(Z)-Orantinib

210644-62-5

310.35

DMSO : 50 mg/mL (161.11 mM; Need ultrasonic)

Protein Tyrosine Kinase/RTK; Protein Tyrosine Kinase/RTK; Protein Tyrosine Kinase/RTK

(Z)-Orantinib ((Z)-SU6668) is a potent, selective, orally active and ATP competitive inhibitor of Flk?1/KDR, PDGFRbeta, and FGFR1, with IC₅₀s of 2.1, 0.008, and 1.2 uM, respectively. (Z)-Orantinib is a potent antiangiogenic and antitumor agent that induces regression of established tumors^[1][2]. In Vitro: SU6668 (5-15 min) inhibits Flk-1 trans-phosphorylation (K_i=2.1 uM), FGFR1 trans-phosphorylation (K_i=1.2 uM), and PDGFR autophosphorylation (K_i=0.008 uM)^[1].
SU6668 (0.03-10 uM; 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 uM, respectively^[1].
In Vivo: 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].