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Triflusal is an antithrombotic and antiplatelet agent structurally related to salicylic acid, but not a direct derivative of acetylsalicylic acid (aspirin)[1][2][5]. It irreversibly inhibits cyclooxygenase‑1 (COX‑1) in platelets, thereby preventing the formation of thromboxane B2 and inhibiting platelet aggregation[1][2][5]. Unlike aspirin, triflusal spares the arachidonic acid pathway in endothelial cells and promotes nitric oxide production as well as increases cyclic nucleotide concentrations, leading to vasodilation[2][5]. It also exhibits antioxidant and anti-inflammatory effects by modulating NF-kappa B activity and inducible nitric oxide synthase (iNOS), contributing to neuroprotective properties observed in animal models[6][7]. Clinically, triflusal is used for secondary prevention of ischemic stroke, myocardial infarction, and thromboprophylaxis in atrial fibrillation—especially as an alternative for patients intolerant to aspirin due to its lower risk of bleeding complications[4][8]. Developed by J. Uriach and Company, it is marketed in several countries but not approved by the FDA or EMA[2].
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