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[Ridogrel, a new platelet antiaggregant molecule with a double mechanism of action. A pharmacological and clinical profile].

Ridogrel has a double mechanism of action: it is a combined thromboxane A2 synthetase inhibitor and thromboxane A2/prostaglandin endoperoxide receptor blocker, demonstrated in vitro, as well as in vivo in animals and in man. In man, ridogrel is quickly absorbed after oral administration (30-60 min). The half-life is about 6-9 hours. At the oral dose of 300 mg b.i.d., the steady state has been reached at the third day of administration. Pharmacodynamic studies in healthy volunteers as well as in patients demonstrate a marked decrease in TXB2 serum level and an increase in 6ketoPGF1 alpha level. Moreover ridogrel inhibits the human platelet aggregation induced by U46619, collagen and arachidonic acid (thromboxane A2/prostaglandin endoperoxide receptor blocker). During the ridogrel treatment there have been neither variations of coagulative parameters (PTT, APTT, plasmatic fibrinogen) nor variations of other metabolic parameters except for those concerning the antiaggregant activity. To conclude, the preliminary data on about 100 healthy volunteers and more than 100 patients show that pharmacologic combined actions on enzyme and on receptors could be more efficacious than one single activity in eliminating circulatory flux resistance, in potentiating thrombolysis and in preventing or postponing vessels reocclusions. According to the above-mentioned results, ridogrel could have a good application in correction of thrombotic disorders due to platelet activation.