What best describes the mechanism of action of alteplase in managing ischaemic stroke?

Alteplase is a thrombolytic agent, and its primary mechanism of action involves the acceleration of plasminogen to plasmin conversion. In the context of ischaemic stroke, the formation of a blood clot (thrombus) obstructs blood flow to the brain. Alteplase works by binding to fibrin in the clot and converting bound plasminogen into plasmin, which then breaks down fibrin and leads to the dissolution of the thrombus. This restoration of blood flow is crucial in minimizing neurological damage from the ischaemic event.

The other options describe mechanisms related to different classes of drugs. Adenosine diphosphate (ADP) P2Y12 receptor antagonism pertains to certain antiplatelet agents, which prevent platelet aggregation rather than breaking down existing clots. Cyclooxygenase-1 inhibition is a mechanism associated with non-steroidal anti-inflammatory drugs (NSAIDs) and aspirin, which can reduce clot formation but do not directly dissolve clots. Lastly, Factor Xa inhibition is the action of anticoagulants like rivaroxaban, which prevent new clot formation by targeting the coagulation cascade rather than directly lysing existing thrombi. Thus, the mechanism of action of altepl