U.S. Department of Health & Human Services Divider Arrow National Institutes of Health Divider Arrow NCATS
This repository is under review for potential modification in compliance with Administration directives.

Details

Stereochemistry ACHIRAL
Molecular Formula C6H13NO2
Molecular Weight 131.1729
Optical Activity NONE
Defined Stereocenters 0 / 0
E/Z Centers 0
Charge 0

SHOW SMILES / InChI
Structure of AMINOCAPROIC ACID

SMILES

NCCCCCC(O)=O

InChI

InChIKey=SLXKOJJOQWFEFD-UHFFFAOYSA-N
InChI=1S/C6H13NO2/c7-5-3-1-2-4-6(8)9/h1-5,7H2,(H,8,9)

HIDE SMILES / InChI

Molecular Formula C6H13NO2
Molecular Weight 131.1729
Charge 0
Count
MOL RATIO 1 MOL RATIO (average)
Stereochemistry ACHIRAL
Additional Stereochemistry No
Defined Stereocenters 0 / 0
E/Z Centers 0
Optical Activity NONE

Description

6-Aminocaproic acid (epsilon-aminocaproic acid, marketed as Amicar) is an ant fibrinolytic agent that acts by inhibiting plasminogen activators, which have fibrinolytic properties. It is useful in enhancing hemostasis when fibrinolysis contributes to bleeding. In life threatening situations, transfusion of appropriate blood products and other emergency measures may be required. Fibrinolytic bleeding may frequently be associated with surgical complications following heart surgery (with or without cardiac bypass procedures) and portacaval shunt; hematological disorders such as a megakaryocytic thrombocytopenia (accompanying aplastic anemia); hepatic cirrhosis; and neoplastic disease such as carcinoma of the prostate, lung, stomach, and cervix. 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. The drug should NOT be administered without a definite diagnosis and/or laboratory finding indicative of hyperfibrinolysis (hyperplasminemia). Inhibition of fibrinolysis by aminocaproic acid may theoretically result in clotting or thrombosis. However, there is no definite evidence that administration of aminocaproic acid has been responsible for the few reported cases of intravascular clotting which followed this treatment. Rather, it appears that such intravascular clotting was most likely due to the patient's preexisting clinical condition, e.g., the presence of DIC. It has been postulated that extravascular clots formed in vivo may not undergo spontaneous lysis as do normal clots. Reports have appeared in the literature of an increased incidence of certain neurological deficits such as hydrocephalus, cerebral ischemia, or cerebral vasospasm associated with the use of ant fibrinolytic agents in the treatment of subarachnoid hemorrhage (SAH). All of these events have also been described as part of the natural course of SAH, or as a consequence of diagnostic procedures such as angiography. Drug relatedness remains unclear. Aminocaproic acid may change the conformation of apoliprotein, changing its binding properties and potentially preventing the formation of lipoprotein.

CNS Activity

Approval Year

Targets

Primary TargetPharmacologyConditionPotency
0.009 mM [Kd]

Conditions

ConditionModalityTargetsHighest PhaseProduct
Preventing
AMICAR

Cmax

ValueDoseCo-administeredAnalytePopulation
164 μg/mL
5 g single, oral
AMINOCAPROIC ACID plasma
Homo sapiens

AUC

ValueDoseCo-administeredAnalytePopulation
39000 mg × min/L
150 mg/kg single, intravenous
AMINOCAPROIC ACID plasma
Homo sapiens

T1/2

ValueDoseCo-administeredAnalytePopulation
2 h
5 g single, oral
AMINOCAPROIC ACID plasma
Homo sapiens
6.2 h
30 mg/kg/h single, intravenous
AMINOCAPROIC ACID plasma
Homo sapiens

Doses

AEs

PubMed

Sample Use Guides

In Vivo Use Guide
For the treatment of acute bleeding syndromes due to elevated fibrinolytic activity, it is suggested that 5 AMICAR (aminocaproic acid) 1000 mg Tablets or 10 AMICAR 500 mg Tablets (5 g) or 4 teaspoonfuls of AMICAR Oral Solution (5 g) be administered during the first hour of treatment, followed by a continuing rate of 1 AMICAR 1000 mg Tablet or 2 AMICAR 500 mg Tablets (1 g) or 1 teaspoonful of AMICAR Oral Solution (1.25 g) per hour. This method of treatment would ordinarily be continued for about 8 hours or until the bleeding situation has been controlled.
Route of Administration: Oral
In Vitro Use Guide
in vitro epsilon-aminocaproic acid (EACA) (final concentration 1.25-5 mg/ml) substantially inhibited the activity of the inhibitors, while the same concentration of EACA had no effect on other immunological reactions like red cell agglutination and immunofluorescence.
Substance Class Chemical
Record UNII
U6F3787206
Record Status Validated (UNII)
Record Version