Cediranib (AZD2171) Product Overview Product Name: Cediranib (AZD2171) Alternate Name/Synonyms: AZD2171, Recentin Description: Cediranib (AZD2171) is a tyrosine kinase inhibitor that targets vascular endothelial growth factor receptors (VEGFR) 1, 2, and 3, c-KIT, and platelet-derived growth factor receptors. Studies show cediranib to be generally well tolerated as monotherapy at doses of 45 mg/d or less. Peptide Sequence: N/A Appearance: Crystalline solid Formulation: N/A CAS Number: 288383-20-0 Molecular Formula: C₂₅H₂₇FN₄O₃ Molecular Weight: 450.51 Purity: ≥98% Solubility:DMSO (10 mM) Storage Temp.: -20°C Shipping Conditions: RT Handling: Protect from air and moisture SMILES: CC1=CC2=C(N1)C=CC(=C2F)OC3=NC=NC4=CC(=C(C=C43)OC)OCCCN5CCCC5 InChi: 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 PubChem CID: 9933475 MDL Number: MFCD09954115 USAGE: For Research Use Only! Not For Use in Humans.
Cediranib (AZD2171) Product Overview Product Name: Cediranib (AZD2171) Alternate Name/Synonyms: AZD2171, Recentin Description: Cediranib (AZD2171) is a tyrosine kinase inhibitor that targets vascular endothelial growth factor receptors (VEGFR) 1, 2, and 3, c-KIT, and platelet-derived growth factor receptors. Studies show cediranib to be generally well tolerated as monotherapy at doses of 45 mg/d or less. Peptide Sequence: N/A Appearance: Crystalline solid Formulation: N/A CAS Number: 288383-20-0 Molecular Formula: C₂₅H₂₇FN₄O₃ Molecular Weight: 450.51 Purity: ≥98% Solubility:DMSO (10 mM) Storage Temp.: -20°C Shipping Conditions: RT Handling: Protect from air and moisture SMILES: CC1=CC2=C(N1)C=CC(=C2F)OC3=NC=NC4=CC(=C(C=C43)OC)OCCCN5CCCC5 InChi: 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 PubChem CID: 9933475 MDL Number: MFCD09954115 USAGE: For Research Use Only! Not For Use in Humans.
C-4300 Cediranib, Free Base, >99% Synonyms: [AZD2171] Related Terms: [Recentin]M.W. 450.51 C25H27FN4O3 [288383-20-0] Storage: Store at or below -20 ºC. Solubility: Soluble in DMSO. Disposal: A •Cediranib is a highly potent inhibitor of recombinant KDR tyrosine kinase activity in vitro (IC50 < 1 nM). Inhibitory activity was also observed against the kinase associated with Flt-1 (IC50 = 5 nM), the VEGF-C and VEGF-D receptor Flt-4 (IC50 ≤ 3 nM), recombinant PDGFR-related kinase c-Kit (IC50 = 2 nM), and PDGFRβ tyrosine kinase (IC50 = 5 nM). In HUVEC, it inhibited VEGF-stimulated phosphorylation of KDR, c-Kit, PDGFR-α, PDGFR-β in a dose-dependent manner with IC50 values of 0.5, 1, 5, and 8 nM, respectively. It inhibited VEGF-stimulated HUVEC proliferation potently with an IC50 value of 0.4 nM. Consistent with potent activity against VEGF signaling, cediranib inhibited vessel branching, length, and area in vitro with IC50 values of 0.1, 0.1, and 0.2 nM, respectively. It also completely abolished VEGF-induced angiogenesis in vivo. However, it inhibited tumor cell proliferation in vitro only at comparatively high concentrations, showing IC50 values of 3.0 µM for SKOV-3 cells, 3.8 µM for MDA-MB-231 cells, 5.8 µM for PC-3 cells, 6.4 µM for Calu-6 cells, and 7.4 µM for SW620 cells. It also inhibited the growth of these five tumor models in nude mice. Furthermore, cediranib induced vascular regression in human lung tumor xenografts. Wedge, S.R., et al. "AZD2171: a highly potent, orally bioavailable, vascular endothelial growth factor receptor-2 tyrosine kinase inhibitor for the treatment of cancer." Cancer Res. 65: 4389-4400 (2005). •Cediranib significantly increased survival of mice wth glioblastoma by decreasing tumor vessel permeability, normalizing perivascular cell coverage, and thinning of the basement membrane, thus controlling edema. Kamoun, W.S., et al. "Edema control by cediranib, a vascular endothelial growth factor receptor-targeted kinase inhibitor, prolongs survival despite persistent brain tumor growth in mice." J. Clin. Oncol. 