Clinical pharmacology of the adenosine diphosphate (ADP) receptor antagonist, clopidogrel

Vasc Med. 1998;3(3):247-51. doi: 10.1177/1358836X9800300312.

Abstract

Antiplatelet compounds interfere with the platelet activation cascade at different levels. The antiplatelet effect of the thienopyridine, clopidogrel, results from antagonism of a platelet ADP receptor, P2T, resulting in inhibition of platelet activation. This antagonism is non-competitive, irreversible, and results in a 50-70% inhibition of platelet fibrinogen binding. Additionally, clopidogrel may also antagonize the ADP-induced inhibition of adenylate cyclase, possibly resulting in an elevated platelet cyclic adenosine monophosphate level after stimulation by an appropriate agonist, such as prostacyclin. This spectrum of antiplatelet activities is different from that of aspirin. Further, clopidogrel is associated with a reduction in gastrointestinal hemorrhage, making it a valuable therapeutic alternative to aspirin in oral, long-term prevention of atherothrombotic vascular occlusion.

Publication types

  • Comparative Study
  • Review

MeSH terms

  • Adenosine Diphosphate / physiology
  • Animals
  • Arteriosclerosis / drug therapy
  • Arteriosclerosis / etiology
  • Aspirin / therapeutic use
  • Clopidogrel
  • Humans
  • Platelet Activation / physiology
  • Platelet Aggregation Inhibitors / pharmacology*
  • Platelet Aggregation Inhibitors / therapeutic use
  • Purinergic P2 Receptor Antagonists*
  • Rats
  • Receptors, Purinergic P2 / metabolism
  • Signal Transduction
  • Thrombosis / drug therapy
  • Thrombosis / etiology
  • Thrombosis / physiopathology
  • Ticlopidine / analogs & derivatives*
  • Ticlopidine / pharmacology
  • Ticlopidine / therapeutic use

Substances

  • Platelet Aggregation Inhibitors
  • Purinergic P2 Receptor Antagonists
  • Receptors, Purinergic P2
  • Adenosine Diphosphate
  • Clopidogrel
  • Ticlopidine
  • Aspirin