Comparative Pharmacology
Head-to-head clinical analysis: AMINOCAPROIC versus AMINOCAPROIC ACID.
Peer-Reviewed Evidence
Head-to-head clinical analysis: AMINOCAPROIC versus AMINOCAPROIC ACID.
AMINOCAPROIC vs AMINOCAPROIC ACID
Comparing the clinical profiles, pharmacokinetic behaviors, and safety indices of these two therapeutic agents.
Competitive inhibition of plasminogen activation and, to a lesser extent, noncompetitive inhibition of plasmin, thereby preventing fibrinolysis and promoting clot stability.
Competitive inhibition of plasminogen activation, reducing fibrinolysis by binding to plasminogen and blocking its conversion to plasmin.
4-5 g orally or intravenously as a loading dose, followed by 1 g/hour continuous infusion or 1 g every 4-6 hours orally. Maximum dose 30 g/day.
Loading dose: 4-5 g intravenously (IV) over 1 hour, followed by continuous IV infusion of 1 g/hour for 8 hours or until bleeding controlled. Oral: 1 g every hour for 8 hours, then 1 g every 2 hours for 8 additional hours.
None Documented
None Documented
Clinical Note
moderateAminocaproic acid + Tretinoin
"Aminocaproic acid may increase the thrombogenic activities of Tretinoin."
Terminal elimination half-life: 2 hours (normal renal function); prolonged to 4–10 hours in renal impairment. Clinically, dosing interval must be adjusted in renal dysfunction to avoid accumulation.
Terminal elimination half-life is approximately 2 hours (range 1-3 hours) in patients with normal renal function. Prolonged in renal impairment (up to 20 hours in anuria).
Primarily renal (>95%) as unchanged drug via glomerular filtration and tubular secretion. Less than 1% biliary/fecal.
Primarily renal (80-90% unchanged). A small fraction (<5%) is excreted as metabolites. No significant biliary/fecal elimination.
Category C
Category C
Antifibrinolytic
Antifibrinolytic