Network Version
Semaxinib Data Sheet
| Product Name: | Semaxinib |
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|---|---|---|
| CAS No.: | 204005-46-9 | |
| Cat. No.: | HY-10374 | |
| MWt: | 238.28 | |
| Formula: | C15H14N2O | |
| Purity : | >98% | |
| Solubility: | DMSO : 20 mg/mL (83.93 mM; Need ultrasonic); DMF : 50 mg/mL (209.84 mM; Need ultrasonic) | |
| Mechanisms: | Target: Cancer | |
| Biological Activity: | ||
| Semaxinib (SU5416) is a potent and selective inhibitor of VEGFR (Flk-1/KDR) with an IC50 of 1.23 μM[1]. IC50 & Target: IC50: 1.23±0.2 μM (Flk-1 receptor)[1] 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[1]. 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[1]. 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[2]. | ||
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