SU10944
SU10944 is a selective, orally active VEGFR inhibitor, with an IC50 of 6 nM against VEGFR-1, an IC50 of 96 nM and a Ki of 21 nM against VEGFR-2. SU10944 only exhibits weak inhibitory activity against PDGFRβ (IC50 = 1 μM), SCFR (IC50 = 1.58 μM) and FGFR-1 (IC50 = 1.6 μM). SU10944 selectively inhibits VEGFR receptor downstream signaling, neovascularization, vascular permeability, VEGF-mediated tissue factor production, and induces tumor growth delay. SU10944 can be used in research related to diabetic retinopathy, exudative age-related macular degeneration or cancer.
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- CAS No.: 515821-11-1
- Formule: C17H16N2O3
- Masse moléculaire:296.33
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Activité biologique
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Chemical Information
- Pureté et documentation
- Références
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Activité biologique
|
VEGFR1 6 nM (IC50) |
VEGFR2 96 nM (IC50) |
FGFR1 1/6 μM (IC50) |
SU10944 (2 h) inhibits VEGFR-2 autophosphorylation in transiently transfected human embryonic kidney 293T cells with an IC50 of 227 nM[1].
SU10944 (0.2-25 μM; 20 h) dose-dependently inhibits VEGF-induced VEGFR-2 autophosphorylation in stably transfected NIH/3T3 cells, with maximal inhibition at 25 μM[1].
SU10944 (varying concentrations; 4 h) inhibits VEGF-induced tissue factor production in human umbilical vein endothelial cells with an IC50 of 102 nM, without affecting PMA-stimulated tissue factor production[1].
SU10944 (varying concentrations; 20 h (3T3 assays); 3 days (MO7e assay)) inhibits SCFR-dependent MO7e cell survival (IC50 = 1.6 μM) and PDGFRβ-dependent 3T3 cell proliferation (IC50 = 30.6 μM), but does not inhibit EGFR- or FGFR-1-dependent 3T3 cell proliferation (IC50 > 50 μM) and is not cytotoxic to 3T3 cells at concentrations up to 50 μM[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:NIH/3T3 cells (stably expressing mouse VEGFR-2)
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Concentration:0.2, 1, 5 and 25 μM
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Incubation Time:20 h
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Result:Dose-dependently inhibited VEGF-induced VEGFR-2 autophosphorylation, with near-complete inhibition at 25 μM.
SU10944 (3-100 mg/kg; p.o.; single dose) time- and dose-dependently inhibits VEGF-induced vascular permeability in athymic mice, with a plasma concentration of 250 ng/mL correlating to 50% inhibition[1].
SU10944 (150 mg/kg; p.o.; once daily; 12 days) induces 76% growth inhibition of C6 glioma xenografts in nu/nu mice, accompanied by modest antiangiogenic activity[2].
SU10944 (150 mg/kg; p.o.; once daily; 15 days) induces 95% growth inhibition and maintains stasis of MV4;11 leukemia xenografts in nu/nu mice, with modest antiangiogenic activity[2].
SU10944 (150 mg/kg; p.o.; once daily; 18 days) induces 55% growth inhibition of HT-29 colon carcinoma xenografts in nu/nu mice[2].
SU10944 (150 mg/kg; p.o.; once daily; 14 days) induces 90% growth inhibition of 786-O renal carcinoma xenografts in nu/nu mice, accompanied by significant antiangiogenic activity[2].
SU10944 (150 mg/kg; p.o.; once daily; 29 days) induces 82% growth inhibition of WM-266-4 melanoma xenografts in nu/nu mice, with modest antiangiogenic activity[2].
SU10944 (150 mg/kg; p.o.; once daily; 14 days) induces 28% growth inhibition of H226 lung carcinoma xenografts in nu/nu mice, with moderate antiangiogenic activity[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Athymic[1]
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Dosage:3 mg/kg; 30 mg/kg; 100 mg/kg
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Administration:p.o.; single dose
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Result:Inhibited VEGF-induced vascular permeability in a time- and dose-dependent manner.
Sustained maximum inhibition up to 2 hours at 100 mg/kg, with 50% inhibition still apparent 24 hours postdose.
Showed maximum inhibition at 1 hour and decreased to zero by 24 hours at 30 mg/kg.
Associated 50% inhibition of VEGF-mediated vascular permeability with a plasma concentration of 250 ng/mL (844 nM).
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Animal Model:nu/nu (female, 8-12 weeks old, 25 g, rat C6 glioma cells implanted s.c. into hindflank)[2]
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Dosage:150 mg/kg
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Administration:p.o.; once daily; 12 days
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Result:Induced 76% tumor growth inhibition.
Reduced tumor microvessel density (MVD) by 20% relative to vehicle-treated controls.
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Animal Model:nu/nu (female, 8-12 weeks old, 25 g, human MV4;11 FLT3-ITD-mutated leukemia cells implanted s.c. into hindflank with 50% Matrigel)[2]
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Dosage:150 mg/kg
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Administration:p.o.; once daily; 15 days
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Result:Induced 95% tumor growth inhibition.
Maintained tumor stasis.
Reduced tumor microvessel density (MVD) by 40% relative to vehicle-treated controls.
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Animal Model:nu/nu (female, 8-12 weeks old, 25 g, human HT-29 colon carcinoma cells implanted s.c. into hindflank with 50% Matrigel)[2]
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Dosage:150 mg/kg
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Administration:p.o.; once daily; 18 days
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Result:Induced 55% tumor growth inhibition.
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Animal Model:nu/nu (female, 8-12 weeks old, 25 g, human 786-O renal carcinoma cells implanted s.c. into hindflank with 50% Matrigel)[2]
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Dosage:150 mg/kg
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Administration:p.o.; once daily; 14 days
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Result:Induced 90% tumor growth inhibition.
Reduced tumor microvessel density (MVD) by 54% relative to vehicle-treated controls.
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Animal Model:nu/nu (female, 8-12 weeks old, 25 g, human WM-266-4 melanoma cells implanted s.c. into hindflank)[2]
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Dosage:150 mg/kg
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Administration:p.o.; once daily; 29 days
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Result:Induced 82% tumor growth inhibition.
Reduced tumor microvessel density (MVD) by 23% relative to vehicle-treated controls.
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Animal Model:nu/nu (female, 8-12 weeks old, 25 g, human H226 lung carcinoma cells implanted s.c. into hindflank)[2]
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Dosage:150 mg/kg
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Administration:p.o.; once daily; 14 days
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Result:Induced 28% tumor growth inhibition.
Reduced tumor microvessel density (MVD) by 42% relative to vehicle-treated controls.
Chemical Information
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CAS No. 515821-11-1
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Masse moléculaire 296.33
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Formule C17H16N2O3
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SMILES
O=C(O)CCC=1C=C(NC1C=C2C(=O)NC=3C=CC=CC32)C
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Pureté et documentation
Références
[1]. Patel N, et al. A selective and oral small molecule inhibitor of vascular epithelial growth factor receptor (VEGFR)-2 and VEGFR-1 inhibits neovascularization and vascular permeability. J Pharmacol Exp Ther. 2003;306(3):838-845. [Content Brief]
[2]. Potapova O, et al. Contribution of individual targets to the antitumor efficacy of the multitargeted receptor tyrosine kinase inhibitor SU11248. Mol Cancer Ther. 2006;5(5):1280-1289. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
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