Prevention of repeated vascular disorders of an ischemic nature, such as: heart attack; stable and unstable angina; cerebrovascular non-hemorrhagic transient or permanent circulatory disorders. Prevention of shunt occlusion after coronary artery bypass surgery.
active substance: triflusal;
1 capsule contains 300 mg of triflusal;
Disgren Dosage form
Basic physical and chemical properties: colorless hard gelatin capsules of size 1, containing a white or almost white powder.
Antithrombotic agents. Platelet aggregation inhibitors, excluding heparin.
ATX code B01A C18.
Triflusal reduces thromboxane biosynthesis by irreversible inhibition of platelet cyclooxygenase, due to its insignificant effect on vascular COX in a therapeutic dose, does not affect prostacyclin biosynthesis. Also, the main metabolite of triflusal, 2-hydroxy-4- (trifluoromethyl) benzoic acid (HTB), is a reversible inhibitor of platelet cyclooxygenase and, due to its long half-life (34 hours), contributes to the antithrombotic action of triflusal. Both triflusal and HTB can increase the concentration of cyclic adenosine 5-monophosphate (c-AMP) in platelets by inhibiting platelet PDE. In addition, it has been demonstrated in vitro and ex vivo that triflusal stimulates the release of nitric oxide in human neutrophils, which also contributes to antithrombotic action. Triflusal has been shown to inhibit platelet aggregation in both healthy volunteers and patients. In ex vivo experiments in healthy volunteers after administration of triflusal at a dose of 600 mg after 24 hours, platelet aggregation induced by arachidonic acid decreased by 65%. Repeated use of triflusal (600 mg / day for 7 days) resulted in 50-75% inhibition of platelet aggregation induced by arachidonic acid, ADP (adenosine diphosphate), epinephrine or collagen.
Prevention of recurrent ischemic vascular disorders, such as:
stable and unstable angina pectoris;
cerebrovascular non-hemorrhagic transient or permanent circulatory disorders.
Prevention of graft occlusion after coronary artery bypass grafting.
Hypersensitivity to the active substance or other salicylates. History of active ulcer and its complications. Acute bleeding.
Interaction with other medicinal products and other types of interactions
In vitro experiments have shown an increase in the free fraction of the main triflusal metabolite, 2-hydroxy-4- (trifluoromethyl) benzoic acid (HTB), in the presence of NSAIDs. On the other hand, increasing the concentration of HTB increases the effect of NSAIDs, glisentide and warfarin. The dose of these drugs may need to be changed if they are used with triflusal.
In patients with acute myocardial infarction, the safety of using triflusal together with thrombolytic agents (rt-PA and streptokinase) was evaluated. The number of cases of intracerebral bleeding was less than in patients receiving acetylsalicylic acid and thrombolytic agents (0.1% versus 1.1%; p = 0.04).