Cediranib | VEGFR inhibitor

Cediranib chemical structure

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Cediranib (288383-20-0) is a highly potent (IC50 =  <1 nM) inhibitor of VEGFR-2.1 It also inhibits VEGFR-1, VEGFR-3, c-Kit, and PDGFRß (IC50s respectively: 5 nM, 3 nM, 2nM, and 5 nm). It displays broad-spectrum activity in various human tumor models. Cediranib normalized tumor vasculature decreasing permeability, increasing blood perfusion, and allowing better drug delivery in glioblastoma patients.2,3 It enhanced transcription of MHC-I leading to enhanced CD8+ T cell infiltration and improved efficacy of anti-PD-L1 therapy.4

References/Citations:

  1. Wedge et al. (2005), AZD2171: a highly potent, orally bioavailable, vascular endothelial growth factor receptor-2 tyrosine kinase inhibitor for the treatment of cancer; Cancer Res. 65 4389
  2. Sorensen et al. (2011), Increased Survival in Glioblastoma Patients to Anti-angiogenic Therapy with Elevated Blood Perfusion; Cancer Res. 72 402
  3. Batchelor et al. (2013), Increased tumor oxygenation and survival in glioblastoma patients who shoe increased blood perfusion after cediranib and chemoradiation; Proc. Natl. Acad. Sci. USA 110 19059
  4. Zhang et al. (2024), Cediranib enhances the transcription of MHC-I by upregulating IRF-1; Biochem. Pharmacol. 221 116036
288383-20-0, AZD-2171, AZD2171, AZD2171 supplier, cediranib, Cediranib supplier
Alternate Name:
AZD2171

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Cediranib (288383-20-0) is a highly potent (IC50 =  <1 nM) inhibitor of VEGFR-2.1 It also inhibits VEGFR-1, VEGFR-3, c-Kit, and PDGFRß (IC50s respectively: 5 nM, 3 nM, 2nM, and 5 nm). It displays broad-spectrum activity in various human tumor models. Cediranib normalized tumor vasculature decreasing permeability, increasing blood perfusion, and allowing better drug delivery in glioblastoma patients.2,3 It enhanced transcription of MHC-I leading to enhanced CD8+ T cell infiltration and improved efficacy of anti-PD-L1 therapy.4

References/Citations:

  1. Wedge et al. (2005), AZD2171: a highly potent, orally bioavailable, vascular endothelial growth factor receptor-2 tyrosine kinase inhibitor for the treatment of cancer; Cancer Res. 65 4389
  2. Sorensen et al. (2011), Increased Survival in Glioblastoma Patients to Anti-angiogenic Therapy with Elevated Blood Perfusion; Cancer Res. 72 402
  3. Batchelor et al. (2013), Increased tumor oxygenation and survival in glioblastoma patients who shoe increased blood perfusion after cediranib and chemoradiation; Proc. Natl. Acad. Sci. USA 110 19059
  4. Zhang et al. (2024), Cediranib enhances the transcription of MHC-I by upregulating IRF-1; Biochem. Pharmacol. 221 116036