Suramin, an anticancer and angiosuppressive agent, inhibits endothelial cell binding of basic fibroblast growth factor, migration, proliferation, and induction of urokinase-type plasminogen activator.

摘要: Suramin, an anticancer agent in current clinical trials, is a prototype of pharmacological antagonist growth factors, including basic fibroblast factor (bFGF). Suramin inhibited angiogenesis the chick chorioallantoic membrane assay dose-dependent fashion. 200 mg/kg i.v., rat corneal induced by bFGF-impregnated polymers; addition heparin stimulated and counteracted inhibition suramin. The half-maximal inhibitory concentration (IC50) suramin was determined for key cellular mechanisms that regulate angiogenesis: (a) low high affinity binding bFGF to bovine capillary endothelial (BCE) cells with IC50s, respectively, 24.3 71.5 micrograms/ml; (b) spontaneous migration pulmonary artery normal AG 7680 fetal aortic cells; bFGF-stimulated BCE transformed GM 7373 IC50s 200-320 (c) proliferation at > 100 micrograms/ml 250 (d) urokinase-type plasminogen activator activity IC50 211 micrograms/ml, but not phorbol 12-myristate 13-acetate. multiple control points angiogenesis, those bFGF. Because tumor dependent, efficacy may relate, part, angiosuppression.