Famitinib (SHR1020), an orally active multi-targeted kinase inhibitor, inhibits the activity of c-kit, VEGFR-2 and PDGFRβ with IC50 values of 2.3 nM, 4.7 nM and 6.6 nM, respectively[1]. Famitinib exerts powerful antitumor activity in human gastric cancer cells and xenografts. Famitinib triggers apoptosis[2].
Famitinib inhibits the VEGF-induced proliferation, migration and tubule formation of human umbilical vein endothelial cells, and micro-vessel spouting from matrigel-embedded rat aortic rings[1].Famitinib inhibits cell proliferation by inducing cell cycle arrest at the G2/M phase and causes cell apoptosis in a dose-dependent manner in gastric cancer cell lines. Famitinib (0.6-20.0 µM) inhibits gastric cancer cell growth in a dose-dependent manner[2].
Famitinib exhibits broad and potent anti-tumor activity, leading to regression or growth arrest of various established xenografts derived from human tumor cell lines [1].Famitinib significantly slows tumor growth in vivo via inhibition of angiogenesis in BGC-823 xenograft models. Famitinib (50 and 100 mg/kg;gavage) reduces xenograft growth in vivo via inhibition of angiogenesis[2].
[1]. Liguang Lou, et al. Abstract 3604: Preclinical antitumor study of famitinib, an orally available multi-targeted kinase inhibitor of VEGFR/PDGFR/c-Kit in phase I clinical trials.
[2]. Sai Ge, et al. Famitinib exerted powerful antitumor activity in human gastric cancer cells and xenografts. Oncol Lett. 2016 Sep;12(3):1763-1768.