Thrombolytic agents are used to lyse already formed blood clots in clinical settings where ischemia may be fatal ( acute mycardial infarction, pulmonary embolism, ischemic stroke, and arterial thrombosis). Very precise indications rule the use of these drugs, which are not free from serious side effects ( bleeding).


The image below shows how serine protease thrombin (also called activated factor II) converts fibrinogen to fibrin.

Fibrin polymerizes and constitutes a “mesh” that acts as hemostatic clot (in conjunction with platelets) over a wounded site.

fibrin mesh

This plasmin meshwork can be cleaved by plasmin, which derives from an inactive precursor: plasminogen.
Plasminogen can be activated by the tissue plasminogen activator (t-PA), which  is released by endothelial cells.


As can be seen in the image, streptokinase acts by activating plasminogen conversion into plasmin, which promotes clot lysis.

Since streptokinase is a protein obtained from Streptococci cultures, it is capable of eliciting antigenic responses in humans.

The following animation integrates  the concepts previously explained, showing how endothelial cells release t-PA.


Agent Abbreviation Source
Streptokinase (Streptase) SK Streptococcal culture
Urokinase UK Renal cell culture
Alteplase or Tissue plasminogen activator(trade names Retavase, Rapilysin) t-PA Recombinant technology
Anistreplase or Acylated plasminogen: streptokinase activator) APSAC Streptococcal
Prourokinase or Single-chain urokinase plasminogen activator SCU-PA Renal cell culture

Pharmacological properties

Streptokinase is a protein produced by Beta-hemolytic streptococci as a component of that organism tissue destroying machinery.

There are two drawbacks for streptokinase therapy:

Since t-PA is produced by endothelial cells, it is nonantigenic and causes a more selective thrombolysis than streptokinase. Alteplase, the recombinant t-PA, is produced by recombinant DNA technology. It is effective in recanalizing occluded coronary arteries, limiting cardiac dysfunction and reducing  mortality following an ST elevation myocardial infarction. At pharmacologic doses it can trigger a systemic lytic state and cause unwanted bleeding.

A genetically engineered variant of t-PA. Tecneplase has a longer half life than t-PA which allows it to be administered as a single weight-based bolus.

It has an increased half life than t-PA and increased specificity for fibrin. Its efficacy and adverse effect profile are similar to those of streptokinase and t-PA.

Therapeutic considerations

Agent Indication
Streptokinase ST elevation myocardial infarction.Arterial thrombosis.

Deep vein thrombosis.

Pulmonary embolism.

Intra-arterial or intravenous catheter occlusion.

t-PA Acute myocardial infarction.Acute cerebrovascular thrombosis.

Pulmonary embolism.

Central venous catheter occlusion

Tenecteplase (TNK) and reteplase Acute myocardial infarction

Adverse effects common to all agents of the class:

Steptokinase adverse effects:

Relative contraindications to thrombolytic therapy


Harvey, Richard; Champe, Pamela (series editors). “Lippincott illustrated reviews: Pharmacology”, 4th edition. LWW: 2009.

Lullmann, Heinz; Mohr Klaus. “Color Atlas of Pharmacology”, 2nd edition. Thieme: 1999.

Golan, David E (editor). “Principles of Pharmacology: The Pathophysiologic Basis of Drug Therapy”, 2nd edition. LWW: 2008.

Fauci, Anthony S., Braunwald, Eugene, Kasper,Dennis L. “Harrison’s Principles of Internal Medicine”, 17 edition. Mc Graw Hill: 2008.

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