Reteplase (DB00015): A Comprehensive Pharmacological and Clinical Monograph

Executive Summary & Introduction

Overview

Reteplase is a potent, third-generation thrombolytic agent developed through recombinant biotechnology for the emergency management of thromboembolic events.[1] Classified as a plasminogen activator, its primary function is to dissolve intravascular thrombi (blood clots) that cause acute medical emergencies, most notably ST-elevation myocardial infarction (STEMI), commonly known as a heart attack.[2] By enzymatically degrading the fibrin matrix of an occlusive thrombus, Reteplase restores blood flow to ischemic tissue, thereby reducing infarct size, preserving organ function, and decreasing the associated risks of mortality and heart failure.[5] Its common trade name in the United States is Retavase.[2]

Development and Positioning

Reteplase represents a significant milestone in the evolution of thrombolytic therapy. It is not a naturally occurring enzyme but rather a specifically engineered deletion mutein of native human tissue plasminogen activator (t-PA), the molecule from which the second-generation thrombolytic alteplase is derived.[1] The molecular architecture of Reteplase was deliberately modified to optimize its pharmacokinetic profile, resulting in a longer plasma half-life compared to alteplase.[8] This key modification underpins its principal clinical advantage: a simplified double-bolus intravenous administration regimen that obviates the need for a complex, weight-adjusted infusion.[10] This feature enhances its utility in time-critical settings such as emergency departments and pre-hospital care. Large-scale clinical trials have established its therapeutic equivalence to other major fibrinolytics in the management of STEMI, and compelling recent evidence suggests its potential for superior efficacy in the treatment of acute ischemic stroke, positioning it for a possible expansion of its therapeutic