What is the mechanism of action for tenecteplase 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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Tenecteplase was approved by the FDA as a fibrinolytic agent in 2000. It is produced by recombinant DNA technology using Chinese hamster ovary cells. Its mechanism of action is similar to that of alteplase, and it is currently indicated for the management of AMI.

Tenecteplase is a 527-amino-acid glycoprotein (GP) that sustained several modifications in amino acid molecules. These modifications consist of substitution of asparagine for threonine 103 and glutamine for asparagine 117, as well as a tetra-alanine substitution at amino acids 296-299 in the protease domain.

These changes give tenecteplase a longer plasma half-life and greater fibrin specificity. Tenecteplase has a half-life ranging initially from 20-24 minutes to 130 minutes for final clearance, mostly through liver metabolism. [7] In addition, these amino acid modifications allow single-bolus administration and yield decreased bleeding side effects as a consequence of the high fibrin specificity.

The ASSENT-2 trial evaluated the efficacy and safety of tenecteplase compared with alteplase in patients with AMI and found the former to be noninferior to the latter in terms of 30-day mortality. [8] Tenecteplase was associated with fewer bleeding complications, fewer major bleeding events (4.66% vs 5.94%), and less need for blood transfusion (4.25% vs 5.49%). Rates for intracranial hemorrhage were similar (0.93% vs 0.94%). [9] Follow-up study showed that mortality was similar in the two active therapy groups after 1 year. [8]

Several clinical trials have been initiated to assess possible new indications for tenecteplase (eg, in AIS and massive PE).

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