27: 2542-2552 (2009). •Hypertension induced by cediranib is reported to be manageable. Langenberg, M.H., et al. "Effective strategies for management of hypertension after vascular endothelial growth factor signaling inhibition therapy: results from a phase II randomized, factorial, double-blind study of Cediranib in patients with advanced solid tumors." J. Clin. Oncol. 27: 6152-6159 (2009). •Cediranib demonstrated potent antitumor and antiangiogenic efficacy in the murine renal cell carcinoma model. Medinger, M., et al. "Antitumor and antiangiogenic activity of cediranib in a preclinical model of renal cell carcinoma." Anticancer Res. 29: 5065-5076 (2009). •Combined treatments of cediranib with radiation in Calu-6 lung xenografts induced a significantly enhanced growth delay when compared with either modality alone. Williams, K.J., et al. "Inhibition of vascular endothelial growth factor signalling using cediranib (RECENTIN; AZD2171) enhances radiation response and causes substantial physiological changes in lung tumour xenografts." Br. J. Radiol. 81: S21-S27 (2008). •Cediranib reverses ABCB1 (P-glycoprotein)- and ABCC1 (MRP1)-mediated multidrug resistance by directly inhibiting their drug efflux function. Tao, L.Y., et al. "Cediranib (recentin, AZD2171) reverses ABCB1- and ABCC1-mediated multidrug resistance by inhibition of their transport function." Cancer Chemother. Pharmacol. 64: 961-969 (2009). •Cediranib is the active ingredient in the drug formulation designated by the trade name Recentin®. This drug has been in human clinical trials for use in patients with non-small cell lung cancer, small cell lung cancer, kidney cancer, colorectal cancer, breast cancer, liver and ovarian cancer, melanoma, mesothelioma, and glioblastoma. NOTE: THE CEDIRANIB, FREE BASE RE
C-4300 Cediranib, Free Base, >99% Synonyms: [AZD2171] Related Terms: [Recentin]M.W. 450.51 C25H27FN4O3 [288383-20-0] Storage: Store at or below -20 ºC. Solubility: Soluble in DMSO. Disposal: A •Cediranib is a highly potent inhibitor of recombinant KDR tyrosine kinase activity in vitro (IC50 < 1 nM). Inhibitory activity was also observed against the kinase associated with Flt-1 (IC50 = 5 nM), the VEGF-C and VEGF-D receptor Flt-4 (IC50 ≤ 3 nM), recombinant PDGFR-related kinase c-Kit (IC50 = 2 nM), and PDGFRβ tyrosine kinase (IC50 = 5 nM). In HUVEC, it inhibited VEGF-stimulated phosphorylation of KDR, c-Kit, PDGFR-α, PDGFR-β in a dose-dependent manner with IC50 values of 0.5, 1, 5, and 8 nM, respectively. It inhibited VEGF-stimulated HUVEC proliferation potently with an IC50 value of 0.4 nM. Consistent with potent activity against VEGF signaling, cediranib inhibited vessel branching, length, and area in vitro with IC50 values of 0.1, 0.1, and 0.2 nM, respectively. It also completely abolished VEGF-induced angiogenesis in vivo. However, it inhibited tumor cell proliferation in vitro only at comparatively high concentrations, showing IC50 values of 3.0 µM for SKOV-3 cells, 3.8 µM for MDA-MB-231 cells, 5.8 µM for PC-3 cells, 6.4 µM for Calu-6 cells, and 7.4 µM for SW620 cells. It also inhibited the growth of these five tumor models in nude mice. Furthermore, cediranib induced vascular regression in human lung tumor xenografts. Wedge, S.R., et al. "AZD2171: a highly potent, orally bioavailable, vascular endothelial growth factor receptor-2 tyrosine kinase inhibitor for the treatment of cancer." Cancer Res. 65: 4389-4400 (2005). •Cediranib significantly increased survival of mice wth glioblastoma by decreasing tumor vessel permeability, normalizing perivascular cell coverage, and thinning of the basement membrane, thus controlling edema. Kamoun, W.S., et al. "Edema control by cediranib, a vascular endothelial growth factor receptor-targeted kinase inhibitor, prolongs survival despite persistent brain tumor growth in mice." J. Clin. Oncol. 