What is the mechanism of action for alteplase in thrombolytic therapy?

Updated: Aug 04, 2021
  • Author: Wanda L Rivera-Bou, MD, FAAEM, FACEP; Chief Editor: Erik D Schraga, MD  more...
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Alteplase was the first recombinant tissue-type plasminogen activator and is identical to native tPA. In vivo, tissue-type plasminogen activator is synthesized and made available by cells of the vascular endothelium. It is the physiologic thrombolytic agent responsible for most of the body’s natural efforts to prevent excessive thrombus propagation.

Alteplase is fibrin-specific and has a plasma half-life of 4-6 minutes. It is the fibrinolytic agent most familiar to emergency department (ED) physicians, in that it is the lytic agent most often used for treatment of coronary artery thrombosis, PE, and AIS. Alteplase is FDA-approved for treatment of ST-elevation myocardial infarction (STEMI), AIS, acute massive PE, and occluded CVADs. [4, 5] At present, it is the only thrombolytic drug approved for AIS.

In theory, alteplase should be effective only at the surface of fibrin clot. In practice, however, a systemic lytic state is seen, with moderate amounts of circulating fibrin degradation products and a substantial risk of systemic bleeding. Alteplase may be readministered as necessary; it is not antigenic and is almost never associated with any allergic manifestations.

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