Summary
Halofenate free acid (HFA), the major metabolite of the hypolipemic agent halofenate,
blocked the secondary phase of human platelet aggregation induced by ADP, epinephrine,
or thrombin; higher concentrations of clohbrate free acid (CFA) were required to produce
similar inhibitory effects on platelet aggregation. HFA and CFA inhibited collagen-induced
aggregation of human, rat, or guinea pig platelets. Halofenate orally administered
to rats caused inhibition of collagen-induced aggregation when plasma levels of HFA
exceeded 300 μg/ml, a clinically achievable human plasma concentration. The platelet
inhibitory effects of clofibrate administration were less than those observed with
halofenate administration.