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Year : 2004  |  Volume : 36  |  Issue : 3  |  Page : 133--139

Glycoprotein IIb/IIIa receptor and its inhibition: A platelet-directed therapeutic strategy

HD Shah, RK Goyal 
 Department of Pharmacology, L. M. College of Pharmacy, Navrangpura, Ahmedabad, Gujarat, India

Correspondence Address:
R K Goyal
Department of Pharmacology, L. M. College of Pharmacy, Navrangpura, Ahmedabad, Gujarat
India

Platelets play a key role in atherosclerosis, thrombosis and acute coronary syndromes. Drugs that dissolve blood clot (thrombolytic agents) and that prevent clot propagation (antiplatelet and anticoagulant agents) are used to treat a broad array of cardiovascular diseases. Therapeutic manipulation of platelet function has focused principally on the use of aspirin which has proved effective in many clinical situations, despite its relatively weak antiplatelet action as compared to newer agents like ticlopidine, clopidogrel and more recently, platelet glycoprotein (GP) IIb/IIIa receptor inhibitors. The platelet GP IIb/IIIa receptor has been identified as a pivotal mediator of platelet aggregation, making it a logical target for the control of the platelet response to vascular injury. The primary mechanism of GP IIb/IIIa antagonists is the inhibition of the final common pathway of platelet aggregation: fibrinogen binding to the GP IIb/IIIa complex. Various antagonists of the GP IIb/IIIa receptor are currently receiving considerable attention and are being investigated for various clinical settings including angina, myocardial infarction and interventional cardiology.


How to cite this article:
Shah H D, Goyal R K. Glycoprotein IIb/IIIa receptor and its inhibition: A platelet-directed therapeutic strategy.Indian J Pharmacol 2004;36:133-139


How to cite this URL:
Shah H D, Goyal R K. Glycoprotein IIb/IIIa receptor and its inhibition: A platelet-directed therapeutic strategy. Indian J Pharmacol [serial online] 2004 [cited 2021 Jul 29 ];36:133-139
Available from: https://www.ijp-online.com/article.asp?issn=0253-7613;year=2004;volume=36;issue=3;spage=133;epage=139;aulast=Shah;type=0