Abstract

A COMPREHENSIVE REVIEW ON THE DRUG PROFILE OF TENECTEPLASE

S. Rajesh Raja* H. Sravani Bai, J. Lavanya and M. Sumalatha

ABSTRACT

Stroke is the second leading cause of death globally and ischemic stroke constituted more than 60% of all incident strokes in 2019. ST-elevation myocardial infarction (STEMI) occurs due to coronary vessel occlusion causing trans mural myocardial ischaemia and subsequent necrosis. Intravenous thrombolysis is the first-line therapy for ischemic stroke, and alteplase has been used as an intravenous thrombolysis drug for over 20 years. However, considering its low rate of recanalization and risk of intracerebral hemorrhage, alteplase may not be the optimal thrombolytic drug of choice for ischemic stroke. Tenecteplase (TNK) is a genetically engineered, mutant, tissue plasminogen activator that is a potential substitute to alteplase in ischemic stroke. The pharmacokinetic advantages of TNK include greater fibrin selectivity than alteplase and prolonged half-life time. TNK (Tenecteplase) is a tissue plasminogen activator (tPA) produced by recombinant DNA technology using an established mammalian cellline (Chinese Hamster Ovary cells). Tenecteplase is a 527 amino acid glycoprotein developed by introducing the following modifications to the complementary DNA (cDNA) for natural human TPA are substitution of threonine 103 with asparagine, and a substitution of asparagine 117 with glutamine, both within the kringle 1 domain, and a tetra-alanine substitution at amino acids 296–299 in the protease domain.

Keywords: ST-elevation myocardial infarction (STEMI), TNK (Tenecteplase), tissue plasminogen activator (tPA).