| Indication |
For use in the treatment of excessive postoperative bleeding. |
| Pharmacodynamics |
Aminocaproic acid works as an antifibrinolytic. It is a
derivative of the amino acid lysine. The fibrinolysis-inhibitory effects
of aminocaproic acid appear to be exerted principally via inhibition of
plasminogen activators and to a lesser degree through antiplasmin
activity. Aminocaproic acid may be a possible prophylactic for vascular
disease, as it may prevent formation of lipoprotein (a), a risk factor
for vascular disease. |
| Mechanism of action |
Aminocaproic acid binds reversibly to the kringle domain of
plasminogen and blocks the binding of plasminogen to fibrin and its
activation to plasmin. With NO activation of plasmin, there is a
reduction in fibrinolysis. This consequently will reduce the amount of
bleeding post surgery. Elevated plasma levels of lipoprotein(a) have
been shown to increase the risk of vascular disease. Lipoprotein 9a)a
has two components, apolipoprotein B-100, linked to apolipoprotein (a).
Aminocaproic acid may change the conformation of apoliprotein (a),
changing its binding properties and potentially preventing the formation
of lipoprotein (a). |
| Absorption |
Absorbed rapidly following oral administration. In adults, oral
absorption appears to be a zero-order process with an absorption rate of
5.2 g/hr. The mean lag time in absorption is 10 minutes. After a single
oral dose of 5 g, absorption was complete (F=1). |
| Volume of distribution |
|
| Protein binding |
Not Available |
| Metabolism |
Sixty-five percent of the dose is recovered in the urine as
unchanged drug and 11% of the dose appears as the metabolite adipic
acid. |
| Route of elimination |
Renal excretion is the primary route of elimination, whether aminocaproic acid is administered orally or intravenously. |
| Half life |
The terminal elimination half-life is approximately 2 hours. |
| Clearance |
|
| Toxicity |
A few cases of acute overdosage with intravenous administration
have been reported. The effects have ranged from no reaction to
transient hypotension to severe acute renal failure leading to death.
The intravenous and oral LD50 were 3.0 and 12.0 g/kg
respectively in the mouse and 3.2 and 16.4 g/kg respectively in the rat.
An intravenous infusion dose of 2.3 g/kg was lethal in the dog. |
