AZD2171 MedChemExpress (MCE)

Product Name	Cediranib
Synonyms	AZD2171 Recentin Cediranib Cadiranib Cediranib R Cediranib(AZD2171) Cadiranib (AZD2171) Synonyms AZD2171 Recentin Cediranib Cadiranib Cediranib R Cediranib(AZD2171) Cadiranib (AZD2171) 4-(4-Fluoro-2-methylindol-5-yloxy)-6-methoxy-7-[3-(pyrrolidin-1-yl)propoxy]quinazoline 4-[(4-fluoro-2-methyl-1H-indol-5-yl)oxy]-6-methoxy-7-(3-pyrrolidin-1-ylpropoxy)quinazoline
CAS	288383-20-0
EINECS	670-946-2
Chemical Formula	C25H27FN4O3
Molecular Weight	450.51
inchi	InChI=1/C25H27FN4O3/c1-16-12-17-19(29-16)6-7-21(24(17)26)33-25-18-13-22(31-2)23(14-20(18)27-15-28-25)32-11-5-10-30-8-3-4-9-30/h6-7,12-15,29H,3-5,8-11H2,1-2H3
Package	10 mM * 1 mL;1 mg;5 mg;10 mg;50 mg;100 mg
Price	Email to quote
Descriptions	Cediranib Cediranib MedChemExpress (MCE) HY-10205 288383-20-0 AZD2171 99.38% Powder -20°C 3 years 4°C 2 years In solvent -80°C 1 year -20°C 6 months Room temperature in continental US Descriptions Cediranib Cediranib MedChemExpress (MCE) HY-10205 288383-20-0 AZD2171 99.38% Powder -20°C 3 years 4°C 2 years In solvent -80°C 1 year -20°C 6 months Room temperature in continental US may vary elsewhere. Cediranib (AZD2171) is a highly potent, orally available VEGFR tyrosine kinase inhibitor with IC50s of KDR, Flt4, PDGFRα, PDGFRβ, c-Kit, respectively. In human umbilical vein endothelial cells, Cediranib inhibits VEGF-stimulated proliferation and KDR phosphorylation with IC50 values of 0.4 and 0.5 nM, respectively. In a fibroblast/endothelial cell coculture model of vessel sprouting, Cediranib also reduces vessel area, length, and branching at subnanomolar concentrations[1]. Once-daily oral administration of Cediranib ablates experimental (VEGF-induced) angiogenesis and inhibits endochondral ossification in bone or corpora luteal development in ovary physiologic processes that are highly dependent upon neovascularization. The growth of established human tumor xenografts (colon, lung, prostate, breast, and ovary) in athymic mice is inhibited dose-dependently by Cediranib, with chronic administration of 1.5 mg per kg per day producing statistically significant inhibition in all models. A histologic analysis of Calu-6 lung tumors treated with Cediranib reveals a reduction in microvessel density within 52 hours that becomes progressively greater with the duration of treatment. These changes are indicative of vascular regression within tumors[1]. Rats: Young female Alderley Park rats (6 weeks of age, Wistar derived, n=5) are dosed orally, once daily for 28 days with Cediranib (1.25-5 mg per kg per day) or vehicle. Additional rats (five per group) are treated with Cediranib (5 mg per kg per day) or vehicle for 28 days and maintained for a further 28 days without treatment, to examine the effect of compound withdrawal. Histologic paraffin wax sections of the femorotibial joints and ovaries are stained with H&E. Morphometric image analysis of femorotibial sections is done, with growth plate areas from both the femur and tibia in each joint being combined for an analysis of the effect of compound treatment. The area of corpora lutea in H&E-stained ovary sections is similarly determined by morphometric analysis[1]. Proliferation of MG63 osteosarcoma cells is induced by PDGF-AA, which selectively activates PDGFR-α homodimer signaling. Cells are cultured in DMEM without phenol red containing 1% charcoal stripped FCS, 2 mM glutamine, and 1% nonessential amino acids for 24 hours. Cediranib or vehicle is added with PDGF-AA ligand (50 ng/mL) and plates reincubated for 72 hours. Cellular proliferation is determined using a bromodeoxyuridine[1]. The inhibitory activity of Cediranib is determined against a range of recombinant tyrosine kinases [KDR, Flt-1, Flt-4, c-Kit, PDGFR-α, PDGFR-β, CSF-1R, Flt-3, FGFR1, Src, Abl, epidermal growth factor receptor (EGFR), ErbB2, Aur-A, and Aur-B] using ELISA methodology[1]. Flt-1 5 nM (IC50) KDR 1 nM (IC50) Flt-4 3 nM (IC50) PDGFRα 36 nM (IC50) PDGFRβ 5 nM (IC50) c-Kit 2 nM (IC50) \| \| \| \| \| \| \| \| \| \| [1]. Wedge SR, et al. AZD2171: a highly potent, orally bioavailable, vascular endothelial growth factor receptor-2 tyrosine kinase inhibitor for the treatment of cancer. Cancer Res, 2005, 65(10), 4389-4400. [Content Brief] [2]. Zhang L, et al. Pleiotrophin promotes vascular abnormalization in gliomas and correlates with poor survival in patients with astrocytomas. Sci Signal. 2015 Dec 8 8(406):ra125. [Content Brief]
Last Update	2025-04-01 14:45:47

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