
Cellagen Technology
Flk-1/KDR inhibitor
SU5416 (Semaxinib) is a reversible, ATP-competitive, oxindole-based inhibitor of Flk-1/KDR receptor tyrosine kinase. SU5416 inhibits VEGF-dependent phosphorylation of the Flk-1 receptor in Flk-1-overexpressing NIH 3T3 cells with a IC50 of 1.04 uM. In an ELISA-based assay, SU5416 inhibits autophosphorylation of the Flk-1 receptor at an IC50 of 1.23 uM. [1]
In a mitogenic/proliferation assay in HUVECs, the IC50 of SU5416 is extremely time-dependent, ranging from 1 uM to 40 nM at 48h incubation. These data in conjunction with dose-ranging studies support regimens of less than once-daily dosing of SU5416. [2]
More recent studies have shown that SU5416 is also an agonist of the aryl hydrocarbon receptor (AHR), leading to the generation of regulatory T-cells in vitro. SU5416 also upregulates CYP1A1 and CYP1B1. [3]





Cellagen Technology
Flk-1/KDR inhibitor


SU5416 (Semaxinib) is a reversible, ATP-competitive, oxindole-based inhibitor of Flk-1/KDR receptor tyrosine kinase. SU5416 inhibits VEGF-dependent phosphorylation of the Flk-1 receptor in Flk-1-overexpressing NIH 3T3 cells with a IC50 of 1.04 uM. In an ELISA-based assay, SU5416 inhibits autophosphorylation of the Flk-1 receptor at an IC50 of 1.23 uM. [1]
In a mitogenic/proliferation assay in HUVECs, the IC50 of SU5416 is extremely time-dependent, ranging from 1 uM to 40 nM at 48h incubation. These data in conjunction with dose-ranging studies support regimens of less than once-daily dosing of SU5416. [2]
More recent studies have shown that SU5416 is also an agonist of the aryl hydrocarbon receptor (AHR), leading to the generation of regulatory T-cells in vitro. SU5416 also upregulates CYP1A1 and CYP1B1. [3]