Triflusal

Triflusal is an inhibitor of platelet aggregation (IC₅₀s = 48.3 and 693 µM in isolated human whole blood and platelet-rich plasma, respectively).¹ It inhibits production of thromboxane B₂ (TXB₂; Item No. 19030) and 6 keto prostaglandin F_1α (6-keto-PGF_1α; Item No. 15210) induced by arachidonic acid (Item Nos. 90010 | 90010.1 | 10006607) with IC₅₀ values of 468 and 339 µM, respectively, in isolated human whole blood. Triflusal decreases IgG-ovalbumin immune complex-induced NF-κB nuclear translocation and production of nitric oxide (NO) in isolated rat peritoneal macrophages when used at a concentration of 1,000 µM.² Oral administration of triflusal (30 mg/kg) reduces infarct volume and peri-infarct levels of OX-6, a marker of activated microglia, in a rat model of focal ischemia induced by permanent middle cerebral artery occlusion (MCAO).³ It also reduces increases in cortical amyloid-β precursor protein (APP) levels induced by intracerebroventricular administration of amyloid-β (25-35) in rats at the same dose.⁴

WARNING This product is not for human or veterinary use.

1. de la Cruz, J.P., Mata, J.M., and de la Cuesta, F.S. Triflusal vs aspirin on the inhibition of human platelet and vascular cyclooxygenase. Gen. Pharmacol. 23(2), 297-300 (1992).

2. Bayón, Y., Alonso, A., and Crespo, M.S. 4-trifluoromethyl derivatives of salicylate, triflusal and its main metabolite 2-hydroxy-4-trifluoromethylbenzoic acid, are potent inhibitors of nuclear factor κB activation. Br. J. Pharmacol. 126(6), 1359-1366 (1999).

3. Whitehead, S.N., Bayona, N.A., Cheng, G., et al. Effects of triflusal and aspirin in a rat model of cerebral ischemia. Stroke 38(2), 381-387 (2007).

4. Whitehead, S., Cheng, G., Hachinski, V., et al. Interaction between a rat model of cerebral ischemia and β-amyloid toxicity. II. Effects of triflusal. Stroke 36(8), 1782-1789 (2005).