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Chemical Compound Review

Tecnosal     2-acetyloxy-4- (trifluoromethyl)benzoic acid

Synonyms: DRISGEN, Disgren, Grendis, Triflusal, Triflux, ...
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Disease relevance of Triflusal


Psychiatry related information on Triflusal

  • OBJECTIVE: Triflusal has been shown to exert neuroprotective effects by downregulating molecules considered responsible for the development of Alzheimer's disease (AD) [5].
  • Aspirin, triflusal and Ginkgo biloba extract were associated with some stabilization of dementia progression, perhaps due to their antiplatelet effects [6].

High impact information on Triflusal

  • RNase protection assays showed that 2-acetoxy-4-trifluoromethylbenzoic acid (triflusal) inhibited, in a dose-dependent manner, mRNA expression of several cytokine genes, most of which are NFAT-regulated and cyclosporin A (CsA)-sensitive [7].
  • Transactivation experiments performed with several NFAT-dependent and AP-1-dependent reporter genes showed that triflusal strongly inhibited NFAT-dependent transcription at concentrations as low as 0.25 mM [7].
  • These results indicate that triflusal, a drug with a well characterized pharmacological and safety profile currently used as antiplatelet, inhibits cardiomyocyte growth by interfering with the NF-kappaB signaling pathway through a post-transcriptional mechanism involving reduced-proteosome degradation of IkappaBalpha [2].
  • It is noteworthy that banded rats treated with oral triflusal, compared with untreated rats, showed enhanced protein levels of IkappaBalpha, which forms a cytoplasmic inactive complex with the p65-p50 heterodimeric complex [2].
  • Overall, both drugs were well tolerated, although there was a trend towards fewer bleeding episodes with triflusal; significantly fewer central nervous system bleeding episodes were observed in triflusal-treated patients (0.27% vs. 0.97%; P = 0.033) [1].

Chemical compound and disease context of Triflusal


Biological context of Triflusal


Anatomical context of Triflusal


Associations of Triflusal with other chemical compounds


Gene context of Triflusal

  • The closure time in the presence of collagen plus ADP (Coll/ADP-CT), ICAM-1, VCAM-1, and NO(2)(-)+NO(3)(-) were not modified either by triflusal or aspirin [11].
  • CONCLUSIONS: This study suggests that triflusal neuroprotection is associated with a decrease of iNOS and other inflammatory mediators and therefore may constitute a good therapeutic agent in pathological situations in which regulation of inflammatory genes constitutes a relevant step in the outcome of the neurodegenerative event [21].
  • However, only triflusal and aspirin inhibited purified COX-2 enzyme [20].
  • Triflusal and HTB may exert beneficial effects in processes in which de novo COX-2 expression is involved and, in a broader sense, in pathological situations in which genes under nuclear factor-kappaB control are up-regulated [20].
  • Plasma P-selectin and vWF were reduced by triflusal but not by aspirin [11].

Analytical, diagnostic and therapeutic context of Triflusal

  • Electrophoretic mobility shift assay revealed an increase in the NF-kappaB binding activity in cardiac nuclear extracts of banded rats that was prevented by triflusal treatment [2].
  • After administration of triflusal, we observed a reduction in microalbuminuria (59 +/- 25 vs. 33 +/- 22 micrograms/min, P less than 0.01), an increase in RPF (648 +/- 119 vs. 722 +/- 134 ml.min-1 x 1.73 m-2, P less than 0.01), and a reduction in filtration fraction (0.24 +/- 0.04 vs. 0.20 +/- 0.03, P less than 0.01) [22].
  • One week old Long-Evans black hooded rat pups received three oral administrations of triflusal (30 mg/kg) and were sacrificed at 9 days of age [14].
  • The biological effects of a new antiplatelet agent, triflusal, were evaluated in patients with cardiac valvular prostheses [17].
  • RESULTS: After treatment with triflusal, there was an increase in NO production by neutrophils and an increase in endothelial nitric oxide synthase (eNOS) protein expression in neutrophils [13].


