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Aspirin is best thought of as an antiplatelet medication. It works by irreversibly inhibiting the enzyme cyclooxygenase-1 in platelets, which blocks the production of thromboxane A2, a chemical that promotes platelet activation and aggregation. Because platelets don’t have nuclei, they can’t replace the COX-1 enzyme, so the antiplatelet effect lasts for the life of the platelet (about 7–10 days). This direct action to prevent platelets from clumping explains its primary use in reducing clot formation and preventing heart attacks and strokes. While aspirin also has analgesic and anti-inflammatory effects, its classification here reflects its main clinical role and mechanism—preventing platelets from aggregating. It is not an anticoagulant, which would target the broader coagulation cascade, nor an antibiotic.