Pharmacology: Injection: Tranexamic acid is an antifibrinolytic agent that inhibits the activation of plasminogen to plasmin (fibrinolysin-enzyme that degrades fibrin clots), fibrinogen, and other plasma proteins, including the procoagulant factors V and VIII. And at much higher concentrations, a noncompetitive inhibitor of plasmin ie, have actions similar to aminocaproic acid. Tranexamic acid is about 10 times more potent in vitro than aminocaproic acid. Tranexamic acid binds more strongly than aminocaproic acid to both the strong and weak receptor sites of the plasminogen molecule. Tranexamic acid in a concentration of 1 mg per mL does not aggregate platelets in vitro. In patients with hereditary angioedema, inhibition of the formation and activity of plasmin by Tranexamic acid may prevent attacks of angioedema by decreasing plasmin-induced activation of the first complement protein (C1).
Plasma protein binding is 3% at the therapeutic plasma levels. The plasma protein binding seems fully accounted for by its binding to plasminogen. Tranexamic acid is excreted unchanged in the urine.
Approximately 90% of an intravenously administered Tranexamic acid dose is excreted largely unchanged in the urine within 24 hours.
Pharmacokinetics: Capsule: Tranexamic acid is rapidly absorbed from the gastrointestinal tract: absorption is 30 to 50%. It is widely distributed throughout the body, diffuses across the placenta and has been detected in breast milk. It has a plasma elimination half-life of about 2 hours. It is excreted in the urine mainly as unchanged drug.