| Clinical data | |
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| Routes of administration | Oral |
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| Eliminationhalf-life | 12 to 35 hours |
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| CompTox Dashboard(EPA) | |
| ECHA InfoCard | 100.196.628 |
| Chemical and physical data | |
| Formula | C25H27FN4O3 |
| Molar mass | 450.514 g·mol−1 |
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Cediranib (AZD-2171; tentative trade nameRecentin) is a potentinhibitor ofvascular endothelial growth factor (VEGF) receptortyrosine kinases.[1][2][3]
The drug is being developed byAstraZeneca as a possible anti-cancer chemotherapeutic agent for oral administration.
Beginning in 2007, it underwentphase Iclinical trials for the treatment ofnon-small celllung cancer,kidney cancer, andcolorectal cancer in adults, as well as tumors of thecentral nervous system in children. Phase I trials of interactions with other drugs used in cancer treatment were also undertaken.[citation needed]
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-leaderbevacizumab.[4]In 2016, AstraZeneca completed a phase III trial comparing the efficacy of cediranib alone and cediranib withlomustine to the efficacy of lomustine alone in patients with recurrentglioblastoma. The trial failed to meet its primary endpoint and survival was not extended with cediranib.[5]
Findings from a federally funded, NCI-sponsored phase II clinical trial[6] presented at the 50th Annual Meeting of theAmerican Society of Clinical Oncology (May 30 - June 3, 2014, Chicago, Ill; Abstract No: LBA5500),[7] show that the combination of two investigational oral drugs,olaparib, a PARP inhibitor, and cediranib is significantly more active against recurrent, platinum chemotherapy-sensitive disease or ovarian cancer related to mutations in BRCA genes than olaparib alone.[8]