Triflusal

248.16

248.16

206-297-5

1Z0YFI05OO

DTXSID8045305

B - Blood and blood forming organs

2918990090

63.6

2.1

white to off-white

1.4±0.1 g/cm3

121 °C

316°C at 760 mmHg

144.9±27.9 °C

1.484

H2O: <1 mg/ml;DMSO: >30mg/mL

2-8°C

NONH for all modes of transport

3

22-36/37/38-43

26-36/37

GP4250000

Xn

P261-P280-P305 + P351 + P338

H302-H315-H317-H319-H335

There is the possibility of producing major systemic hemorrhages.

Triflusal binds almost completely to plasma proteins reaching a 99% of the administered dose.

Triflusal is indicated as prophylaxis of thromboembolic disorders. It has been registered in Spain and in other countries of Europe, South America and South Korea for the prevention of Stroke and myocardial infarction.

Triflusal is an antithrombotic anticoagulant. It irreversibly inhibits the production of thromboxane-B2 in platelets by acetylating cycloxygenase-1. Triflusal affects many other targets such as NF kappa B, which is a gene expression regulatory factor for cycloxygenase-a and cytokines. Numerous studies comparing the efficacy and safety profile (i.e. systemic hemorrhage) between triflusal and acetylsalsylic acid has shown either no significant difference or a better effacy and safety profile for triflusal. Triflusal has been shown to protect cerebral tissue due to its inhibition of lipid peroxidation resulting from anoxia-reoxygenation.

Drugs or agents which antagonize or impair any mechanism leading to blood platelet aggregation, whether during the phases of activation and shape change or following the dense-granule release reaction and stimulation of the prostaglandin-thromboxane system. (See all compounds classified as Platelet Aggregation Inhibitors.)

Absorbed in the small intestine with a bioavailability range from 83% to 100%. There is no significant difference between the absorption of the oral solution and capsule formulation. Triflusal displays a Cmax of 11.6 mcg/ml and a tmax of 0.88 h. The major metabolite of triflusal presents different pharmacokinetic properties by showing a Cmax and tmax of 92.7 mcg/ml and 4.96 h, respectively.|The elimination pathway of triflusal is primarily renal. Urine analysis has shown the presence of unchanged triflusal, HTB and the glycine conjugate of HTB.|The reported volume of distribution for triflusal is of 34L.|Renal clearance is 0.8 +/- 0.2L/h and 0.18 +/1 0.04L/h for triflusal and HTB, respectively.

In the liver, triflusal undergoes deacetylation, forming its main metabolite 2-OH-4-trifluoromethyl benzoic acid (HTB). This major metabolite seems to have marked antiplatelet properties in vitro.

In the healthy human, the half-life is 0.5 +/- 0.1h, while that of HTB is 34.3 +/- 5.3h.

Triflusal is chemically related to acetylsalicylic acid (ASA) and irreversibly inhibits cycloxygenase-1 (COX-1) in platelets. Acetylation of the active group of COX-1 prevents the formation of thromboxane-B2 in platelets. However, it is unique because it spares the arachidonic acid metabolic pathway in endothelial cells. In addition, it favors the production of nitric oxide, a vasodilator.

2-acetoxy-4-trifluoromethylbenzoic acid