Cediranib

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Cediranib
File:AZD2171.svg
Systematic (IUPAC) name
4-[(4-fluoro-2-methyl-1H-indol-5-yl)oxy]-6-methoxy-7-[3-(pyrrolidin-1-yl)propoxy]quinazoline
Clinical data
Routes of
administration		 Oral
Pharmacokinetic data
Biological half-life 12 to 35 hours
Identifiers
CAS Number 288383-20-0 YesY
ATC code L01XE32 (WHO)
PubChem CID: 9933475
IUPHAR/BPS 5664
ChemSpider 8109103 N
UNII NQU9IPY4K9 YesY
ChEMBL CHEMBL491473 N
Chemical data
Formula C25H27FN4O3
Molecular mass 450.505 g/mol
  • Cc4nc5ccc(Oc3ncnc2cc(OCCCN1CCCC1)c(OC)cc23)c(F)c5c4
  • 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 N
  • Key:XXJWYDDUDKYVKI-UHFFFAOYSA-N N
 NYesY (what is this?)  (verify)

Cediranib (AZD-2171; tentative trade name Recentin) is a potent inhibitor of vascular endothelial growth factor (VEGF) receptor tyrosine kinases.[1][2][3]

The drug is being developed by AstraZeneca as a possible anti-cancer chemotherapeutic agent for oral administration.

Beginning in 2007, it underwent Phase I clinical trials for the treatment of non-small cell lung cancer, kidney cancer, and colorectal cancer in adults, as well as tumors of the central nervous system in children. Phase I trials of interactions with other drugs used in cancer treatment were also undertaken.

On February 27, 2008, AstraZeneca announced that the use of cediranib in non-small cell lung cancer will not progress into phase III after failing to meet its main goal. On 8 March 2010, AstraZeneca issued a press-release stating that cediranib had failed Phase III clinical trials for use in first-line metastatic colorectal cancer when it was compared clinically with the market-leader bevacizumab.[4] As of November 2012, it was being assessed in double-blind studies for the treatment of methylated Glioblastoma Multiforme at the University of Washington Medical Center at a 20 mg daily dose.

Combination trials

Findings from a federally funded, NCI-sponsored phase II clinical trial[5] presented at the 50th Annual Meeting of the American Society of Clinical Oncology (May 30 - June 3, 2014, Chicago, Ill; Abstract No: LBA5500),[6] show that the combination of two investigational oral drugs, olaparib (AZD-2281; AstraZeneca), a potential first-in-class poly ADP ribose polymerase or PARP inhibitor and cediranib (AZD-2171; AstraZeneca), an anti-angiogenesis drug, is significantly more active against recurrent, platinum chemotherapy-sensitive disease or ovarian cancer related to mutations in BRCA genes than olaparib alone.[7]

References

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External links

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  6. ↑ Liu J, Barry WT, Birrer MJ, et al. A randomized phase 2 trial comparing efficacy of the combination of the PARP inhibitor olaparib and the antiangiogenic cediranib against olaparib alone in recurrent platinum-sensitive ovarian cancer; J Clin Oncol 32:5s, 2014 (suppl; abstr LBA5500))
  7. ↑ Combination of Targeted Drugs May Significantly Increase Progression-Free Survival in Women with Recurrent Ovarian Cancer, Study Shows - Onco'Zine - The International Oncology Network; June 2, 2014
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