Vandetanib trifluoroacetate (D6474 trifluoroacetate) is a potent, orally active inhibitor ofVEGFR2/KDRtyrosine kinase activity (IC₅₀=40 nM). Vandetanib trifluoroacetate also has activity versus the tyrosine kinase activity ofVEGFR3/FLT4(IC₅₀=110 nM) andEGFR/HER1(IC₅₀=500 nM)^[1].

Vandetanib inhibits VEGFR3 and EGFR with IC₅₀of 110 nM and 500 nM, respectively. Vandetanib is not sensitive to PDGFRβ, Flt1, Tie-2 and FGFR1 with IC₅₀of 1.1-3.6 μM, while almost has no activity against MEK, CDK2, c-Kit, erbB2, FAK, PDK1, Akt and IGF-1R with IC₅₀above 10 μM. Vandetanib inhibits VEGF-, EGF- and bFGF-stimulated HUVEC proliferation with IC₅₀of 60 nM, 170 nM and 800 nM, with no effect on basal endothelial cell growth. Vandetanib inhibits tumor cell growth with IC₅₀of 2.7 μM (A549) to 13.5 μM (Calu-6)^[1]. Odanacatib is a weak inhibitor of antigen presentation, measured in a mouse B cell line (IC₅₀=1.5±0.4 μM), compared to the Cat S inhibitor LHVS (IC₅₀=0.001 μM) in the same assay. Odanacatib also shows weak inhibition of the processing of the MHC II invariant chain protein Iip10 in mouse splenocytes compared to LHVS (minimum inhibitory concentration 1-10 μM versus 0.01 μM, respectively)^[2]. Vandetanib suppresses phosphorylation of VEGFR-2 in HUVECs and EGFR in hepatoma cells and inhibits cell proliferation^[4].

Vandetanib (15 mg/kg, p.o.) has a superior anti-tumor effect than gefitinib in the H1650 xenograft model, and suppresses tumor growth with IC₅₀of 3.5±1.2 μM^[3]. In tumor-bearing mice, vandetanib (50 or 75 mg/kg) suppresses phosphorylation of VEGFR-2 and EGFR in tumor tissues, significantly reduces tumor vessel density, enhances tumor cell apoptosis, suppresses tumor growth, improves survival, reduces number of intrahepatic metastases, and upregulates VEGF, TGF-α, and EGF in tumor tissues^[4].

589.38

C₂₄H₂₅BrF₄N₄O₄

338992-53-3

凡德他尼三氟醋酸盐

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Please store the product under the recommended conditions in the Certificate of Analysis.