Semaxinib

本公司产品仅用于科研实验，不得用于人体或动物的临床与诊断

Semaxanib (SU5416) 是一种有效的选择性 VEGFR(Flk-1/KDR) 抑制剂。

Semaxanib (SU5416) is a potent and selective VEGFR(Flk-1/KDR) inhibitor with IC50 of 1.23μM, 20-fold more selective for VEGFR than PDGFR beta, lack of activity against EGFR, InsR and FGFR.(In Vitro):Semaxinib (SU5416) inhibits VEGF-driven mitogenesis in a dose-dependent manner with an IC50 of 0.04±0.02 μM (n=3). In contrast, Semaxinib (SU5416) blocks FGF-dependent mitogenesis of HUVECs with an IC50 of 50 μM (n=10). An IC50 of 20.26±5.2 μM, which is about 20-fold less in potency on PDGF-dependent autophosphorylation, is observed when SU5416 is tested in NIH 3T3 cells overexpressing the human PDGF receptor β(In Vivo):Daily administration of Semaxinib (SU5416) (i.p., 3 mg/kg/day) inhibits the local growth of C6 tumors in the colon. A comparable level of growth inhibition (62% by day 16; P=0.001) is observed for tumors growing in the colon in comparison with ones growing in the hindflank region (54% by day 18; P=0.001). These results indicate that Semaxinib (SU5416) could inhibit tumor growth at a site other than the subcutaneous implantation site, where the preexisting vasculature may be different. Daily treatment with Semaxinib (SU5416) (25 mg/kg) results in a significantly lower tumor growth rate with tumor masses of up to 8% of that present in control animals by day 22 after implantation. Inhibition of tumor growth is clearly preceded by a marked reduction of the tissue area covered by the newly formed glioma microvasculature in the Semaxinib-treated group, indicating a reduced initial tumor vascularization.

Semaxinib (SU5416) inhibits VEGF-driven mitogenesis in a dose-dependent manner with an IC50 of 0.04±0.02 μM (n=3). In contrast, Semaxinib (SU5416) blocks FGF-dependent mitogenesis of HUVECs with an IC50 of 50 μM (n=10). An IC50 of 20.26±5.2 μM, which is about 20-fold less in potency on PDGF-dependent autophosphorylation, is observed when SU5416 is tested in NIH 3T3 cells overexpressing the human PDGF receptor β.

Daily administration of Semaxinib (SU5416) (i.p., 3 mg/kg/day) inhibits the local growth of C6 tumors in the colon. A comparable level of growth inhibition (62% by day 16; P=0.001) is observed for tumors growing in the colon in comparison with ones growing in the hindflank region (54% by day 18; P=0.001). These results indicate that Semaxinib (SU5416) could inhibit tumor growth at a site other than the subcutaneous implantation site, where the preexisting vasculature may be different. Daily treatment with Semaxinib (SU5416) (25 mg/kg) results in a significantly lower tumor growth rate with tumor masses of up to 8% of that present in control animals by day 22 after implantation. Inhibition of tumor growth is clearly preceded by a marked reduction of the tissue area covered by the newly formed glioma microvasculature in the Semaxinib-treated group, indicating a reduced initial tumor vascularization.

SU 5416

Angiogenesis

VEGFR

Flk1

Cancer

Solid Tumors

204005-46-9

238.28

C15H14N2O

>98% (HPLC)

DMSO: 10 mM

O=C1NC2=C(C=CC=C2)/C1=C/C3=C(C)C=C(C)N3

(Z)-3-((3,5-dimethyl-1H-pyrrol-2-yl)methylene)indolin-2-one

(-20℃)

With Ice Pack

≥ 2 years