Triflusal is aplatelet aggregation inhibitor that was discovered and developed in the Uriach Laboratories, and commercialised inSpain since 1981. Currently, it is available in 25 countries in Europe, Asia, Africa and America. It is aderivative ofacetylsalicylic acid (ASA; Aspirin) in which a hydrogen atom on thebenzene ring has been replaced by atrifluoromethyl group. Trade names includeDisgren,Grendis,Aflen andTriflux.[1]
In the 2008, guidelines for stroke management from the European Stroke Organization,[3] triflusal was for the first time recommended as lone therapy, as an alternative toacetylsalicylic acid (ASA)(Aspirin) plusdipyridamole, orclopidogrel alone for secondary prevention ofatherothrombotic stroke. This recommendation was based on the double-blind, randomised TACIP and TAPIRSS trials, which found triflusal to be as effective asAspirin (acetylsalicylic acid, ASA, which Triflusal is derived from) in preventing post-stroke vascular events, while having a more favourable safety profile.[4][5][6]
It is absorbed in thesmall intestine and itsbio-availability ranges from 83% to 100%.[7][8] The active metabolite of Triflusal is 2-hydroxy-4-trifluoromethyl-benzoic acid, which is when Triflusal gets metabolized by anesterase.
^Murdoch D, Plosker GL (2006). "Triflusal: a review of its use in cerebral infarction and myocardial infarction, and as thromboprophylaxis in atrial fibrillation".Drugs.66 (5):671–92.doi:10.2165/00003495-200666050-00009.PMID16620146.S2CID195684205.
^Culebras A, Rotta-Escalante R, Vila J, Domínguez R, Abiusi G, Famulari A, et al. (April 2004). "Triflusal vs aspirin for prevention of cerebral infarction: a randomized stroke study".Neurology.62 (7):1073–80.doi:10.1212/01.wnl.0000113757.34662.aa.PMID15079004.S2CID9065395.
^Ramis J, Mis R, Conte L, Forn J (1990). "Rat and human plasma protein binding of the main metabolite of triflusal".Eur J Pharmacol.183 (5):1867–1868.doi:10.1016/0014-2999(90)92202-T.
^Ramis J, Mis R, Forn J, Torrent J, Gorina E, Jané F (1991). "Pharmacokinetics of triflusal and its main metabolite HTB in healthy subjects following a single oral dose".European Journal of Drug Metabolism and Pharmacokinetics.16 (4):269–73.doi:10.1007/BF03189971.PMID1823870.S2CID6287466.