  1. Randomized comparative trial of triflusal and aspirin following acute myocardial infarction. Cruz-Fernández, J.M., López-Bescós, L., García-Dorado, D., López García-Aranda, V., Cabadés, A., Martín-Jadraque, L., Velasco, J.A., Castro-Beiras, A., Torres, F., Marfil, F., Navarro, E. Eur. Heart J. (2000) [Pubmed]
  2. Inhibition of cardiac hypertrophy by triflusal (4-trifluoromethyl derivative of salicylate) and its active metabolite. Planavila, A., Rodríguez-Calvo, R., de Arriba, A.F., Sánchez, R.M., Laguna, J.C., Merlos, M., Vazquez-Carrera, M. Mol. Pharmacol. (2006) [Pubmed]
  3. Triflusal. McNeely, W., Goa, K.L. Drugs (1998) [Pubmed]
  4. Triflusal : a review of its use in cerebral infarction and myocardial infarction, and as thromboprophylaxis in atrial fibrillation. Murdoch, D., Plosker, G.L. Drugs (2006) [Pubmed]
  5. Access of HTB, main metabolite of triflusal, to cerebrospinal fluid in healthy volunteers. Valle, M., Barbanoj, M.J., Donner, A., Izquierdo, I., Herranz, U., Klein, N., Eichler, H.G., Müller, M., Brunner, M. Eur. J. Clin. Pharmacol. (2005) [Pubmed]
  6. Perspectives in the treatment of vascular dementia. Romàn, G. Drugs of today (Barcelona, Spain : 1998) (2000) [Pubmed]
  7. A new pharmacological effect of salicylates: inhibition of NFAT-dependent transcription. Aceves, M., Dueñas, A., Gómez, C., San Vicente, E., Crespo, M.S., García-Rodríguez, C. J. Immunol. (2004) [Pubmed]
  8. Triflusal versus oral anticoagulation for primary prevention of thromboembolism after bioprosthetic valve replacement (trac): prospective, randomized, co-operative trial. Aramendi, J.I., Mestres, C.A., Mestres, C.A., Martinez-León, J., Campos, V., Muñoz, G., Navas, C. European journal of cardio-thoracic surgery : official journal of the European Association for Cardio-thoracic Surgery. (2005) [Pubmed]
  9. Effects of triflusal and acetylsalicylic acid on microthrombi formation in experimental brain ischemia. Heye, N., Campos, A., Kannuki, S., Cervós-Navarro, J. Experimental pathology. (1991) [Pubmed]
  10. Triflusal for preventing serious vascular events in people at high risk. Costa, J., Ferro, J.M., Matias-Guiu, J., Alvarez-Sabin, J., Torres, F. Cochrane database of systematic reviews (Online) (2005) [Pubmed]
  11. Inhibition of thromboxane biosynthesis by triflusal in type 2 diabetes mellitus. Falco, A., Salvati, F., Vitacolonna, E., Avellone, G., Pinto, A., Di Febbo, C., Ballone, E., Di Nicola, M., Ciabattoni, G., Davì, G. Atherosclerosis (2005) [Pubmed]
  12. Effect of 4-trifluoromethyl derivatives of salicylate on nuclear factor kappaB-dependent transcription in human astrocytoma cells. Hernández, M., de Arriba, A.F., Merlos, M., Fuentes, L., Crespo, M.S., Nieto, M.L. Br. J. Pharmacol. (2001) [Pubmed]
  13. A 4-trifluoromethyl derivative of salicylate, triflusal, stimulates nitric oxide production by human neutrophils: role in platelet function. De Miguel, L.S., Jiménez, A., Montón, M., Farré, J., Del Mar Arriero, M., Rodríguez-Feo, J.A., García-Cañete, J., Rico, L., Gómez, J., Núñez, A., Casado, S., Farré, A.L. Eur. J. Clin. Invest. (2000) [Pubmed]
  14. Oral administration of the anti-inflammatory substance triflusal results in the downregulation of constitutive transcription factor NF-kappaB in the postnatal rat brain. Acarin, L., González, B., Castellano, B. Neurosci. Lett. (2000) [Pubmed]
  15. Effects of triflusal on oxidative stress, prostaglandin production and nitric oxide pathway in a model of anoxia-reoxygenation in rat brain slices. González-Correa, J.A., Arrebola, M.M., Ureña, I.M., Guerrero, A., Muñoz-Marín, J., Ruiz-Villafranca, D., Sánchez De La Cuesta, F., De La Cruz, J.P. Brain Res. (2004) [Pubmed]
  16. Comparison of in vitro effects of triflusal and acetysalicylic acid on nitric oxide synthesis by human neutrophils. Sánchez de Miguel, L., Casado, S., Farré, J., García-Durán, M., Rico, L.A., Montón, M., Romero, J., Bellver, T., Sierra, M.P., Guerra, J.I., Mata, P., Esteban, A., López-Farré, A. Eur. J. Pharmacol. (1998) [Pubmed]
  17. Effects of triflusal in patients with prosthetic heart valves. Dominguez, M.J., Vacas, M., Sáez, Y., Olabarría, I., Velasco, A., Iriarte, J.A., Forn, J. Clinical therapeutics. (1985) [Pubmed]
  18. Influence of triflusal on platelet activation after coronary artery bypass graft. Prieto, M.A., De La Cruz, J.P., Del Prado, M.F., Sánchez de la Cuesta, F. Blood Coagul. Fibrinolysis (2000) [Pubmed]
  19. Effects of triflusal and aspirin in a rat model of cerebral ischemia. Whitehead, S.N., Bayona, N.A., Cheng, G., Allen, G.V., Hachinski, V.C., Cechetto, D.F. Stroke (2007) [Pubmed]
  20. Inhibition of cyclooxygenase-2 expression by 4-trifluoromethyl derivatives of salicylate, triflusal, and its deacetylated metabolite, 2-hydroxy-4-trifluoromethylbenzoic acid. Fernández de Arriba, A., Cavalcanti, F., Miralles, A., Bayón, Y., Alonso, A., Merlos, M., García-Rafanell, J., Forn, J. Mol. Pharmacol. (1999) [Pubmed]
  21. Decrease of proinflammatory molecules correlates with neuroprotective effect of the fluorinated salicylate triflusal after postnatal excitotoxic damage. Acarin, L., González, B., Castellano, B. Stroke (2002) [Pubmed]
  22. Effects of thromboxane synthesis inhibitor triflusal on renal hemodynamics in microalbuminuric diabetic patients. Esmatjes, E., Conget, J.I., Gaya, J., Fernandez, M.R., Ferrer, J.P., Rivera, F., Vilardell, E. Diabetes Care (1990) [Pubmed]
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