Vimseltinib: Difference between revisions
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{{Drugbox | {{Drugbox | ||
| verifiedfields = changed | | verifiedfields = changed | ||
| verifiedrevid = | | verifiedrevid = 477002547 | ||
| IUPAC_name = (3R,4R)-3-[[5-[(3,5-difluorophenyl)methyl]-1H-pyrazol-3-yl]amino]-4-hydroxy-1-[[2-(methylsulfonyl)ethyl]amino]pyrrolidin-2-one | |||
| image = Vimseltinib.svg | | image = Vimseltinib.svg | ||
| image2 = | | image2 = | ||
| | | tradename = | ||
| | | synonyms = | ||
| | | CAS_number = 1802250-71-5 | ||
| ATC_prefix = | |||
| ATC_suffix = | |||
| PubChem = 129073382 | |||
| DrugBank = | |||
| ChemSpiderID = 59719492 | |||
| UNII = | |||
| KEGG = | |||
| ChEMBL = 4297640 | |||
| C=19 | H=21 | F=2 | N=5 | O=3 | S=1 | |||
| smiles = | |||
| StdInChI = | |||
| StdInChIKey = | |||
}} | }} | ||
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==Mechanism of Action== | ==Mechanism of Action== | ||
Vimseltinib functions by inhibiting the activity of CSF1R, a receptor tyrosine kinase that is | Vimseltinib functions by inhibiting the activity of CSF1R, a receptor tyrosine kinase that is critical for the survival and proliferation of macrophages. In TGCT, overexpression of CSF1 leads to the recruitment and proliferation of macrophages, which contribute to the tumor's growth and associated symptoms. By blocking CSF1R, vimseltinib reduces the number of macrophages in the tumor microenvironment, thereby alleviating symptoms and potentially reducing tumor size. | ||
==Clinical Development== | ==Clinical Development== | ||
Vimseltinib is currently undergoing clinical trials to evaluate its efficacy and safety in patients with TGCT. Early-phase studies have shown promising results, with significant reductions in tumor size and improvements in | Vimseltinib is currently undergoing clinical trials to evaluate its efficacy and safety in patients with TGCT. Early-phase studies have shown promising results, with significant reductions in tumor size and improvements in patient-reported outcomes. The drug is administered orally, which offers a convenient option for patients compared to intravenous therapies. | ||
==Pharmacokinetics== | ==Pharmacokinetics== | ||
The pharmacokinetic profile of vimseltinib includes rapid absorption following oral administration, with a half-life that supports once-daily dosing. The drug is metabolized primarily in the liver, and its metabolites are excreted via the urine and feces. The pharmacokinetics of vimseltinib may be influenced by factors such as liver function and concomitant medications. | |||
== | ==Adverse Effects== | ||
Common | Common adverse effects observed in clinical trials include fatigue, nausea, and liver enzyme elevations. These side effects are generally manageable with dose adjustments or supportive care. Serious adverse events are rare but may include severe liver toxicity or hematological abnormalities. | ||
==Related Pages== | ==Related Pages== | ||
* [[Tyrosine kinase inhibitor]] | * [[Tyrosine kinase inhibitor]] | ||
* [[Colony-stimulating factor 1 receptor]] | * [[Colony-stimulating factor 1 receptor]] | ||
* [[Tenosynovial giant cell tumor]] | |||
[[Category:Tyrosine kinase inhibitors]] | [[Category:Tyrosine kinase inhibitors]] | ||
[[Category:Experimental cancer drugs]] | [[Category:Experimental cancer drugs]] | ||
Latest revision as of 01:36, 7 March 2025
A CSF1R inhibitor used in the treatment of tenosynovial giant cell tumor
{{Drugbox
| verifiedfields = changed
| verifiedrevid = 477002547
| IUPAC_name = (3R,4R)-3-[[5-[(3,5-difluorophenyl)methyl]-1H-pyrazol-3-yl]amino]-4-hydroxy-1-[[2-(methylsulfonyl)ethyl]amino]pyrrolidin-2-one
| image = Vimseltinib.svg
| image2 =
| tradename =
| synonyms =
| CAS_number = 1802250-71-5
| ATC_prefix =
| ATC_suffix =
| PubChem = 129073382
| DrugBank =
| ChemSpiderID = 59719492
| UNII =
| KEGG =
| ChEMBL = 4297640
| C=19 | H=21 | F=2 | N=5 | O=3 | S=1
| smiles =
| StdInChI =
| StdInChIKey =
}}
Vimseltinib is a small molecule tyrosine kinase inhibitor that specifically targets the colony-stimulating factor 1 receptor (CSF1R). It is being developed for the treatment of tenosynovial giant cell tumor (TGCT), a rare and often debilitating condition characterized by the proliferation of synovial-like mononuclear cells and multinucleated giant cells.
Mechanism of Action[edit]
Vimseltinib functions by inhibiting the activity of CSF1R, a receptor tyrosine kinase that is critical for the survival and proliferation of macrophages. In TGCT, overexpression of CSF1 leads to the recruitment and proliferation of macrophages, which contribute to the tumor's growth and associated symptoms. By blocking CSF1R, vimseltinib reduces the number of macrophages in the tumor microenvironment, thereby alleviating symptoms and potentially reducing tumor size.
Clinical Development[edit]
Vimseltinib is currently undergoing clinical trials to evaluate its efficacy and safety in patients with TGCT. Early-phase studies have shown promising results, with significant reductions in tumor size and improvements in patient-reported outcomes. The drug is administered orally, which offers a convenient option for patients compared to intravenous therapies.
Pharmacokinetics[edit]
The pharmacokinetic profile of vimseltinib includes rapid absorption following oral administration, with a half-life that supports once-daily dosing. The drug is metabolized primarily in the liver, and its metabolites are excreted via the urine and feces. The pharmacokinetics of vimseltinib may be influenced by factors such as liver function and concomitant medications.
Adverse Effects[edit]
Common adverse effects observed in clinical trials include fatigue, nausea, and liver enzyme elevations. These side effects are generally manageable with dose adjustments or supportive care. Serious adverse events are rare but may include severe liver toxicity or hematological abnormalities.