27: 2542-2552 (2009). •Hypertension induced by cediranib is reported to be manageable. Langenberg, M.H., et al. "Effective strategies for management of hypertension after vascular endothelial growth factor signaling inhibition therapy: results from a phase II randomized, factorial, double-blind study of Cediranib in patients with advanced solid tumors." J. Clin. Oncol. 27: 6152-6159 (2009). •Cediranib demonstrated potent antitumor and antiangiogenic efficacy in the murine renal cell carcinoma model. Medinger, M., et al. "Antitumor and antiangiogenic activity of cediranib in a preclinical model of renal cell carcinoma." Anticancer Res. 29: 5065-5076 (2009). •Combined treatments of cediranib with radiation in Calu-6 lung xenografts induced a significantly enhanced growth delay when compared with either modality alone. Williams, K.J., et al. "Inhibition of vascular endothelial growth factor signalling using cediranib (RECENTIN; AZD2171) enhances radiation response and causes substantial physiological changes in lung tumour xenografts." Br. J. Radiol. 81: S21-S27 (2008). •Cediranib reverses ABCB1 (P-glycoprotein)- and ABCC1 (MRP1)-mediated multidrug resistance by directly inhibiting their drug efflux function. Tao, L.Y., et al. "Cediranib (recentin, AZD2171) reverses ABCB1- and ABCC1-mediated multidrug resistance by inhibition of their transport function." Cancer Chemother. Pharmacol. 64: 961-969 (2009). •Cediranib is the active ingredient in the drug formulation designated by the trade name Recentin®. This drug has been in human clinical trials for use in patients with non-small cell lung cancer, small cell lung cancer, kidney cancer, colorectal cancer, breast cancer, liver and ovarian cancer, melanoma, mesothelioma, and glioblastoma. NOTE: THE CEDIRANIB, FREE BASE RE
C-4300 Cediranib, Free Base, >99% Synonyms: [AZD2171] Related Terms: [Recentin]M.W. 450.51 C25H27FN4O3 [288383-20-0] Storage: Store at or below -20 ºC. Solubility: Soluble in DMSO. Disposal: A •Cediranib is a highly potent inhibitor of recombinant KDR tyrosine kinase activity in vitro (IC50 < 1 nM). Inhibitory activity was also observed against the kinase associated with Flt-1 (IC50 = 5 nM), the VEGF-C and VEGF-D receptor Flt-4 (IC50 ≤ 3 nM), recombinant PDGFR-related kinase c-Kit (IC50 = 2 nM), and PDGFRβ tyrosine kinase (IC50 = 5 nM). In HUVEC, it inhibited VEGF-stimulated phosphorylation of KDR, c-Kit, PDGFR-α, PDGFR-β in a dose-dependent manner with IC50 values of 0.5, 1, 5, and 8 nM, respectively. It inhibited VEGF-stimulated HUVEC proliferation potently with an IC50 value of 0.4 nM. Consistent with potent activity against VEGF signaling, cediranib inhibited vessel branching, length, and area in vitro with IC50 values of 0.1, 0.1, and 0.2 nM, respectively. It also completely abolished VEGF-induced angiogenesis in vivo. However, it inhibited tumor cell proliferation in vitro only at comparatively high concentrations, showing IC50 values of 3.0 µM for SKOV-3 cells, 3.8 µM for MDA-MB-231 cells, 5.8 µM for PC-3 cells, 6.4 µM for Calu-6 cells, and 7.4 µM for SW620 cells. It also inhibited the growth of these five tumor models in nude mice. Furthermore, cediranib induced vascular regression in human lung tumor xenografts. Wedge, S.R., et al. "AZD2171: a highly potent, orally bioavailable, vascular endothelial growth factor receptor-2 tyrosine kinase inhibitor for the treatment of cancer." Cancer Res. 65: 4389-4400 (2005). •Cediranib significantly increased survival of mice wth glioblastoma by decreasing tumor vessel permeability, normalizing perivascular cell coverage, and thinning of the basement membrane, thus controlling edema. Kamoun, W.S., et al. "Edema control by cediranib, a vascular endothelial growth factor receptor-targeted kinase inhibitor, prolongs survival despite persistent brain tumor growth in mice." J. Clin. Oncol. 