Is tenecteplase ready to replace alteplase to treat acute ischaemic stroke? The knowns and unknowns
Yi Donga, Yi Suib c, Xin Chenga, David Z. Wangd✉
- aDepartment of Neurology, Huashan Hospital Fudan University, Shanghai, China
- bDepartment of Neurology, Shenyang Brain Hospital, Shenyang Medical College, Shenyang, China
- cDepartment of Neurology, The First People's Hospital of Shenyang, Shenyang, China
- dDepartment of Neurology, Barrow Neurological Institute, Phoenix, Arizona, USA
- ✉Corresponding author
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Abstract
Tenecteplase (TNKase, TNK-tPA or TNK) is a thrombolytic agent derived from the tissue plasminogen activator (tPA). It is a 527-amino acid glycoprotein developed by replacing three amino acids at the T, N and K positions of the glycoprotein structure of tPA under genetic recombinant technology. After replacing threonine 103 with asparagine, asparagine 117 with glutamine and a tetra-alanine at amino acids 296–299, TNK is about eightfold more potent in dissolving clot, 80-fold higher resistance to plasminogen activator inhibitor-1 and 14-fold enhanced relative fibrin specificity, and with a longer half-life (20 min).1 Hence, TNK is administered as a single intravenous bolus. TNK 0.5 mg/kg intravenous bolus is the choice in treating acute myocardial infarction (MI),2 and was approved by the United States Food and Drug Administration in 2000. In comparison, the optimal dosages of TNK used alone or as a part of the bridging therapy remain to be further defined. For Caucasians patients with acute ischaemic stroke (AIS), TNK was tested at doses of 0.1, 0.25, 0.4 or 0.5 mg/kg.3–7 In the current issue of the journal, Tenecteplase Reperfusion Therapy in Acute Ischemic Cerebrovascular Events (TRACE) trial tested three different doses of TNK versus standard dose of tPA in Chinese patients with AIS within 3 hours of onset.8 The trial is a …