Thromb Haemost 1976; 35(02): 358-363
DOI: 10.1055/s-0038-1647929
Original Article
Schattauer GmbH

The Effect of Halofenate or Halofenate Free Acid on Human, Rat and Guinea Pig Platelet Aggregation

D.H Minsker
1   Merck Institute for Therapeutic Research, West Point, Pennsylvania 19486, USA
,
P.T Jordan
1   Merck Institute for Therapeutic Research, West Point, Pennsylvania 19486, USA
,
P Kling
1   Merck Institute for Therapeutic Research, West Point, Pennsylvania 19486, USA
,
A MacMillan
1   Merck Institute for Therapeutic Research, West Point, Pennsylvania 19486, USA
,
H.B Hucker
1   Merck Institute for Therapeutic Research, West Point, Pennsylvania 19486, USA
,
D.J Tocco
1   Merck Institute for Therapeutic Research, West Point, Pennsylvania 19486, USA
› Author Affiliations
Further Information

Publication History

Received 10 April 1975

Accepted 28 July 1975

Publication Date:
02 July 2018 (online)

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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.