27: 2542-2552 (2009). •Hypertension induced by cediranib is reported to be manageable. Langenberg, M.H., et al. "Effective strategies for management of hypertension after vascular endothelial growth factor signaling inhibition therapy: results from a phase II randomized, factorial, double-blind study of Cediranib in patients with advanced solid tumors." J. Clin. Oncol. 27: 6152-6159 (2009). •Cediranib demonstrated potent antitumor and antiangiogenic efficacy in the murine renal cell carcinoma model. Medinger, M., et al. "Antitumor and antiangiogenic activity of cediranib in a preclinical model of renal cell carcinoma." Anticancer Res. 29: 5065-5076 (2009). •Combined treatments of cediranib with radiation in Calu-6 lung xenografts induced a significantly enhanced growth delay when compared with either modality alone. Williams, K.J., et al. "Inhibition of vascular endothelial growth factor signalling using cediranib (RECENTIN; AZD2171) enhances radiation response and causes substantial physiological changes in lung tumour xenografts." Br. J. Radiol. 81: S21-S27 (2008). •Cediranib reverses ABCB1 (P-glycoprotein)- and ABCC1 (MRP1)-mediated multidrug resistance by directly inhibiting their drug efflux function. Tao, L.Y., et al. "Cediranib (recentin, AZD2171) reverses ABCB1- and ABCC1-mediated multidrug resistance by inhibition of their transport function." Cancer Chemother. Pharmacol. 64: 961-969 (2009). •Cediranib is the active ingredient in the drug formulation designated by the trade name Recentin®. This drug has been in human clinical trials for use in patients with non-small cell lung cancer, small cell lung cancer, kidney cancer, colorectal cancer, breast cancer, liver and ovarian cancer, melanoma, mesothelioma, and glioblastoma. NOTE: THE CEDIRANIB, FREE BASE RE
C-4300 Cediranib, Free Base, >99% Synonyms: [AZD2171] Related Terms: [Recentin]M.W. 450.51 C25H27FN4O3 [288383-20-0] Storage: Store at or below -20 ºC. Solubility: Soluble in DMSO. Disposal: A •Cediranib is a highly potent inhibitor of recombinant KDR tyrosine kinase activity in vitro (IC50 < 1 nM). Inhibitory activity was also observed against the kinase associated with Flt-1 (IC50 = 5 nM), the VEGF-C and VEGF-D receptor Flt-4 (IC50 ≤ 3 nM), recombinant PDGFR-related kinase c-Kit (IC50 = 2 nM), and PDGFRβ tyrosine kinase (IC50 = 5 nM). In HUVEC, it inhibited VEGF-stimulated phosphorylation of KDR, c-Kit, PDGFR-α, PDGFR-β in a dose-dependent manner with IC50 values of 0.5, 1, 5, and 8 nM, respectively. It inhibited VEGF-stimulated HUVEC proliferation potently with an IC50 value of 0.4 nM. Consistent with potent activity against VEGF signaling, cediranib inhibited vessel branching, length, and area in vitro with IC50 values of 0.1, 0.1, and 0.2 nM, respectively. It also completely abolished VEGF-induced angiogenesis in vivo. However, it inhibited tumor cell proliferation in vitro only at comparatively high concentrations, showing IC50 values of 3.0 µM for SKOV-3 cells, 3.8 µM for MDA-MB-231 cells, 5.8 µM for PC-3 cells, 6.4 µM for Calu-6 cells, and 7.4 µM for SW620 cells. It also inhibited the growth of these five tumor models in nude mice. Furthermore, cediranib induced vascular regression in human lung tumor xenografts. Wedge, S.R., et al. "AZD2171: a highly potent, orally bioavailable, vascular endothelial growth factor receptor-2 tyrosine kinase inhibitor for the treatment of cancer." Cancer Res. 65: 4389-4400 (2005). •Cediranib significantly increased survival of mice wth glioblastoma by decreasing tumor vessel permeability, normalizing perivascular cell coverage, and thinning of the basement membrane, thus controlling edema. Kamoun, W.S., et al. "Edema control by cediranib, a vascular endothelial growth factor receptor-targeted kinase inhibitor, prolongs survival despite persistent brain tumor growth in mice." J. Clin. Oncol. 