Aspirin and Antiplatelet Medications

  • Medical Author:
    Omudhome Ogbru, PharmD

    Dr. Ogbru received his Doctorate in Pharmacy from the University of the Pacific School of Pharmacy in 1995. He completed a Pharmacy Practice Residency at the University of Arizona/University Medical Center in 1996. He was a Professor of Pharmacy Practice and a Regional Clerkship Coordinator for the University of the Pacific School of Pharmacy from 1996-99.

  • Medical Author: Daniel Lee Kulick, MD, FACC, FSCAI
    Daniel Lee Kulick, MD, FACC, FSCAI

    Dr. Kulick received his undergraduate and medical degrees from the University of Southern California, School of Medicine. He performed his residency in internal medicine at the Harbor-University of California Los Angeles Medical Center and a fellowship in the section of cardiology at the Los Angeles County-University of Southern California Medical Center. He is board certified in Internal Medicine and Cardiology.

  • Medical Editor: Jay W. Marks, MD
    Jay W. Marks, MD

    Jay W. Marks, MD

    Jay W. Marks, MD, is a board-certified internist and gastroenterologist. He graduated from Yale University School of Medicine and trained in internal medicine and gastroenterology at UCLA/Cedars-Sinai Medical Center in Los Angeles.

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What are antiplatelet agents and how do they work?

Antiplatelet agents are medications that block the formation of blood clots by preventing the clumping of platelets. There are four types of antiplatelet agents:

  1. aspirin,
  2. thienopyridines and other ADP receptor blockers,
  3. glycoprotein IIb/IIIa inhibitors, and
  4. Par-1 antagonist

These agents differ in the way they work, their potency (how strongly they prevent clumping), how rapidly they work, and their cost.

What are platelets, and how do they work?

Platelets are particles (actually, remnants of cells) circulating in the blood that are needed in order for blood clots to form. Platelets initiate the formation of blood clots by sticking together (clumping or aggregating), a process called platelet aggregation. Clumps of platelets then are further bound together by a protein (fibrin) formed by factors present in the blood that promote the formation of fibrin. The clumps of platelets and fibrin make up the blood clot.

Blood clots are important because they stop bleeding (for example, a cut or laceration on the skin). When bleeding occurs from a cut, platelets become activated and form a network by attaching to the blood vessel wall at the site of bleeding, and also by attracting other clotting factors in the blood to promote the formation of fibrin to stop ongoing bleeding rapidly.

However, if a blood clot forms inside an artery, it blocks the flow of blood to the tissue that the artery supplies, which can damage the tissue. For example, a blood clot that forms in a coronary artery supplying blood to the muscle of the heart causes a heart attack, and a blood clot that forms in an artery supplying blood to the brain causes a stroke.

How do antiplatelet agents work?


Aspirin prevents blood from clotting by blocking the production by platelets of thromboxane A-2, the chemical that causes platelets to clump. Aspirin accomplishes this by inhibiting the enzyme cyclo-oxygenase-1 (COX-1) that produces thromboxane A-2. While other NSAIDs also inhibit the COX-1 enzyme, aspirin is the preferred NSAID for use as an antiplatelet agent because its inhibition of the COX-1 enzyme lasts much longer than the other NSAIDs (aspirin's antiplatelet effect lasts days while the other NSAIDs' antiplatelet effects last only hours).

Thienopyridines and other ADP receptor blockers

In addition to thromboxane A-2, platelets also produce adenosine diphosphate (ADP). When ADP attaches to receptors on the surface of platelets, the platelets clump. The thienopyridines, for example, ticlopidine (no longer available), prasugrel (Effient), and clopidogrel (Plavix), block the ADP receptor. Blocking the ADP receptor prevents ADP from attaching to the receptor and the platelets from clumping. Ticagrelor (Brilinta) also blocks the ADP receptor but it is chemically not a thienopyridine.

Glycoprotein IIb/IIIa inhibitors

The glycoprotein IIb/IIIa inhibitors, such as abciximab (Reopro) and eptifibatide (Integrilin), prevent clumping by inhibiting a different receptor on the surface of platelets, the receptor for glycoprotein IIb/IIIa. The glycoprotein IIb/IIIa inhibitors that are approved by the FDA must be given intravenously (in the veins).


This is a new class of anti-platelet drug, and the only approved drug in this class is vorapaxar (Zontivity). Vorapaxar works by blocking protease-activated receptor-1 (PAR-1) found on platelets. This prevents platelets from clumping together in response to a proclotting factor called thrombin. Vorapaxar is active in the body for many days.

What is the relative potency of the antiplatelet agents?

  • Since aspirin blocks only one of the several pathways by which platelet aggregation can occur, aspirin is a weak antiplatelet agent because platelet aggregation can be stimulated via another pathway.
  • Since glycoprotein IIb/IIIa inhibitors block the final common pathway for platelet aggregation (platelet aggregation is blocked regardless of the nature of the initial stimuli), glycoprotein IIb/IIIa inhibitors are the most potent antiplatelet agents. The maximal antiplatelet effect of glycoprotein IIb/IIIa inhibitors is approximately nine times that of aspirin.
  • The maximal antiplatelet effect of thienopyridines and vorapaxar is in between that of aspirin and the glycoprotein IIb/IIIa inhibitors.
Medically Reviewed by a Doctor on 10/15/2015

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