Fibrinolytics. Antiplatelet Drugs
Fibrinolytics are enzymes that help dissolve blood clots, primarily by activating plasminogen to plasmin, which degrades fibrin clots. Antiplatelet drugs inhibit platelet aggregation, thus preventing the formation of blood clots.
Classification
- Aspirin and its derivatives:
- Acetylsalicylic acid, Clopidogrel, Prasugrel (Clopidogrel and Prasugrel are actually ADP receptor inhibitors too, but they're often grouped with aspirin for convenience due to similar clinical use.)
- ADP receptor inhibitors:
- Ticagrelor, Cangrelor, Ticlopidine (Note: These inhibit the P2Y12 receptor, a key in platelet activation.)
- GPIIb/IIIa inhibitors:
- Eptifibatide, Tirofiban (Used mostly in acute coronary syndromes and during PCI procedures.)
Fibrinolytics:
- Alteplase, Reteplase, Tenecteplase (These are tissue plasminogen activators used for clot lysis in emergency settings.)
Pharmacodynamics
- Aspirin and its derivatives inhibit platelet aggregation by irreversibly blocking cyclooxygenase (COX-1 and COX-2), preventing the synthesis of thromboxane A2, a potent platelet aggregator and vasoconstrictor.
- ADP receptor inhibitors (e.g., Ticagrelor, Ticlopidine) prevent platelet activation by antagonizing the ADP P2Y12 receptor on the platelet surface.
- GPIIb/IIIa inhibitors (e.g., Eptifibatide, Tirofiban) block the final common pathway of platelet aggregation by inhibiting the binding of fibrinogen and von Willebrand factor to the GPIIb/IIIa receptor.
- Fibrinolytics (e.g., Alteplase, Reteplase, Tenecteplase) promote fibrinolysis by activating plasminogen to plasmin, which breaks down fibrin clots.