Small molecule
PubChem CID 2244
Aspirin
Bayer
- Mechanism of action
- Irreversible COX-1 inhibitor (antiplatelet)
- In plain language
- Blocks a clotting-related enzyme in platelets so they can't stick together as easily, which lowers the risk of dangerous blood clots.
- How it works
- Aspirin irreversibly acetylates a serine residue in the active site of cyclooxygenase-1 (COX-1), permanently disabling the enzyme's ability to convert arachidonic acid into prostaglandin H2, the precursor of thromboxane A2 (TXA2). Because platelets are anucleate and cannot synthesize new COX-1, this inhibition persists for the platelet's roughly 7-10 day lifespan, producing a sustained antiplatelet effect even at low doses (e.g., 81 mg). At higher doses, aspirin also inhibits COX-1/COX-2 in other tissues, reducing prostaglandin-mediated pain, fever, and inflammation. The net effect is reduced thromboxane A2-driven platelet aggregation and vasoconstriction, lowering the risk of arterial thrombosis, alongside analgesic and antipyretic activity from broader prostaglandin suppression.
- Therapeutic applications
- Aspirin is FDA-indicated (via OTC monograph and NDA-approved formulations) for temporary relief of minor aches and pain, headache, muscle and joint pain, toothache, menstrual cramps, and fever/pain associated with the common cold, as well as minor arthritis pain. Low-dose formulations are additionally used, under physician direction, for secondary prevention of myocardial infarction and ischemic stroke/TIA in patients with established atherosclerotic cardiovascular disease, and in combination products for reduction of stroke risk. It is also used in acute coronary syndrome management per clinical practice guidelines.
- Class
- Small molecule
- Therapeutic area
- Antiplatelet / Analgesic
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