Semaxinib

SKU: orb1225736

Description

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.

Key Properties

• CAS Number: 204005-46-9
• MW: 238.28
• Purity: >98% (HPLC)
• Formula: C₁₅H₁₄N₂O
• SMILES: O=C1NC2=C(C=CC=C2)/C1=C/C3=C(C)C=C(C)N3
• Target: VEGFR
• Solubility: DMSO: 10 mM

Bioactivity

• 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.
• 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.

Storage & Handling

• Storage: Storage temperature: -20°C. Stability: ≥ 2 years
• Expiration Date: 12 months from date of receipt.
• Disclaimer: For research use only

Alternative Names

SU 5416

Quick Database Links

Gene Symbol

VEGFR