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Clinical data
AHFS/Drugs.comInternational Drug Names
ATC code
  • 2-acetyloxy-4-(trifluoromethyl)benzoic acid
CAS Number
PubChem CID
CompTox Dashboard (EPA)
ECHA InfoCard100.005.726 Edit this at Wikidata
Chemical and physical data
Molar mass248.157 g·mol−1
3D model (JSmol)
  • CC(=O)Oc1cc(ccc1C(=O)O)C(F)(F)F
  • InChI=1S/C10H7F3O4/c1-5(14)17-8-4-6(10(11,12)13)2-3-7(8)9(15)16/h2-4H,1H3,(H,15,16) ☒N
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Triflusal is a platelet aggregation inhibitor that was discovered and developed in the Uriach Laboratories, and commercialised in Spain since 1981. Currently, it is available in 25 countries in Europe, Asia, Africa and America. It is a derivative of acetylsalicylic acid (ASA) in which a hydrogen atom on the benzene ring has been replaced by a trifluromethyl group. Trade names include Disgren, Grendis, Aflen and Triflux.[1]

Mechanism of action

Triflusal is a selective platelet antiaggregant through;

  • blocks cyclooxygenase, thereby inhibiting thromboxane A2, and thus preventing aggregation
  • preserves vascular prostacyclin, thus promoting anti-aggregant effect
  • blocks phosphodiesterase thereby increasing cAMP concentration, thereby promoting anti-aggregant effect due to inhibition of calcium mobilization


Triflusal is indicated for;

Prevention of stroke

In the 2008 guidelines for stroke management from the European Stroke Organization, triflusal was for the first time recommended as lone therapy, as an alternative to acetylsalicylic acid plus dipyridamole, or clopidogrel alone for secondary prevention of atherothrombotic stroke. This recommendation was based on the double-blind, randomised TACIP and TAPIRSS trials, which found triflusal to be equally as effective as Aspirin in preventing post-stroke vascular events, while having a more favourable safety profile.[2][3][4]


It is absorbed in the small intestine and its bio-availability ranges from 83% to 100%.[5][6]


  1. ^ 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. PMID 16620146.
  2. ^ Matías-Guiu J, Ferro JM, Alvarez-Sabín J, Torres F, Jiménez MD, Lago A, Melo T (April 2003). "Comparison of triflusal and aspirin for prevention of vascular events in patients after cerebral infarction: the TACIP Study: a randomized, double-blind, multicenter trial". Stroke. 34 (4): 840–8. doi:10.1161/01.STR.0000063141.24491.50. PMID 12649515. S2CID 1387069.
  3. ^ 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. PMID 15079004. S2CID 9065395.
  4. ^ European Stroke Organisation (ESO) Executive Committee, ESO Writing Committee. (2008). "Guidelines for management of ischaemic stroke and transient ischaemic attack 2008". Cerebrovascular Diseases. 25 (5): 457–507. doi:10.1159/000131083.
  5. ^ 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: 1867–1868.
  6. ^ 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. PMID 1823870. S2CID 6287466.