All Photos(1)
Synonym(s):
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-(1-pyrrolidinyl)propoxy]quinazoline, 4-[(4-Fluoro-2-methyl-1H-indol-5-yl)oxy]-6-methoxy-7-[3-(pyrrolidin-1-yl)propoxy]quinazoline, AZD 2171, AZD2171
Empirical Formula (Hill Notation):
C25H27FN4O3
CAS Number:
Molecular Weight:
450.51
MDL number:
UNSPSC Code:
12352200
NACRES:
NA.77
Recommended Products
Quality Level
Assay
≥98% (HPLC)
form
powder
color
white to beige
solubility
DMSO: 2 mg/mL, clear
storage temp.
2-8°C
InChI
1S/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
InChI key
XXJWYDDUDKYVKI-UHFFFAOYSA-N
Biochem/physiol Actions
Cediranib (AZD2171) is an orally active anticancer agent and a highly potent ATP-competitive receptor tyrosine kinase (RTK) inhibitor against VEGFR (IC50 = 5 nM/Flt-1 (VEGFR1), <1 nM/KDR (VEGFR2), ≤3 nM/Flt-4 (VEGFR3), c-Kit (IC50 = 2 nM), PDGFR1/2 (IC50 = 5/36 nM), and FGFR1 (IC50 = 26 nM). Cediranib exhibits reduced activity against CSF-1R, Src, Abl (IC50 = 110, 130, 260 nM, respectively) and little or no potency toward Flt-3, EGFR, ErbB2 (Her-2/neu), CDK2/4, Aurora A/B, and MEK.
WGK
WGK 3
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Regulatory Information
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Kathy D Miller et al.
Clinical cancer research : an official journal of the American Association for Cancer Research, 12(1), 281-288 (2006-01-07)
This pilot study combined physiologic imaging, microcomputed tomography, and histologic tumor evaluation with a xenograft model of breast cancer to identify surrogates likely to correlate with response to AZD2171, an inhibitor of the vascular endothelial growth factor (VEGF) receptor tyrosine
A L R Bordinhão et al.
Oncology reports, 36(6), 3197-3206 (2016-10-18)
Cediranib, a pan-tyrosine kinase inhibitor is showing promising results for the treatment of several solid tumours. In breast cancer, its effects remain unclear, and there are no predictive biomarkers. Several studies have examined the expression profiles of microRNAs (miRNAs) in response
Ji Yeong Kim et al.
Anticancer research, 39(7), 3785-3793 (2019-07-03)
This study investigated drugs able to sensitize P-glycoprotein (P-gp)-overexpressing resistant KBV20C cancer cells to vincristine or eribulin treatment and assessed their associated mechanisms of action. Eight tyrosine kinase inhibitors (lapatinib, gefitinib, imatinib, erlotinib, nilotinib, pazopanib, cediranib, and vandetanib) and one
Carolyn Cao et al.
Cancer research, 66(23), 11409-11415 (2006-12-06)
The vascular endothelial growth factor receptor (VEGFR) tyrosine kinases are being explored as targets for antiangiogenic cancer therapy. Radiotherapy also inhibits tumor growth and affects vasculature. We investigated the combination of the potent VEGFR tyrosine kinase inhibitor AZD2171 and ionizing
Stephen R Wedge et al.
Cancer research, 65(10), 4389-4400 (2005-05-19)
Inhibition of vascular endothelial growth factor-A (VEGF) signaling is a promising therapeutic approach that aims to stabilize the progression of solid malignancies by abrogating tumor-induced angiogenesis. This may be accomplished by inhibiting the kinase activity of VEGF receptor-2 (KDR), which
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