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The effects of a synthetic tripeptide, Gyki 14,451(Boc-D Phe-Pro-Arg-H)have been studied in vitro on human platelet aggregation and arachidonic acid (AA) metabolism and in vivo on experimentally induced venous thrombosis in the rat.  1 μM Gyki 14,451 concentration selectively inhibits thrombin induced platelet aggregation as well as malondial- dehyde (MDA) and thromboxane B2 (TXB2) formation by platelet rich plasma (PRP) stimulated with thrombin. Far higher concentrations (400μM)of the peptide are required to exert an inhibitory effect when collagen, ADP and AA are used to stimulate platelets. No effect has been observed on the conversion of 14C AA to metabolites using unstimulated platelets. Kinetic studies of MDA production by platelets stimulated with thrombin and its inhibition by Gyki 14,451 (0.15,0.3,0.6 uM) suggest that the peptide interacts with thrombin by an apparently competitive mechanism.  4 mg/Kg of Gyki 14,451, intravenously injected in the rat caudal vein, completely inhibited the occurrence of venous thrombosis, obtained by vena cava ligature.  The oral administration of the peptide (50 mg/Kg by gastric intubation) failed to reduce the percentage of incidence of venous thrombosis (88% in controls versus 90% in treated rats) resulting only in a reduction of the thrombus weight. These data suggest that the anticoagulant peptide Gyki 14,451, given intravenously, possesses a consistent activity in the prevention of experimentally induced venous thrombosis.

Gyki 14,451, A Specific Inhibitor Of Thrombin:“In Vitro” And“In Vivo”Studies