Currently Enrolling Trials
Retavase (reteplase) is a tissue plasminogen activator (tPA).
Retavase is specifically indicated for treatment of acute ST-elevation myocardial infarction (STEMI) to reduce the risk of death and heart failure.
Retavase is supplied as an injection for intravenous administration. The recommended dose is two 10 unit intravenous injections, each administered over 2 minutes, 30 minutes apart. No other medication should be injected or infused simultaneously via the same intravenous line or added to the injection solution.
Mechanism of Action
Retavase (reteplase) is a recombinant plasminogen activator which catalyzes the cleavage of endogenous plasminogen to generate plasmin. Plasmin in turn degrades the fibrin matrix of the thrombus, thereby exerting its thrombolytic action.
The most common adverse reaction (>5%) is bleeding.
Retavase was evaluated in three controlled clinical studies comparing RETAVASE to other thrombolytic agents. In all three studies, patients were treated with aspirin (initial doses of 160 mg to 350 mg and subsequent doses of 75 mg to 350 mg) and heparin (a 5,000 unit IV bolus prior to the administration of Retavase or control, followed by a 1000 unit/hour continuous IV infusion for at least 24 hours).
The INJECT study compared Retavase to streptokinase on mortality rates at 35 days following acute ST-elevation myocardial infarction (STEMI). INJECT was a double-blind study in which 6,010 patients with no more than 12 hours of chest pain consistent with coronary ischemia and either ST segment elevation or bundle branch block on ECG were randomized 1:1 to Retavase (10 + 10 unit) or streptokinase (1.5 million units over 60 minutes). The study was designed to determine whether the effect of Retavaseon survival was non-inferior to that of streptokinase by ruling out with 95% confidence that 35-day mortality among RETAVASE patients was no more than 1% higher than among streptokinase patients. This endpoint was reached.
The other two studies (RAPID 1 and RAPID 2) compared coronary artery patency of Retavase to two regimens of alteplase in patients with STEMI. In RAPID 1 patients within 6 hours of the onset of symptoms were randomized to open-label administration of one of three regimens of RETAVASE (doses of 10 + 10 unit, 15 unit, or 10 + 5 unit) or to alteplase (100 mg over 3 hours). In RAPID 2 patients within 12 hours of the onset of symptoms were randomized to open-label administration of either Retavase (10 + 10 unit) or alteplase (100 mg over 1.5 hours). The primary endpoint for both studies was patency of the infarct-related artery 90 minutes after initiation of therapy. Interpretation of coronary angiograms was blinded. A higher percentage of subjects administered Retavase had complete flow (TIMI grade 3) and partial or complete flow (TIMI grades 2 or 3) compared to both regimens of alteplase. The relationship between coronary artery patency and clinical efficacy has not been established. In both clinical trials the re-occlusion rates were similar for Retavase and alteplase.