1865733-40-9

Product Details:

CasNo： 1865733-40-9

Molecular Formula： C23H20ClFN6O2

Purity： 99%

Synonyms: Capmatinib hydrochloride Hydrate; Capmatinib HCl hydrate; Capmatinib 2HCl.H2O; INC-280 2HCl.H2O; INCB28060 2HCl.H2O; NVP-INC280 2HCl.H2O; Capmatinib Hydrochloride Hydrate(INCB28060)
Color: White to light yellow
Form: Solid
Storage temp.: 4°C, sealed storage, away from moisture and light.

Description:
Capmatinib dihydrochloride hydrate is a orally active,reversible MET tyrosine kinase inhibitor that received approval for advanced non-small cell lung cancer(NSCLC) harboring MET exon 14 skipping mutationa. Capmatinib dihydrochloride hydrate 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 dihydrochloride hydrate potently inhibits c-MET-dependent tumor cell proliferation and migration and effectively induces apoptosis. Antitumor activity. Capmatinib dihydrochloride hydrate is largely metabolized by CYP3A4 and aldehyde oxidase.

Origin:
Capmatinib was first reported in 2011 by Liu et al., who showed that in both in vivo and in vitro mice studies using human cell lines, capmatinib had a 10,000-fold selectivity for c-met over a large panel of human kinase. They showed that capmatinib can block the c-MET phosphorylation and activation of downstream targets, including HGF. They further showed that activated c-met upregulates cancer-promoting EGFR and HER-3 pathways. Baltschukat et al. further investigated capmatinib in NSCLC.

Mechanism of action:
Tabrecta (capmatinib) is a kinase inhibitor that targets MET, including the mutant variant produced by exon 14 skipping. MET exon 14 skipping results in a protein with a missing regulatory domain that reduces its negative regulation, leading to increased downstream MET signaling.