Hemanex Mechanism of Action

Pharmacology: Pharmacodynamics: Tranexamic acid is an anti-fibrinolytic agent. It is a competitive inhibitor of plasminogen activation and at much higher concentrations is a noncompetitive inhibitor of plasmin.
Human plasminogen contains lysine binding sites that are important for interactions not only with synthetic antifibrinolytic amino acid derivatives but also with .₂-antiplasmin and fibrin. One of these binding sites has a high affinity for tranexamic acid; the others have low affinity.
Tranexamic acid almost completely blocks the interaction of plasminogen and the heavy chain of plasmin with the lysine binding site of plasminogen. Saturation of this site with tranexamic acid prevents binding of plasminogen to the surface of fibrin. This process retards fibrinolysis because, although plasmin is still formed, it is unable to bind to fibrinogen or fibrin monomer. Conversely, when tranexamic acid blocks the binding site of plasmin, inactivation by .₂-antiplasmin is impossible.
In vitro, tranexamic acid 1 mg per mL does not aggregate platelets. Tranexamic acid in concentrations up to 10 mg per mL blood has no influence on platelet count, the coagulation time or various coagulation factors in whole blood or citrated blood from normal subjects. In contrast, tranexamic acid in concentrations of 10 mg and 1 mg per mL blood prolongs thrombin time.
Pharmacokinetics: Tranexamic acid is rapidly absorbed from the gastrointestinal tract. Peak plasma levels after oral administration of 1 or 2 g are 8 or 15 mg/L, both obtained three hours after dosing. Bioavailability is about 30 to 50%. Food intake does not influence absorption.
Tranexamic acid is widely distributed in the body and has very low protein binding, i.e., about 3% at therapeutic plasma levels and is accounted for by binding to plasminogen. It does not bind to serum albumin. Tranexamic acid's antifibrinolytically active concentration (10 μg/mL) remains in different tissues for about 17 hours and in the serum for up to 7 or 8 hours when administered 36 to 48 hours before surgery in four doses of 10 to 20 mg/kg body weight.
Tranexamic acid crosses the placenta but secretion in breast milk is low. No data are available concerning the concentration in gastric juice, but the clinical effect of tranexamic acid on gastrointestinal hemorrhage has been clearly demonstrated.
Acetylation or deamination followed by oxidation or reduction are possible routes of biotransformation. After oral administration, approximately 50% of the parent compound, 2% of the deaminated dicarboxylic acid and 0.5% of the acetylated product are excreted.
Tranexamic acid is excreted in the urine by glomerular filtration mainly as unchanged drug. The total amount of metabolites excreted in urine within 72 hours is less than 5%. After administration of a 10 to 15 mg/kg oral dose, the urinary excretion at 24 and 48 hours is 39 and 41%, respectively. Tranexamic acid's plasma half-life is approximately two hours.