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SML2850

Sigma-Aldrich

Cediranib

≥98% (HPLC)

Synonyme(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

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About This Item

Formule empirique (notation de Hill):
C25H27FN4O3
Numéro CAS:
288383-20-0
Poids moléculaire :
450.51
Numéro MDL:
MFCD09954115
Code UNSPSC :
12352200
Nomenclature NACRES :
NA.77

Niveau de qualité

100

Pureté

≥98% (HPLC)

Forme

powder

Couleur

white to beige

Solubilité

DMSO: 2 mg/mL, clear

Température de stockage

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

Clé InChI

XXJWYDDUDKYVKI-UHFFFAOYSA-N

Actions biochimiques/physiologiques

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.

Code de la classe de stockage

11 - Combustible Solids

Classe de danger pour l'eau (WGK)

WGK 3

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable

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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
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
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
Z Ping Lin et al.
PloS one, 13(11), e0207399-e0207399 (2018-11-18)
PARP inhibitors target BRCA mutations and defective homologous recombination repair (HRR) for the treatment of epithelial ovarian cancer (EOC). However, the treatment of HRR-proficient EOC with PARP inhibitors remains challenging. The objective of this study was to determine whether the
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