[1] As a medication it is used to break down clots in some cases of myocardial infarction (heart attack), pulmonary embolism, and arterial thromboembolism.

[2] Side effects include nausea, bleeding, low blood pressure, and allergic reactions.

[7] If percutaneous coronary intervention (PCI) is not available within 90–120 minutes of first contact, streptokinase is recommended intravenously as soon as possible after the onset of a ST elevation myocardial infarction (STEMI).

Extra production of plasmin caused by streptokinase breaks down unwanted blood clots, for example, in the lungs (pulmonary embolism).

[11] The amino group of Val562 then forms a salt-bridge with Asp740, which triggers a conformational change producing the active protease plasmin.

Therefore, another residue must substitute for the free amino group of Val562 and provide a counterion for Asp740 in this active complex.

Staphylokinase is considered a virulence factor,[16] although its presence after the establishment of infection actually decreases disease severity.

Initially used in treatment of fibrinous pleural exudates, hemothorax and tuberculous meningitis, its role in acute myocardial infarction was serendipitous.

One study using animal models (rats) found that when used with a PHBV membrane drug-delivery system, it was 90 percent effective in preventing adhesions.