| Indication |
For use in patients with hemophilia for short term use (two to
eight days) to reduce or prevent hemorrhage and reduce the need for
replacement therapy during and following tooth extraction. It can also
be used for excessive bleeding in menstruation, surgery, or trauma
cases. |
| Pharmacodynamics |
Tranexamic acid is an antifibrinolytic that competitively
inhibits the activation of plasminogen to plasmin. Tranexamic acid is a
competitive inhibitor of plasminogen activation, and at much higher
concentrations, a noncompetitive inhibitor of plasmin, i.e., 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 in a ratio corresponding to the
difference in potency between the compounds. 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). |
| Mechanism of action |
Tranexamic acid competitively inhibits activation of plasminogen
(via binding to the kringle domain), thereby reducing conversion of
plasminogen to plasmin (fibrinolysin), an enzyme that degrades fibrin
clots, fibrinogen, and other plasma proteins, including the procoagulant
factors V and VIII. Tranexamic acid also directly inhibits plasmin
activity, but higher doses are required than are needed to reduce
plasmin formation. |
| Absorption |
Absorption of tranexamic acid after oral administration in humans
represents approximately 30 to 50% of the ingested dose and
bioavailability is not affected by food intake. |
| Volume of distribution |
|
| Protein binding |
The plasma protein binding of tranexamic acid is about 3% at
therapeutic plasma levels and seems to be fully accounted for by its
binding to plasminogen (does not bind serum albumin). |
| Metabolism |
Only a small fraction of the drug is metabolized (less than 5%). |
| Route of elimination |
Urinary excretion is the main route of elimination via glomerular filtration. |
| Half life |
Biological half-life in the joint fluid is about 3 hours. |
| Clearance |
|
| Toxicity |
Oral LD50 in mice is >10 gm/kg. Symptoms of overdosage may be nausea, vomiting, orthostatic symptoms and/or hypotension. |
