In vitro effect of mopidamol on platelet-subendothelium interaction.

Chemical substitutions in the structure of the pyrimido-pyrimidine nucleus give rise to pyrimidopyrimidine compounds with platelet antiaggregatory effects, such as RA-8 (dipyridamole), RA233 (mopidamol) and RA-642. All these compounds inhibit platelet aggregation-induced by ADP through an increase in platelet CAMP levels (1,2). Mopidamol, however, is 3-10 times more potent than dipyridamole and RA-642 both in whole blood and platelet-rich plasma (3) and determines an increase in CAMP levels which is almost 22 times greater than that caused by equimolar concentrations of dipyridamole and RA-642 (2). In contrast to dipyridamole which causes an increase in prostacyclin synthesis, the effect of mopidamol on arachidonic acid metabolism is negligible. On the other hand, platelet thromboxane synthesis is inhibited by mopidamol but unaffected by dipyridamole (4).