Vatalanib dihydrochloride

VEGFR2/KDR；VEGFR1/FLT1；VEGFR2/Flk1；PDGFRβ；VEGFR3/FLT4

419.73

DMSO : 50 mg/mL (119.12 mM; ultrasonic and warming and heat to 80°C)

Vatalanib also inhibits Flk, c-Kit and PDGFRβ with IC50 of 270 nM, 730 nM and 580 nM, respectively. Furthermore, Vatalanib shows the anti-proliferation effect by inhibiting thymidine incorporation induced by VEGF in HUVECs with and IC50 of 7.1 nM, and dose-dependently suppresses VEGF-induced survival and migration of endothelial cells in the same dose range without cytotoxic or antiproliferative effect on cells that do not express VEGF receptors. A recent study shows that Vatalanib significantly inhibits the growth of hepatocellular carcinoma cells and enhances the IFN/5-FU induced apoptosis by increasing proteins levels of Bax and reduced Bcl-xL and Bcl-2.

Vatalanib induces dose-dependent inhibition of the angiogenic response to VEGF and PDGF in both a growth factor implant model and a tumor cell-driven angiogenesis model after once-daily oral dosing (25-100 mg/kg). In the same dose range, Vatalanib also inhibits the growth and metastasesof several human carcinomas in nude mice without significant effect on circulating blood cells or bone marrow leukocytes.

瓦他拉尼二盐酸盐；Vatalanib dihydrochloride；PTK787 dihydrochloride；CGP-797870 dihydrochloride；ZK-222584 dihydrochloride

C₂₀H₁₅ClN₄·2HCl

212141-51-0