CapmatinibCapmatinib
MedChemExpress (MCE)
HY-13404
1029712-80-8
INC280
INCB28060
99.92%
Powder -20°C 3 years 4°C 2 years In solvent -80°C 2 years -20°C 1 year
Room temperature in continental US
may vary elsewhere.
Capmatinib (INC280
INCB28060) is a potent, orally active, selective, and ATP competitive c-Met kinase inhibitor (IC50=0.13 nM). Capmatinib can inhibit phosphorylation of c-MET as well as c-MET pathway downstream effectors such as ERK1/2, AKT, FAK, GAB1, and STAT3/5. Capmatinib potently inhibits c-MET-dependent tumor cell proliferation and migration and effectively induces apoptosis. Antitumor activity. Capmatinib is largely metabolized by CYP3A4 and aldehyde oxidase.
Capmatinib (INCB28060) inhibits c-MET phosphorylation with an IC50 value of approximately 1 nM and a concentration of approximately 4 nM inhibits c-MET more than 90%, which is reversible and the effect is significantly reduced in several hours after the compound is removed and completely disappeared by 48 hours[1]. Capmatinib (INCB28060) (0-10000 nM
72 h) inhibits the proliferation of SNU-5, S114, H441 and U-87MG[1]. Capmatinib (INCB28060) (0.06-62.25 nM
2h) effectively inhibits phosphorylation of c-MET as well as c-MET pathway downstream effectors such as ERK1/2, AKT, FAK, GAB1, and STAT3/5[1]. Capmatinib (INCB28060) (0.24-63 nM
over night) prevents HGF-stimulated H441 cell migration[1]. Capmatinib (INCB28060) (0.5-50 nM
20 min) suppresses phosphorylation of both EGFR and HER-3 rapidly[1]. Capmatinib (INCB28060) (0-333 nM
24 h) induces apoptosis in SNU-5 cells[1].
Capmatinib (INCB28060) (1-30 mg/kg
PO, twice daily, for 2 weeks) exhibits dose-dependent inhibition of tumor growth, and shows well tolerance at all doses during the treatment periods, with no evidence of overt toxicity or weight loss in U-87MG tumor mice model[1]. Capmatinib (INCB28060) (0.03-10 mg/kg
PO, single dosage) causes inhibition of c-MET phosphorylation in S114 tumor mice model[1].
IC50: 0.13 nM (c-MET)[1] Cellular Effect Cell Line Type Value Description References
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[1]. Liu X, et al. A novel kinase inhibitor, INCB28060, blocks c-MET-dependent signaling, neoplastic activities, and cross-talk with EGFR and HER-3. Clin Cancer Res. 2011 Nov 15
17(22):7127-38. [Content Brief]
[2]. Baltschukat S, et al. Capmatinib (INC280) Is Active Against Models of Non-Small Cell Lung Cancer and Other Cancer Types with Defined Mechanisms of MET Activation. Clin Cancer Res. 2019 May 15
25(10):3164-3175. [Content Brief]
[3]. Dhillon S. Capmatinib: First Approval. Drugs. 2020 Jul
80(11):1125-1131. [Content Brief]