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(Z)-Orantinib
本产品不向个人销售，仅用作科学研究，不用于任何人体实验及非科研性质的动物实验。
(Z)-Orantinib图片
CAS NO:210644-62-5
包装与价格：
包装价格(元)
10mM (in 1mL DMSO)电议
10mg电议
50mg电议
100mg电议

产品介绍
(Z)-Orantinib ((Z)-SU6668) 是一种有效，选择性，具有口服活性和 ATP 竞争性的 Flk‐1/KDR，PDGFRβ 和 FGFR1 抑制剂，IC50 值分别为 2.1，0.008 和 1.2 µM。(Z)-Orantinib 是有效的抗血管生成和抗肿瘤剂，可诱导已建立的肿瘤消退。
Cas No.210644-62-5
别名(Z)-SU6668; (Z)-TSU-68
分子式C18H18N2O3
分子量310.35
溶解度DMSO : 50 mg/mL (161.11 mM; Need ultrasonic)
储存条件Store at -20°C
General tipsFor obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.
Shipping ConditionEvaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request
产品描述

(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[1][2].

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)[1].SU6668 (0.03-10 μM; 60 min) inhibits the VEGF-stimulated increase of KDR tyrosine phosphorylation in HUVECs[1].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[1].

SU6668 (4-200 mg/kg/day; p.o. for 21 d) induces dose-dependent inhibition of A431 tumor growth in athymic mice[1].SU6668 (75 mg/kg/day; i.p. for 22 d) significantly suppresses tumor angiogenesis and vascularization in mice[1].SU6668 (200 mg/kg/day; p.o. for 11-27 d) induces striking regression of large established A431 xenografts in athymic mice[1].

[1]. Laird AD, et, al. SU6668 is a potent antiangiogenic and antitumor agent that induces regression of established tumors. Cancer Res. 2000 Aug 1;60(15):4152-60.
[2]. Laird ad, et, al. SU6668 inhibits Flk-1/KDR and PDGFRbeta in vivo, resulting in rapid apoptosis of tumor vasculature and tumor regression in mice. FASEB J. 2002 May;16(7):681-90.