27: 2542-2552 (2009). •Hypertension induced by cediranib is reported to be manageable. Langenberg, M.H., et al. "Effective strategies for management of hypertension after vascular endothelial growth factor signaling inhibition therapy: results from a phase II randomized, factorial, double-blind study of Cediranib in patients with advanced solid tumors." J. Clin. Oncol. 27: 6152-6159 (2009). •Cediranib demonstrated potent antitumor and antiangiogenic efficacy in the murine renal cell carcinoma model. Medinger, M., et al. "Antitumor and antiangiogenic activity of cediranib in a preclinical model of renal cell carcinoma." Anticancer Res. 29: 5065-5076 (2009). •Combined treatments of cediranib with radiation in Calu-6 lung xenografts induced a significantly enhanced growth delay when compared with either modality alone. Williams, K.J., et al. "Inhibition of vascular endothelial growth factor signalling using cediranib (RECENTIN; AZD2171) enhances radiation response and causes substantial physiological changes in lung tumour xenografts." Br. J. Radiol. 81: S21-S27 (2008). •Cediranib reverses ABCB1 (P-glycoprotein)- and ABCC1 (MRP1)-mediated multidrug resistance by directly inhibiting their drug efflux function. Tao, L.Y., et al. "Cediranib (recentin, AZD2171) reverses ABCB1- and ABCC1-mediated multidrug resistance by inhibition of their transport function." Cancer Chemother. Pharmacol. 64: 961-969 (2009). •Cediranib is the active ingredient in the drug formulation designated by the trade name Recentin®. This drug has been in human clinical trials for use in patients with non-small cell lung cancer, small cell lung cancer, kidney cancer, colorectal cancer, breast cancer, liver and ovarian cancer, melanoma, mesothelioma, and glioblastoma. NOTE: THE CEDIRANIB, FREE BASE RE
C-4300 Cediranib, Free Base, >99% Synonyms: [AZD2171] Related Terms: [Recentin]M.W. 450.51 C25H27FN4O3 [288383-20-0] Storage: Store at or below -20 ºC. Solubility: Soluble in DMSO. Disposal: A •Cediranib is a highly potent inhibitor of recombinant KDR tyrosine kinase activity in vitro (IC50 < 1 nM). Inhibitory activity was also observed against the kinase associated with Flt-1 (IC50 = 5 nM), the VEGF-C and VEGF-D receptor Flt-4 (IC50 ≤ 3 nM), recombinant PDGFR-related kinase c-Kit (IC50 = 2 nM), and PDGFRβ tyrosine kinase (IC50 = 5 nM). In HUVEC, it inhibited VEGF-stimulated phosphorylation of KDR, c-Kit, PDGFR-α, PDGFR-β in a dose-dependent manner with IC50 values of 0.5, 1, 5, and 8 nM, respectively. It inhibited VEGF-stimulated HUVEC proliferation potently with an IC50 value of 0.4 nM. Consistent with potent activity against VEGF signaling, cediranib inhibited vessel branching, length, and area in vitro with IC50 values of 0.1, 0.1, and 0.2 nM, respectively. It also completely abolished VEGF-induced angiogenesis in vivo. However, it inhibited tumor cell proliferation in vitro only at comparatively high concentrations, showing IC50 values of 3.0 µM for SKOV-3 cells, 3.8 µM for MDA-MB-231 cells, 5.8 µM for PC-3 cells, 6.4 µM for Calu-6 cells, and 7.4 µM for SW620 cells. It also inhibited the growth of these five tumor models in nude mice. Furthermore, cediranib induced vascular regression in human lung tumor xenografts. Wedge, S.R., et al. "AZD2171: a highly potent, orally bioavailable, vascular endothelial growth factor receptor-2 tyrosine kinase inhibitor for the treatment of cancer." Cancer Res. 65: 4389-4400 (2005). •Cediranib significantly increased survival of mice wth glioblastoma by decreasing tumor vessel permeability, normalizing perivascular cell coverage, and thinning of the basement membrane, thus controlling edema. Kamoun, W.S., et al. "Edema control by cediranib, a vascular endothelial growth factor receptor-targeted kinase inhibitor, prolongs survival despite persistent brain tumor growth in mice." J. Clin. Oncol. 