Btrol (Tranexamic Acid) Capsules and Injection

Mechanism of Action

The decreased fibrinolysis protects clots from lysis and reduces the bleeding of hemostatic failure. The central process of fibrinolysis is conversion of inactive plasminogen to proteolytic enzyme plasmin. Btrol (tranexamic acid) is the analogue of aminocaproic acid, which is a competitive inhibitor of plasminogen activation and at much higher concentrations, a noncompetitive inhibitor of plasmin. It is 10 times more potent invitro than aminocaproic acid. Btrol in a concentration of 1 mg per ml does not aggregate platelets invitro. In concentrations upto 10 mg per ml blood has no influence on the platelet count, the coagulation time or various coagulation factors in whole blood or citrated blood from normal subjects. On the other hand, tranexamic acid in concentrations of 10 mg and 1 mg per ml blood prolongs the thrombin time.


Btrol capsules and injections are indicated in situations where excessive haemorrhage cannot be controlled e.g.:


Absorption of tranexamic acid after oral administration represents approximately 30-50% of ingested dose and bioavailability is not affected by food intake. After an intravenous dose of 1gm the plasma concentration-time curve shows a triexponential decay with a half life of about 2 hours for the terminal elimination phase. The plasma peak level after 1 gm orally is 8mg/l and after 2gm, 15mg/l,both obtained three hours after dosing. The initial volume of distribution is about 9-12 litres. Only a small fraction of drug is metabolized. Urinary excretion is the main route of elimination via glomerular filtration. Antifibrinolytic concentration of tranexamic acid remains in different tissues for about 17 hours and in the serum, upto 7 or 8 hours.

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