Molecular Formula | C20H17Cl3N4
|
Molar Mass | 419.74 |
Melting Point | 268-2700C |
Solubility | Soluble in DMSO (up to 20 mg/ml with warming) or in Water (up to 100 mg/ml) |
Appearance | solid |
Color | White or off-white |
Storage Condition | Inert atmosphere,Store in freezer, under -20°C |
Stability | Stable for 2 years from date of purchase as supplied. Solutions in DMSO or distilled water may be stored at -20°C for up to 3 months. |
In vitro study | Vatalanib effectively inhibits VEGFR tyrosine kinase, and when it acts on VEGF receptor/KDR,VEGF receptor/Flt-1, VEGF receptor/Flk, c-Kit and PDGFR-β, the IC50 is 0.037 μm and 0.077 μm respectively, 0.27 μm, 0.73 μm and 0.58 μm. Vatalanib inhibited the phosphorylation induced by VEGF with IC50 of 17 nM and 34 nM in HUVECs and CHO cells, respectively. Moreover, Vatalanib acts on HUVECs, which has an anti-proliferation effect by inhibiting the uptake of pectin induced by VEGF, with an IC50 of 7.1 nM, and inhibits the survival and migration of endothelial cells induced by VEGF in the same dose range, this effect is dose-dependent and has no toxicity or antiproliferative effect on cells that do not express VEGF receptors. Recent studies have shown that Vatalanib significantly inhibits the growth of hepatoma cells and enhances IFN/5-FU-induced apoptosis by increasing Bax protein levels and decreasing Bcl-xL and Bcl-2 protein levels. |
In vivo study | In Vivo, Vatalanib was administered orally at a dose of 25-100 mg/kg, once daily, in a growth factor transplantation model and a tumor cell-driven angiogenesis model, to inhibit angiogenic responses to VEGF and PDGF. Treatment of nude mice with the same dose of Vatalanib also inhibited the growth and translocation of some human cancer cells and had no effect on circulating blood cells and bone marrow leukocytes. |