| Identification | |||||||||||||||||||||||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Name | Aminocaproic Acid | ||||||||||||||||||||||||||||||||||||
| Accession Number | DB00513 (APRD00791, EXPT00408) | ||||||||||||||||||||||||||||||||||||
| Type | small molecule | ||||||||||||||||||||||||||||||||||||
| Groups | approved | ||||||||||||||||||||||||||||||||||||
| Description | An antifibrinolytic agent that acts by inhibiting plasminogen activators which have fibrinolytic properties. [PubChem] |
||||||||||||||||||||||||||||||||||||
| Structure |
Download: MOL | SDF | SMILES | InChI Display: 2D Structure | 3D Structure |
||||||||||||||||||||||||||||||||||||
| Synonyms |
|
||||||||||||||||||||||||||||||||||||
| Brand names |
|
||||||||||||||||||||||||||||||||||||
| Brand name mixtures | Not Available | ||||||||||||||||||||||||||||||||||||
| Categories |
|
||||||||||||||||||||||||||||||||||||
| CAS number | 60-32-2 | ||||||||||||||||||||||||||||||||||||
| Weight |
Average: 131.1729 Monoisotopic: 131.094628665 |
||||||||||||||||||||||||||||||||||||
| Chemical Formula | C6H13NO2 | ||||||||||||||||||||||||||||||||||||
| InChI Key | InChIKey=SLXKOJJOQWFEFD-UHFFFAOYSA-N | ||||||||||||||||||||||||||||||||||||
| InChI |
InChI=1S/C6H13NO2/c7-5-3-1-2-4-6(8)9/h1-5,7H2,(H,8,9)
Plain Text
|
||||||||||||||||||||||||||||||||||||
| IUPAC Name |
6-aminohexanoic acid
|
||||||||||||||||||||||||||||||||||||
| SMILES |
NCCCCCC(O)=O
Plain Text
|
||||||||||||||||||||||||||||||||||||
| Mass Spec | show (7.2 KB) | ||||||||||||||||||||||||||||||||||||
| Taxonomy | |||||||||||||||||||||||||||||||||||||
| Kingdom | Organic | ||||||||||||||||||||||||||||||||||||
| Classes |
|
||||||||||||||||||||||||||||||||||||
| Substructures |
|
||||||||||||||||||||||||||||||||||||
| Pharmacology | |||||||||||||||||||||||||||||||||||||
| 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. | ||||||||||||||||||||||||||||||||||||
| Affected organisms |
|
||||||||||||||||||||||||||||||||||||
| Pathways |
|
||||||||||||||||||||||||||||||||||||
| Pharmacoeconomics | |||||||||||||||||||||||||||||||||||||
| Manufacturers |
|
||||||||||||||||||||||||||||||||||||
| Packagers |
|
||||||||||||||||||||||||||||||||||||
| Dosage forms |
|
||||||||||||||||||||||||||||||||||||
| Prices |
|
||||||||||||||||||||||||||||||||||||
| Patents | Not Available | ||||||||||||||||||||||||||||||||||||
| Properties | |||||||||||||||||||||||||||||||||||||
| State | solid | ||||||||||||||||||||||||||||||||||||
| Melting point | 205 oC | ||||||||||||||||||||||||||||||||||||
| Experimental Properties |
|
||||||||||||||||||||||||||||||||||||
| Predicted Properties |
|
||||||||||||||||||||||||||||||||||||
| References | |||||||||||||||||||||||||||||||||||||
| Synthesis Reference | Not Available | ||||||||||||||||||||||||||||||||||||
| General Reference | Not Available | ||||||||||||||||||||||||||||||||||||
| External Links |
|
||||||||||||||||||||||||||||||||||||
| ATC Codes |
|
||||||||||||||||||||||||||||||||||||
| AHFS Codes | Not Available | ||||||||||||||||||||||||||||||||||||
| PDB Entries | |||||||||||||||||||||||||||||||||||||
| FDA label | show (152.1 KB) | ||||||||||||||||||||||||||||||||||||
| MSDS | show (73.6 KB) | ||||||||||||||||||||||||||||||||||||
| Interactions | |||||||||||||||||||||||||||||||||||||
| Drug Interactions |
|
||||||||||||||||||||||||||||||||||||
| Food Interactions |
|
||||||||||||||||||||||||||||||||||||
| Targets |
|---|
|
1. Plasminogen Pharmacological action: yesActions: inhibitor Angiostatin is an angiogenesis inhibitor that blocks neovascularization and growth of experimental primary and metastatic tumors in vivo Organism class: humanUniProt ID: P00747 ![]() Gene: PLG ![]() Protein Sequence: FASTA Gene Sequence: FASTA SNPs: SNPJam Report ![]() References:
2. Tissue-type plasminogen activator Pharmacological action: yesActions: antagonist Converts the abundant, but inactive, zymogen plasminogen to plasmin by hydrolyzing a single Arg-Val bond in plasminogen. By controlling plasmin-mediated proteolysis, it plays an important role in tissue remodeling and degradation, in cell migration and many other physiopathological events. Play a direct role in facilitating neuronal migration Organism class: humanUniProt ID: P00750 ![]() Gene: PLAT ![]() Protein Sequence: FASTA Gene Sequence: FASTA SNPs: SNPJam Report ![]() References:
Pharmacological action: unknown
Actions: other Apo(a) is the main constituent of lipoprotein(a) (Lp(a)). It has serine proteinase activity and is able of autoproteolysis. Inhibits tissue-type plasminogen activator 1. Lp(a) may be a ligand for megalin/Gp 330 Organism class: humanUniProt ID: P08519 ![]() Gene: LPA ![]() Protein Sequence: FASTA Gene Sequence: FASTA SNPs: SNPJam Report ![]() References:
|
| Comments |
|---|
This project is supported by Genome Alberta & Genome Canada, a not-for-profit organization that is leading Canada's national genomics strategy with $600 million in funding from the federal government. This project is also supported in part by GenomeQuest, Inc., an enterprise genomic information company serving the life science community.