Antiplatelets

Irreversible COX-1/COX-2 inhibitor — antiplatelet / NSAID

Irreversibly acetylates COX-1 → blocks thromboxane A2 for the platelet's lifespan (~7–10 days). Antiplatelet effect at low dose; analgesic/anti-inflammatory at high dose.

Thienopyridine P2Y12 receptor inhibitor (irreversible)

Prodrug → active metabolite (CYP2C19) irreversibly blocks the platelet P2Y12 ADP receptor for the platelet lifespan.

Thienopyridine P2Y12 receptor inhibitor (irreversible)

Prodrug → active metabolite irreversibly blocks P2Y12. More potent + more consistent than clopidogrel (not CYP2C19-limited), but more bleeding.

Cyclopentyltriazolopyrimidine — REVERSIBLE P2Y12 inhibitor

Directly and REVERSIBLY inhibits P2Y12 (not a prodrug, not thienopyridine). Faster onset/offset than clopidogrel.

First-generation thienopyridine P2Y12 inhibitor (irreversible)

Irreversibly blocks P2Y12. Largely replaced by clopidogrel due to hematologic toxicity.

Glycoprotein IIb/IIIa receptor inhibitor (monoclonal antibody)

Fab fragment that irreversibly blocks the platelet GP IIb/IIIa receptor → prevents fibrinogen cross-linking (final common pathway of aggregation).

Glycoprotein IIb/IIIa receptor inhibitor (small-molecule)

Reversibly blocks GP IIb/IIIa (final common pathway of platelet aggregation). Short-acting.

Phosphodiesterase inhibitor / adenosine reuptake inhibitor — antiplatelet + vasodilator

Inhibits platelet PDE (↑ cAMP) and adenosine reuptake (↑ adenosine → vasodilation). Weak antiplatelet; also a coronary vasodilator used in stress testing.

Phosphodiesterase-3 inhibitor — antiplatelet + vasodilator

Inhibits PDE3 → ↑ cAMP → antiplatelet + arterial vasodilation. Improves claudication walking distance.

Protease-activated receptor-1 (PAR-1) antagonist — antiplatelet

Blocks the thrombin platelet receptor (PAR-1) → inhibits thrombin-mediated aggregation without affecting the coagulation cascade itself.