SU5416 inhibits VEGF-driven mitogenesis in a dose-dependent manner with an IC50 of 0.04±0.02 μM (n=3). In contrast, SU5416 blocked FGF-dependent mitogenesis of HUVECs with an IC50 of 50 μM (n=10). The selective activity of SU5416 on Flk-1 is supported by the fact that testing of SU5416 using NIH 3T3 cells overexpressing either the EGF or insulin receptors indicated a complete lack of activity (IC50>100 μM). This observation is confirmed by immunoblotting after ligand stimulation. An IC50 of 20.26±5.2 μM (n=7), 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].

Daily administration of 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 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 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 SU5416-treated group, indicating a reduced initial tumor vascularization[2].