Actranex Film-Coated Tablet Mechanism of Action

Antifibrinolytic.
Pharmacology: Pharmacodynamics: Tranexamic acid is an antifibrinolytic compound which is a potent competitive inhibitor of the activation of plasminogen to plasmin. It is a non-competitive plasmin inhibitor at much larger concentrations. Tranexamic acid inhibits plasminogen activation by urokinase 6-100 times more than aminocaproic acid, and streptokinase 6-40 times more than aminocaproic acid. Tranexamic acid has about ten times the antifibrinolytic action of aminocaproic acid.
Mechanism of action: Tranexamic acid is a synthetic derivative of the amino acid lysine and binds the 5 lysine binding sites on plasminogen. This inhibits plasmin formation and displaces plasminogen from the fibrin surface. It may also directly inhibit plasmin and partially inhibit fibrinogenolysis at higher concentrations. Tranexamic acid is also thought to exert an anti-inflammatory effect (by inhibiting plasmin-mediated activation of complement, monocytes, and neutrophils) and may improve platelet function in certain circumstances.
Pharmacokinetics: Absorption: Tranexamic acid is absorbed from the gastrointestinal tract. After oral administration of 1 or 2 g, the peak plasma concentrations are 8 or 15 mg/L, both obtained 3 hours after dosing. About 30 to 50% of the drug is bioavailable. Food intake does not influence absorption of the drug.
Distribution: Tranexamic acid has very low protein binding and widely distributed in the body, about 3% at therapeutic plasma concentrations and is accounted for by binding to plasminogen. It does not bind to serum albumin. The initial volume of distribution is 9 to 12 L. The active concentration of Tranexamic acid (antifibrinolytic) is 10 mcg/mL. When administered 36 to 48 hours before surgery in four doses of 10 to 20 mg/kg body weight, the drug remains in different tissues for about 17 hours and in serum up to 7 or 8 hours.
No data are available concerning the concentration in gastric juice, but the clinical effect of tranexamic acid on gastrointestinal bleeding has been demonstrated. Tranexamic acid crosses the placenta and passes into breastmilk.
Biotransformation: The possible routes of biotransformation are acetylation or deamination followed by oxidation or reduction. Approximately 50% of the parent compound, 2% of deaminated dicarboxylic acid and 0.5% of the acetylated product are excreted.
Excretion: Tranexamic acid is excreted in the urine by glomerular filtration mainly as unchanged drug. Less than 5% of metabolites are excreted in urine within 72 hours. After oral administration of a 10 to 15 mg/kg dose, the urinary excretion at 24 to 48 hours is 39% and 41%, respectively. The approximate plasma half-life of tranexamic acid is 2 hours.