Triflusal

Triflusal irreversibly inhibits the production of thromboxane-B2 in platelets by acetylating cycloxygenase-1. Target: COX Triflusal at 10 mM, 100 mM and 1 M decreases LDH efflux in rat brain slices after anoxia/reoxygenation by 24%, 35% and 49% respectively. Triflusal also reduces inducible NO synthase activity by 18%, 21% and 30% [1]. Triflusal (10 mg/kg i.v.) reduces platelet deposition on subendothelium-induced primary thrombus by about 68% in rabbits. Triflusal (10 mg/kg i.v.) reduces platelet deposition on a fresh thrombus formed over tunica media by about 48% in rabbits. Triflusal (40 mg/kg p.o.) reduces platelet deposition on a primary thrombus triggered by subendothelium and tunica media by 53% in rabbits. Triflusal (40 mg/kg p.o.) significantly reduces Cox-2 mRNA levels and protein levels without influence Cox-1 mRNA levels on the vascular wall in rabbits [2]. Triflusal (600 mg/day for 5 days) results in an increase in NO production by neutrophils and an increase in endothelial nitric oxide synthase (eNOS) protein expression in neutrophils in healthy volunteers [3].

[1]Fernández de Arriba A, et al. Inhibition of cyclooxygenase-2 expression by 4-trifluoromethyl derivatives of salicylate, triflusal, and its deacetylated metabolite, 2-hydroxy-4-trifluoromethylbenzoic acid. Mol Pharmacol. 1999 Apr;55(4):753-60.|[2]Duran, X., et al., Protective effects of triflusal on secondary thrombus growth and vascular cyclooxygenase-2. J Thromb Haemost, 2008. 6(8): p. 1385-92.|[3]De Miguel, L.S., et al., A 4-trifluoromethyl derivative of salicylate, triflusal, stimulates nitric oxide production by human neutrophils: role in platelet function. Eur J Clin Invest, 2000. 30(9): p. 811-7.