![]() ![]() 5 The C max and T max following multiple oral doses (1300 mg three times daily x 5 days) were 16.41 mcg/mL and 2.5 h, respectively. The bioavailability of tranexamic acid after oral administration in humans is approximately 30 to 50% of the ingested dose and is not affected by food intake. The binding of plasminogen to fibrin induces fibrinolysis - by occupying the necessary binding sites tranexamic acid prevents this dissolution of fibrin, thereby stabilizing the clot and preventing hemorrhage. Tranexamic acid competitively and reversibly inhibits the activation of plasminogen via binding at several distinct sites, including four or five low-affinity sites and one high-affinity site, the latter of which is involved in its binding to fibrin. ![]() 6 Consider EEG monitoring of patients with a history of seizure. Off-target antagonism of GABA(A) receptors may be associated with the development of convulsions and hyperexcitability following tranexamic acid administration 1 - the risk appears higher with improper administration or administration during cardiovascular surgery. 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). 6 Tranexamic acid binds more strongly than aminocaproic acid to both the strong and weak receptor sites of the plasminogen molecule in a ratio corresponding to the difference in potency between the compounds. 5 At much higher concentrations it behaves as a noncompetitive inhibitor of plasmin similar to aminocaproic acid, a similar antifibrinolytic which is 10-fold less potent. Tranexamic acid is an antifibrinolytic that competitively inhibits the activation of plasminogen to plasmin. ![]()
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