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1. Antiplasmin action: Tranexamic acid inhibits the binding of plasmin or plasminogen to fibrin by strongly binding to the lysine binding site (LBS) of fibrin which is also the binding site for plasmin and plasminogen. Therefore, Tranexamic acid strongly inhibits fibrinolysis induced by plasmin. In addition, in the presence of antiplasmins, such as a2-macroglobulin in the plasma, the antifibrinolytic action of tranexamic acid is even further strengthened.
2. Hemostatic action: When the blood level of plasmin is abnormally elevated, various phenomena occur, such as inhibition of platelet aggregation and decomposition of coagulation factors occur. Even slight elevation in the blood level of plasmin specifically induces fibrinolysis. Tranexamic acid is considered to exhibit a hemostatic effect by inhibiting fibrinolysis in common hemorrhages.
PHARMACOKINETICS: 1. Blood concentration: When a single dose of 500 mg Tranexamic acid was administered intramuscularly or 1,000 mg was administered intravenously to healthy adults, the time plasma concentration were as follows. (See figure and Table 1.)
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Click on icon to see table/diagram/image2. Distribution: Reference information (animal study): When 14C-tranexamic acid was administered intravenously or intramuscularly to mice, the distribution in the tissue was highest in the liver, kidneys and lungs, followed by pancreas, adrenals, spleen, prostate, colon, uterus, heart and muscle. Levels in the brain were low.
3. Metabolism and excretion: When a single dose of 500 mg Tranexamic acid was administered intramuscularly or 1,000 mg was administered intravenously to healthy adults, it was rapidly absorbed and about 80% and 76% of the administered dose was respectively excreted unchanged form in the urine within 24 hours of administration.
