Cediranib maleate (AZD2171 maleate) is an orally active and highly potent VEGF family receptor tyrosine kinase (VEGFR2) inhibitor that inhibits Flt1, KDR, Flt4, PDGFRα, PDGFRβ, and c-Kit, and up-regulates MHC-I through transcriptional modulation in the study of ovarian cancer.

PDGFRα:36 nM (IC50), PDGFRβ:5 nM (IC50), FLT4:＜3 nM, KDR:＜1 nM, c-Kit:2 nM, FLT1:5 nM

Cediranib maleate (AZD2171) is a highly selective, orally active VEGFR2 inhibitor with IC50 values of 5 nM, ＜1 nM, ＜3 nM, 36 nM, 5 nM, and 2 nM for Flt1, KDR, Flt4, PDGFRα, PDGFRβ, and c-Kit, respectively. in human umbilical vein endothelial cells. Cediranib maleate was able to block VEGF-stimulated proliferation and KDR phosphorylation with IC50 values of 0.4 nM and 0.5 nM, respectively.In a fibroblast/endothelial cell co-culture model of vascular sprouting, Cediranib maleate reduced vascular area, length, and branching at subnanomolar concentrations. [1]

Once-daily oral administration of Cediranib maleate abrogated experimental (VEGF-induced) angiogenesis and inhibited endochondral ossification in bone or luteinization in the ovary; these processes are highly dependent on neointima formation. The growth of human tumor xenografts (colon, lung, prostate, mammary gland, and ovary) established in thymus-free mice was dose-dependently inhibited by Cediranib maleate, and long-term administration at a dose of 1.5 mg/kg/day produced statistically significant inhibition in all models. Histological analysis of Calu-6 lung tumors treated with Cediranib maleate showed a decrease in microvessel density over 52 hours and a further decrease with treatment duration. These changes indicate that the vascularity within the tumor is regressing. [1]

DMSO: 40 mg/mL (70.6 mM), Sonication is recommended.

H2O: 1 mg/mL (1.76 mM), Sonication is recommended.