27: 2542-2552 (2009). •Hypertension induced by cediranib is reported to be manageable. Langenberg, M.H., et al. "Effective strategies for management of hypertension after vascular endothelial growth factor signaling inhibition therapy: results from a phase II randomized, factorial, double-blind study of Cediranib in patients with advanced solid tumors." J. Clin. Oncol. 27: 6152-6159 (2009). •Cediranib demonstrated potent antitumor and antiangiogenic efficacy in the murine renal cell carcinoma model. Medinger, M., et al. "Antitumor and antiangiogenic activity of cediranib in a preclinical model of renal cell carcinoma." Anticancer Res. 29: 5065-5076 (2009). •Combined treatments of cediranib with radiation in Calu-6 lung xenografts induced a significantly enhanced growth delay when compared with either modality alone. Williams, K.J., et al. "Inhibition of vascular endothelial growth factor signalling using cediranib (RECENTIN; AZD2171) enhances radiation response and causes substantial physiological changes in lung tumour xenografts." Br. J. Radiol. 81: S21-S27 (2008). •Cediranib reverses ABCB1 (P-glycoprotein)- and ABCC1 (MRP1)-mediated multidrug resistance by directly inhibiting their drug efflux function. Tao, L.Y., et al. "Cediranib (recentin, AZD2171) reverses ABCB1- and ABCC1-mediated multidrug resistance by inhibition of their transport function." Cancer Chemother. Pharmacol. 64: 961-969 (2009). •Cediranib is the active ingredient in the drug formulation designated by the trade name Recentin®. This drug has been in human clinical trials for use in patients with non-small cell lung cancer, small cell lung cancer, kidney cancer, colorectal cancer, breast cancer, liver and ovarian cancer, melanoma, mesothelioma, and glioblastoma. NOTE: THE CEDIRANIB, FREE BASE RE
C-4300 Cediranib, Free Base, >99% Synonyms: [AZD2171] Related Terms: [Recentin]M.W. 450.51 C25H27FN4O3 [288383-20-0] Storage: Store at or below -20 ºC. Solubility: Soluble in DMSO. Disposal: A •Cediranib is a highly potent inhibitor of recombinant KDR tyrosine kinase activity in vitro (IC50 < 1 nM). Inhibitory activity was also observed against the kinase associated with Flt-1 (IC50 = 5 nM), the VEGF-C and VEGF-D receptor Flt-4 (IC50 ≤ 3 nM), recombinant PDGFR-related kinase c-Kit (IC50 = 2 nM), and PDGFRβ tyrosine kinase (IC50 = 5 nM). In HUVEC, it inhibited VEGF-stimulated phosphorylation of KDR, c-Kit, PDGFR-α, PDGFR-β in a dose-dependent manner with IC50 values of 0.5, 1, 5, and 8 nM, respectively. It inhibited VEGF-stimulated HUVEC proliferation potently with an IC50 value of 0.4 nM. Consistent with potent activity against VEGF signaling, cediranib inhibited vessel branching, length, and area in vitro with IC50 values of 0.1, 0.1, and 0.2 nM, respectively. It also completely abolished VEGF-induced angiogenesis in vivo. However, it inhibited tumor cell proliferation in vitro only at comparatively high concentrations, showing IC50 values of 3.0 µM for SKOV-3 cells, 3.8 µM for MDA-MB-231 cells, 5.8 µM for PC-3 cells, 6.4 µM for Calu-6 cells, and 7.4 µM for SW620 cells. It also inhibited the growth of these five tumor models in nude mice. Furthermore, cediranib induced vascular