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CP 1415 S is a new phenyloxypropanolami ne derivative.  In vitro CP 1415 S inhibits aggregation of human platelets inaucedby collagen (EC50 9 μM) or arachidonic acid (EC50 12μM). It also primary and secondary phases of ADP, thrombin and epinephrine induced platelet aggregation. Effective concentrations are in the same range (10 μM) as concerns the secondary aggregation and higher as concerns the primary phase. In presence of 50 μM CP 1415 S, platelet aggregation is fully prevented. Addition of CP 1415 S to platelets maximally aggregated by ADP causes disaggregation in a dose dependent way (EC50 50 μM); similar effect is observed only with prostacyclin (PGI2) and PGE1Ex-vivo, the antiaggregating properties of CP 1415 S have been demonstrated after single oral administration to rats and Rhesus monkeys (minimal effective dose 10 and 20 mg/kg respectively). After repeated oral administrations, antiaggregating activity was observed from 3 mg/kg/day in rats.  In vivo, in rats, using the tail transsection model, bleeding time was significantly (p &lt; 0.01) prolonged by 10 mg/kg P.o. CP 1415 S or ticlopidine. CP 1415 S given orally up to 100 mg/kg had no effect on prothrombin time. CP 1415 S at 1 mg/kg p.o., 2 hours before testing, protected rats (p &lt; 0.001) against acute thrombocytopenia induced by i.v. injection of ADP whereas acetyl salicylic acid and dipiridamole were inactive at 100 mg/kg and ticlopidine was unsignificantly active. Prostacyclin-like substance production by rat vascular tissue, measured by platelet aggregation bioassay, was not affected in rats after 5 or 10 mg/kg i.v.  CP 1415 S appears to be a potent inhibitor of platelet aggregation in vitro and ex-vivo. Its ability to disaggregate platelets is currently tested in in vivo models of thrombosis.

In Vitro And In Vivo Studies On CP 1415 S A New Platelet Antiaggregating Compound