Question:

How aspirin acts as an antiplatelet?

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Aspirin thins the blood by stopping platelets from making the chemical (thromboxane A 2 ) that makes them clump together. The key is how aspirin chemically alters the enzyme involved.
Updated On: Jun 24, 2026
  • Formation of Acetic acid
  • Breaking down to Salicylic acid
  • Acetylates of COX-1 enzyme
  • Production of Gentisic acid
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The Correct Option is C

Solution and Explanation

Concept:
Aspirin thins the blood by stopping platelets from making the chemical (thromboxane A2) that makes them clump together. The key is how aspirin chemically alters the enzyme involved.

Step 1: Platelets use the enzyme cyclooxygenase-1 (COX-1) to produce thromboxane A2, a strong promoter of platelet aggregation.

Step 2: Aspirin transfers its acetyl group onto a serine residue in COX-1, acetylating the enzyme. This block is irreversible — and since platelets have no nucleus to make new enzyme, the effect lasts the platelet's whole lifespan (about 7–10 days).

Why the others are wrong: Salicylic acid, acetic acid and gentisic acid are just breakdown/metabolic products of aspirin; they are not the cause of the antiplatelet action. The antiplatelet effect comes specifically from acetylation of COX-1.

Answer: Option (3) — Acetylates of COX-1 enzyme.
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