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QuickView for Acenocoumarol (compound)
PubChem
| Name: | Acenocoumarol |
|---|---|
| PubChem Compound ID: | 181809 |
| Description: | A coumarin that is used as an anticoagulant. Its actions and uses are similar to those of WARFARIN. (From Martindale, The Extra Pharmacopoeia, 30th ed, p233) |
| Molecular formula: | C19H15NO6 |
| Molecular weight: | 353.326 g/mol |
| Synonyms: |
66556-77-2; CAS-152-72-7; NCGC00016414-01; ZINC00538563
|
DrugBank
Identification
| Name: | Acenocoumarol |
|---|---|
| Name (isomeric): | DB01418 |
| Drug Type: | small molecule |
| Description: | A coumarin that is used as an anticoagulant. Its actions and uses are similar to those of WARFARIN. (From Martindale, The Extra Pharmacopoeia, 30th ed, p233) |
| Synonyms: |
Acenocoumarolum [INN-latin]; Nitrophenylacetylethyl-4-hydroxycoumarine; Nicoumalone; Acenocoumarin; Nicumalon; Nitrowarfarin; Nitrovarfarian
|
| Brand: | Sincoumar, Sinthrome, Sintrom, Sinthrom, Ascumar, Mini-sintrom, Syncumar, Neositron, Syntrom, Syncoumar, Sinkumar, Zotil |
| Category: | Anticoagulants, Coumarin and Indandione Derivatives |
| CAS number: | 152-72-7 |
Pharmacology
| Indication: | For the treatment and prevention of thromboembolic diseases. More specifically, it is indicated for the for the prevention of cerebral embolism, deep vein thrombosis, pulmonary embolism, thromboembolism in infarction and transient ischemic attacks. It is used for the treatment of deep vein thrombosis and myocardial infarction. |
|---|---|
| Pharmacology: |
Acenocoumarol inhibits the reduction of vitamin K by vitamin K reductase. This prevents carboxylation of certain glutamic acid residues near the N-terminals of clotting factors II, VII, IX and X, the vitamin K-dependent clotting factors. Glutamic acid carboxylation is important for the interaction between these clotting factors and calcium. Without...
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| Mechanism of Action: |
Acenocoumarol inhibits vitamin K reductase, resulting in depletion of the reduced form of vitamin K (vitamin KH2). As vitamin K is a cofactor for the carboxylation of glutamate residues on the N-terminal regions of vitamin K-dependent clotting factors, this limits the gamma-carboxylation and subsequent activation of the vitamin K-dependent coagulan...
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| Absorption: | Rapidly absorbed orally with greater than 60% bioavailability. Peak plasma levels are attained 1 to 3 hours following oral administration. |
| Protein binding: | 98.7% protein bound, mainly to albumin |
| Biotransformation: | Extensively metabolized in the liver via oxidation forming two hydroxy metabolites and keto reduction producing two alcohol metabolites. Reduction of the nitro group produces an amino metabolite which is further transformed to an acetoamido metabolite. Metabolites do not appear to be pharmacologically active. |
| Route of elimination: | Mostly via the kidney as metabolites |
| Half Life: | 8 to 11 hours. |
| Toxicity: | The onset and severity of the symptoms are dependent on the individual's sensitivity to oral anticoagulants, the severity of the overdosage, and the duration of treatment. Bleeding is the major sign of toxicity with oral anticoagulant drugs. The most frequent symptoms observed are: cutaneous bleeding (80%), haematuria (with renal colic) (52%), haematomas, gastrointestinal bleeding, haematemesis, uterine bleeding, epistaxis, gingival bleeding and bleeding into the joints. Further symptoms include tachycardia, hypotension, peripheral circulatory disorders due to loss of blood, nausea, vomiting, diarrhoea and abdominal pains. |
| Affected organisms: | Humans and other mammals |
Interactions
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