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

Autoren

  • 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
Weitere Informationen

Publikationsverlauf

Received 10. April 1975

Accepted 28. Juli 1975

Publikationsdatum:
02. Juli 2018 (online)

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.