Western blot analysis of extracts from NCI-H526 cells, serum-starved overnight and untreated (-) or pretreated with Vatalanib (1000 nM, 2 hr; +) prior to treatment with Human Stem Cell Factor (hSCF) #8925 (100 ng/ml, 5 min; +), using Phospho-c-Kit (Tyr703) (D12E12) Rabbit mAb #3073 (upper) or c-Kit (D13A2) XP® Rabbit mAb #3074 (lower).Learn more about how we get our images
Western blot analysis of extracts from HUVE cells, serum-starved overnight and untreated (-) or pretreated with Vatalanib (1000 nM, 2 hr; +) prior to treatment with Human Vascular Endothelial Growth Factor-165 (hVEGF165) #8065 (50 ng/ml, 5 min; +), using Phospho-VEGF Receptor 2 (Tyr1175) (19A10) Rabbit mAb #2478 (upper) or VEGF Receptor 2 (55B11) Rabbit mAb #2479 (lower).Learn more about how we get our images
Chemical structure of vatalanib.Learn more about how we get our images
Vatalanib is supplied as a lyophilized powder. For a 10 mM stock, reconstitute the 5 mg in 1.19 ml DMSO. Working concentrations and length of treatment can vary depending on the desired effect, but it is typically used as a pretreatment at 0.5-50 μM for 0.5-2 hr prior to treating with a stimulator. It can also be used alone, with varying treatment times lasting up to 72 hr.
Store lyophilized or in solution at -20ºC, desiccated. Protect from light. In lyophilized form, the chemical is stable for 24 months. Once in solution, use within 3 months to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.
Vatalanib is a multi-targeted tyrosine kinase inhibitor. Researchers performing in vitro kinase assays show that vatalanib inhibits VEGFR-1, -2, and -3 with IC50 values of approximately 77 nM, 37 nM, and 640 nM, respectively. Vatalanib also inhibited PDGFR and c-kit at sub micromolar concentrations, but had no activity against several other kinases, including c-Met, EGFR, c-Src, and v-Abl up to 10 μM (1). Vatalanib inhibits VEGF-induced autophosphorylation in HUVE and VEGFR-2 transfected CHO cells with an IC50 of 17 nM and 34 nM, respectively, and effectively blocks VEGF-stimulated HUVE cell proliferation (1). Research studies have demonstrated that vatalanib inhibits proliferation of multiple myeloma (MM) cells in a dose-dependant manner and blocks VEGF-induced ERK phosphorylation and cell migration in MM.1S cells (2). Dose-dependent apoptosis in chronic lymphocytic leukemia (CLL) cells by vatalanib and pazopanib has been observed (3).
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