Triflusal is an antiplatelet agent structurally related to the
salicylates, but it is not derived from ASA. Triflusal and its
metabolite (3-hydroxy-4-triuoro-methylbenzoic acid or
HTB) produce specific inhibition of platelet arachidonic acid
metabolism (McNeely and Goa, 1998). A single 12-month
open-label trial of tritriflusal in 73 VaD patients (López-Pousa
et al., 1997) showed fewer declines in MMSE scores in
the active group compared with untreated subjects. More
recently, triusal was used in patients with amnesic MCI;
257 patients were randomized to receive 900 mg of triflusal
or placebo for 18 months. Triflusal therapy was associated
with a signi cantly lower rate of conversion to dementia
(Gómez-Isla et al., 2008).
Triflusal is an antiplatelet agent structurally related to the salicylates, but it is not derived from ASA. Triflusal and its metabolite (3-hydroxy-4-triuoro-methylbenzoic acid or HTB) produce specic inhibition of platelet arachidonic acid metabolism (McNeely and Goa, 1998). A single 12-month open-label trial of Triflusal in 73 VaD patients (López-Pousa et al., 1997) showed fewer declines in MMSE scores in the active group compared with untreated subjects. More recently, Triflusal was used in patients with amnesic MCI; 257 patients were randomized to receive 900 mg of Triflusal or placebo for 18 months. Triflusal therapy was associated with a signicantly lower rate of conversion to dementia (Gómez-Isla et al., 2008).
An analog of Aspirin; inhibits platelet aggregation. Antithrombotic.
Antithrombotic;Cyclooxygenase inhibitor
ChEBI: 2-acetyloxy-4-(trifluoromethyl)benzoic acid is a member of salicylates, a carboxylic ester and a member of benzoic acids.
2-hydroxy-4-trifluoromethylbenzoic acid (HTB), the deacetylated
metabolite of triflusal, retains significant antiplatelet activity. Triflusal is rapidly absorbed and
metabolized. The area under the concentration–time curve for triflusal is 20.26 mg/L/hour after a
900-mg dose, whereas that for HTB is 42.27 mg/L/hour. Much of the pharmacokinetic data for
triflusal activity is associated with HTB. The inhibition of COX, as measured by reduced production
of thromboxane B2, is 25% after 2 hours and 85% after 7 days with triflusal, whereas the effects of
aspirin on thromboxane B2 is more than 90% reduction after 2 hours and is maintained at this level
after 7 days. It would appear that the presence of a 4-trifluoromethyl group also greatly enhances triflusal's ability to inhibit the activation of nuclear factor κB, which in turn regulates the
expression of the mRNA of vascular
cell adhesion molecule-1 needed for platelet aggregation. In addition, triflusal increases nitric
oxide synthesis in neutrophils, which results in an increased vasodilatory potential. Finally, an
additional site of action for triflusal/HTB is the inhibition of cAMP phosphodiesterase, leading to
increased levels of cAMP. Elevated cAMP levels decrease platelet aggregation through decreased
mobilization of calcium. Aspirin and salicylic acid do not significantly increase cAMP levels.
Triflusal (2-acetoxy-4-trifluoromethyl benzoic acid) is an antiplatelet drug that despite its structural
similarity to aspirin exhibits quite different pharmacological and pharmacokinetic
properties.