regression in human lung tumor xenografts. Wedge, S.R., et al. "AZD2171: a highly potent, orally bioavailable, vascular endothelial growth factor receptor-2 tyrosine kinase inhibitor for the treatment of cancer." Cancer Res. 65: 4389-4400 (2005). •Cediranib significantly increased survival of mice wth glioblastoma by decreasing tumor vessel permeability, normalizing perivascular cell coverage, and thinning of the basement membrane, thus controlling edema. Kamoun, W.S., et al. "Edema control by cediranib, a vascular endothelial growth factor receptor-targeted kinase inhibitor, prolongs survival despite persistent brain tumor growth in mice." J. Clin. Oncol. 27: 2542-2552 (2009). •Hypertension induced by cediranib is reported to be manageable. Langenberg, M.H., et al. "Effective strategies for management of hypertension after vascular endothelial growth factor signaling inhibition therapy: results from a phase II randomized, factorial, double-blind study of Cediranib in patients with advanced solid tumors." J. Clin. Oncol. 27: 6152-6159 (2009). •Cediranib demonstrated potent antitumor and antiangiogenic efficacy in the murine renal cell carcinoma model. Medinger, M., et al. "Antitumor and antiangiogenic activity of cediranib in a preclinical model of renal cell carcinoma." Anticancer Res. 29: 5065-5076 (2009). •Combined treatments of cediranib with radiation in Calu-6 lung xenografts induced a significantly enhanced growth delay when compared with either modality alone. Williams, K.J., et al. "Inhibition of vascular endothelial growth factor signalling using cediranib (RECENTIN; AZD2171) enhances radiation response and causes substantial physiological changes in lung tumour xenografts." Br. J. Radiol. 81: S21-S27 (2008). •Cediranib reverses ABCB1 (P-glycoprotein)- and ABCC1 (MRP1)-mediated multidrug resistance by directly inhibiting their drug efflux function. Tao, L.Y., et al. "Cediranib (recentin, AZD2171) reverses ABCB1- and ABCC1-mediated multidrug resistance by inhibition of their transport function." Cancer Chemother. Pharmacol. 64: 961-969 (2009). •Cediranib is the active ingredient in the drug formulation designated by the trade name Recentin®. This drug has been in human clinical trials for use in patients with non-small cell lung cancer, small cell lung cancer, kidney cancer, colorectal cancer, breast cancer, liver and ovarian cancer, melanoma, mesothelioma, and glioblastoma. NOTE: THE CEDIRANIB, FREE BASE RE
Cediranib Description Cediranib is a potent antitumor and antiangiogenic compound. It inhibits vascular endotheial growth factor(VEGF) receptor tyrosine kinases. Specifications Cas No. 288383-20-0 Product ID C1613 Product Name Cediranib Synonym AZD2171 Formula Wt. 450.51 References Wedge SR, Kendrew J, Hennequin LF, et al Cancer Res. 65:4389-4400 (2005). Medinger M, Esser N, Zirrgiebel U, et al. Anticancer Res. 29:065-76 (2009).
Cediranib Description Cediranib is a potent antitumor and antiangiogenic compound. It inhibits vascular endotheial growth factor(VEGF) receptor tyrosine kinases. Specifications Cas No. 288383-20-0 Product ID C1613 Product Name Cediranib Synonym AZD2171 Formula Wt. 450.51 References Wedge SR, Kendrew J, Hennequin LF, et al Cancer Res. 65:4389-4400 (2005). Medinger M, Esser N, Zirrgiebel U, et al. Anticancer Res. 29:065-76 (2009).
Cediranib Description Cediranib is a potent antitumor and antiangiogenic compound. It inhibits vascular endotheial growth factor(VEGF) receptor tyrosine kinases. Specifications Cas No. 288383-20-0 Product ID C1613 Product Name Cediranib Synonym AZD2171 Formula Wt. 450.51 References Wedge SR, Kendrew J, Hennequin LF, et al Cancer Res. 65:4389-4400 (2005). Medinger M, Esser N, Zirrgiebel U, et al. Anticancer Res. 29:065-76 (2009).
