRAS-MAPK pathway. This prevents proliferation of susceptible cancer cells in which the KRAS-MAPK signaling pathway is overactivated. The Ras-MAPK pathway is often hyperactivated in cancer cells due to specific mutations and rearrangements, such as those seen in KRAS-mutant cancer cells, and drives cancer cell proliferation and survival.
  • Krn5500 - A semisynthetic derivative of the nucleoside-like antineoplastic antibiotic spicamycin, originally isolated from the bacterium Streptomyces alanosinicus. KRN 5500 inhibits protein synthesis by interfering with endoplasmic reticulum and Golgi apparatus functions. This agent also induces cell differentiation and caspase-dependent apoptosis.
  • Ksa-klh conjugate vaccine - A peptide vaccine containing an epitope of human tumor-associated KSA antigen (Ep-CAM) conjugated with keyhole limpet hemocyanin (KLH), with potential antineoplastic activity. KSA antigen, a type-I transmembrane glycoprotein and a cellular adhesion molecule with a molecular mass of 40 kDa, is overexpressed on the majority of epithelial tumor cells. KSA antigen is conjugated with KLH, an immunostimulant and a hapten carrier, to enhance immune recognition. Vaccination with KSA-KLH may result in the production of antibodies as well as eliciting a cytotoxic T-lymphocyte (CTL) response against tumor cells expressing the KSA antigen.
  • Ksp inhibitor azd4877 - A synthetic kinesin spindle protein (KSP) inhibitor with potential antineoplastic activity. AZD4877 selectively inhibits microtubule motor protein KSP (also called kinesin-5 or Eg5), which is essential for the formation of bipolar spindles and the proper segregation of sister chromatids during mitosis. Inhibition of KSP results in an inhibition of mitotic spindle assembly, activation of the spindle assembly checkpoint, induction of cell cycle arrest during the mitotic phase, thereby causing cell death in tumor cells that are actively dividing. Because KSP is not involved in postmitotic processes, such as neuronal transport, AZD4877 may be less likely to cause the peripheral neuropathy often associated with the tubulin-targeting agents.
  • Ksp inhibitor sb-743921 - A synthetic small molecule with potential antineoplastic properties. SB-743921 selectively inhibits kinesin spindle protein (KSP), an important protein involved in the early stages of mitosis that is expressed in proliferating cells. Inhibition of KSP results in inhibition of mitotic spindle assembly and interrupts cell division, thereby causing cell cycle arrest and induction of apoptosis.
  • Kunecatechins ointment - A topical ointment containing a green tea polyphenol mixture (kunecatechins) with potential antiviral, antibacterial, antioxidant, and chemopreventive activities. Kunecatechins is a partially purified fraction of the aqueous extract of green tea leaves from Camellia sinensis and contains catechins and other green tea components. Catechins, polyphenolic antioxidant plant metabolites or flavonoids, comprise most of the drug substance in kunecatechins with epigallocatechin gallate (EGCG) present as the primary catechin. Catechins may inhibit basic functions of human papillomavirus (HPV), counteract specific changes in tumor cells, affect cell signaling, and stimulate the immune system. Topical application of kunecatechins ointment has been reported to reduce HPV-induced genital and anal warts through a not yet fully understood mechanism, which may involve anti-oxidative activity.

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

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