(Z)-Orantinib (Synonyms: (Z)-SU6668; (Z)-TSU-68) |
| Catalog No.GC62291 |
Le (Z)-orantinib ((Z)-SU6668) est un inhibiteur puissant, sélectif, actif par voie orale et compétitif de l'ATP de Flk‐1/KDR, PDGFRβ et FGFR1, avec des IC50 de 2,1, 0,008 et 1,2 μM, respectivement. Le (Z)-orantinib est un puissant agent antiangiogénique et antitumoral qui induit la régression des tumeurs établies.
Products are for research use only. Not for human use. We do not sell to patients.
Cas No.: 210644-62-5
Sample solution is provided at 25 µL, 10mM.
;)
,-1-7$$$37316672.jpg');)
;)
;)
$$$36806353.jpg');)
;33(7)%EF%BC%9A546-561$$$37156877.jpg');)
;)
;)
;)
%201124-1138.$$$35908550.jpg');)
%20766-780.$$$37100057.jpg');)
%20418-432.$$$36893736.jpg');)
%EF%BC%9A-240-255.$$$35108512.jpg');)
533-545$$$36543525.jpg');)
%201-13.$$$36600053.jpg');)
;)
(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.
Average Rating: 5 (Based on Reviews and 38 reference(s) in Google Scholar.)
GLPBIO products are for RESEARCH USE ONLY. Please make sure your review or question is research based.
Required fields are marked with *