Acenocoumarol – a historical overview and its place in modern anticoagulant therapy

Acenocoumarol, a vitamin K antagonist (VKA), has played a pivotal role in anticoagulant therapy for over 60 years. Derived from the coumarin family, acenocoumarol inhibits vitamin K epoxide reductase, disrupting the synthesis of vitamin K-dependent clotting factors (II, VII, IX, X) and effectively preventing thromboembolic events. Compared to warfarin, acenocoumarol offers a rapid onset and shorter half-life, providing clinicians greater therapeutic fl exibility. Despite advances and widespread adoption of direct oral anticoagulants (DOACs), acenocoumarol continues to hold clinical signifi cance, particularly in Europe, Latin America, and Asia, owing to extensive clinical experience, reversibility, and cost-effectiveness. However, its use necessitates regular monitoring of international normalized ratio (INR), with individualized dosage adjustments required due to genetic variability (CYP2C9, VKORC1 polymorphisms), drug-drug interactions, dietary infl uences, and special considerations in the elderly and patients with chronic kidney disease (CKD). Recent clinical trials have expanded our understanding of its effi cacy, safety, and optimal use. Precision dosing strategies, including genotype guidance and advanced INR monitoring based on body-surface area-adjusted estimated glomerular fi ltration rate (BSA-adjusted eGFR) dosing, promise enhanced safety and personalized treatment. Although DOACs are now widely adopted due to their predictable pharmacokinetics and lack of routine monitoring requirements, acenocoumarol remains indispensable in well-defi ned clinical scenarios such as in patients with mechanical heart valves, rheumatic mitral stenosis–associated atrial fi brillation, antiphospholipid syndrome, and other conditions in which individualized dose adjustment offers a therapeutic advantage.