Ex-vivo and in-vivo antithrombotic effect of triflavin, and RGD-containing peptide

Triflavin an Arg-Gly-Asp-containing snake venom peptide inhibits platelet aggregation through the blockade of fibrinogen binding to the activated platelets. It binds to fibrinogen receptors associated with the glycoprotein IIb/IIIa complex with a K(d) value of 7 x 10^-8 M. In this study we found that ¹²⁵I-triflavin reached the maximal binding to human platelets within 5 min at 25°C. In addition, when triflavin was intravenously administered at 1.0 mg kg^-1 to rabbits it reversibly impaired the platelet aggregation of platelet-rich plasma caused by ADP (20 μM) ex-vivo over 30 min. The platelet counts of the experimental rabbits remained unchanged. Triflavin was effective in reducing the mortality of ADP-induced acute pulmonary thromboembolism in mice when administered intravenously at a dose of 2 μg g^-1. Therefore triflavin was proven to be an effective antithrombotic agent in preventing ADP-induced acute pulmonary thromboembolism in mice and impairing reversibly the platelet function of rabbits when given intravenously.