ABSTRACT
The use of thrombolytic drugs has revolutionized the treatment of patients with acute myocardial
infarction. If used within the first 6 h after the onset of symptoms, streptokinase and urokinase,
plus aspirin and heparin, reduce in-hospital mortality by more than half and considerably
improve long-term survival. Although these first-generation fibrinolytic agents (streptokinase,
urokinase) are effective at thrombolysis, they are not fibrin-specific; they also convert circulating
plasminogen to plasmin. Because plasminogen in the thrombus and in the plasma are in
equilibrium, the plasminogen within the thrombus is also gradually depleted. This ‘‘plasminogen
steal’’ reduces clot lysis. Furthermore, streptokinase is immunogenic, resulting in drug resis-
tance, fever, and allergic reactions. To address some of these problems, a complex of
streptokinase and acylated human plasminogen, termed anisoylated streptokinase activator
complex (APSAC) or anistreplase, was developed. This molecule can be administered as a
bolus owing to its longer plasma half-life than that of streptokinase. The hope for a higher fibrin
(thrombus) affinity and fibrinolytic efficacy compared with streptokinase was not fulfilled in
clinical trials. Moreover, the compound still elicits antigenic responses in patients; pyrexia and
hypotension are infrequent adverse reactions.
