TNKase is a genetically engineered variant of the
alteplase molecule. Three different mutations result in an increase of the plasma half-life, of the resistance to
plasminogen-activator inhibitor 1 and of the thrombolytic potency against platelet-rich thrombi. Among available agents in clinical practice,
TNKase is the most
fibrin-specific molecule and can be delivered as a single bolus
intravenous injection. Several large-scale clinical trials have enrolled more than 27,000 patients with acute
myocardial infarction, making the use of this
drug truly evidence-based.
TNKase is equivalent to front-loaded
alteplase in terms of mortality and is the only bolus
thrombolytic drug for which this equivalence has been formally demonstrated.
TNKase appears more potent than
alteplase when symptoms duration lasts more than 4 hours. Also,
TNKase significantly reduces the rate of major bleeds and the need for
blood transfusions. The efficacy of
TNKase may be further improved by
enoxaparin substitution for
unfractionated heparin, provided that
enoxaparin dose adjustment is made for patients more than 75 years old. Hitherto, the small available randomized studies and international clinical registries suggest that pre-hospital
TNKase is as effective as primary angioplasty, thus laying the foundations for a new fibrinolytic,
TNKase-based strategy as the backbone of reperfusion in acute
myocardial infarction.