产品
编 号：F270502
分子式：C18H18N2O3
分子量：310.35
分子式：C18H18N2O3
分子量：310.35
产品类型
规格
价格
是否有货
10mM*1mL in DMSO
询价
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5mg
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10mg
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50mg
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100mg
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结构图
CAS No: 210644-62-5
产品详情
生物活性：
(Z)-Orantinib ((Z)-SU6668) is a potent, selective, orally active and ATP competitive inhibitor of Flk‐1/KDR, PDGFRβ, and FGFR1, with IC50s of 2.1, 0.008, and 1.2 μM, respectively. (Z)-Orantinib is a potent antiangiogenic and antitumor agent that induces regression of established tumors.
体内研究：
SU6668 (4-200 mg/kg/day; p.o. for 21 d) induces dose-dependent inhibition of A431 tumor growth in athymic mice.SU6668 (75 mg/kg/day; i.p. for 22 d) significantly suppresses tumor angiogenesis and vascularization in mice.SU6668 (200 mg/kg/day; p.o. for 11-27 d) induces striking regression of large established A431 xenografts in athymic mice.Animal Model:Female athymic mice (BALB/c, nu/nu) were implanted A431 tumor cells
Dosage:4, 40, 75, 200 mg/kg
Administration:P.o. daily for 21 days
Result:Induced 97% growth inhibition against A431 tumor at the dose of 97%.No mortality was observed in any treatment group.
体外研究：
SU6668 (5-15 min) inhibits Flk-1 trans-phosphorylation (Ki=2.1 μM), FGFR1 trans-phosphorylation (Ki=1.2 μM), and PDGFR autophosphorylation (Ki=0.008 μM).SU6668 (0.03-10 μM; 60 min) inhibits the VEGF-stimulated increase of KDR tyrosine phosphorylation in HUVECs.SU6668 inhibits mitogenesis of HUVECs induced by both VEGF and FGF in a dose-dependent manner with IC50s of 0.34 and 9.6 μM, respectively.
(Z)-Orantinib ((Z)-SU6668) is a potent, selective, orally active and ATP competitive inhibitor of Flk‐1/KDR, PDGFRβ, and FGFR1, with IC50s of 2.1, 0.008, and 1.2 μM, respectively. (Z)-Orantinib is a potent antiangiogenic and antitumor agent that induces regression of established tumors.
体内研究：
SU6668 (4-200 mg/kg/day; p.o. for 21 d) induces dose-dependent inhibition of A431 tumor growth in athymic mice.SU6668 (75 mg/kg/day; i.p. for 22 d) significantly suppresses tumor angiogenesis and vascularization in mice.SU6668 (200 mg/kg/day; p.o. for 11-27 d) induces striking regression of large established A431 xenografts in athymic mice.Animal Model:Female athymic mice (BALB/c, nu/nu) were implanted A431 tumor cells
Dosage:4, 40, 75, 200 mg/kg
Administration:P.o. daily for 21 days
Result:Induced 97% growth inhibition against A431 tumor at the dose of 97%.No mortality was observed in any treatment group.
体外研究：
SU6668 (5-15 min) inhibits Flk-1 trans-phosphorylation (Ki=2.1 μM), FGFR1 trans-phosphorylation (Ki=1.2 μM), and PDGFR autophosphorylation (Ki=0.008 μM).SU6668 (0.03-10 μM; 60 min) inhibits the VEGF-stimulated increase of KDR tyrosine phosphorylation in HUVECs.SU6668 inhibits mitogenesis of HUVECs induced by both VEGF and FGF in a dose-dependent manner with IC50s of 0.34 and 9.6 μM, respectively.
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