For research use only. Not for therapeutic Use.
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 (1.8 and 3.6 μM; 48 h) 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[2].
Famitinib (0.6-20.0 µM; 24-72 h) 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 (50 and 100 mg/kg; p.o. once daily for 3 weeks) reduces tumor growth in vivo via inhibition of angiogenesis[2].
| Catalog Number | I006761 |
| CAS Number | 1044040-56-3 |
| Molecular Formula | C23H27FN4O2 |
| Purity | ≥95% |
| Reference | [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. |
