1.0 2009-07-23 18:26:19 UTC 2026-05-14 17:00:16 UTC T3D3106 Acenocoumarol SmallMolecule Acenocoumarol is an exogenous solid with the formula C19H15NO6 and an average molecular weight of 353.33 g/mol. Acenocoumarol belongs to the hydroxycoumarins, a subclass of coumarins and derivatives within the organic compounds. It is used as an anticoagulant and acts as an inhibitor of EC 1.6.5.2 [NAD(P)H dehydrogenase (quinone)]. This compound is found in amplifiers and in antithrombotic agents within healthcare, pharmaceuticals, and veterinary products, with oral exposure recorded. The protein targets of acenocoumarol include albumin (ALB), alpha-1-acid glycoprotein 1 (ORM1), and vitamin K epoxide reductase complex subunit 1 (VKORC1). Acenocoumarol inhibits vitamin K reductase, which leads to the depletion of the reduced form of vitamin K (vitamin KH2). Because vitamin K serves as a cofactor for the carboxylation of glutamate residues on the N-terminal regions of vitamin K-dependent proteins, this inhibition limits gamma-carboxylation and the subsequent activation of vitamin K-dependent coagulant proteins. Consequently, the synthesis of anticoagulant proteins C and S, as well as vitamin K-dependent coagulation factors II, VII, IX, and X, is inhibited. Drug Synthetic Toxin Organic Compound Aromatic Hydrocarbon Ester Drug Anticoagulant Metabolite Synthetic Compound Human Neurotoxin 3-(alpha-(4'-Nitrophenyl)-beta-acetylethyl)-4-hydroxycoumarin 3-(alpha-(P-Nitrophenol)-beta-acetylethyl)-4-hydroxycoumarin 3-(alpha-Acetonyl-4-nitrobenzyl)-4-hydroxycoumarin 3-(alpha-Acetonyl-P-nitrobenzyl)-4-hydroxycoumarin 3-(alpha-P-Nitrophenyl-beta-acetylethyl)-4-hydroxycoumarin 4-Hydroxy-3-(1-(4-nitrophenyl)-3-oxobutyl)-2H-1-benzopyran-2-one 4-Hydroxy-3-[1-(4-nitrophenyl)-3-oxobutyl]-2H-chromen-2-one Acenocoumarin Acenocoumarolum Acenocumarol Acenocumarolo Acenokumarin Ascumar Mini-sintrom Nicoumalone Nicumalon Nitrophenylacetylethyl-4-hydroxycoumarine Nitrovarfarian Nitrowarfarin Sinkumar Sintrom C19H15NO6 353.3255 353.089937217 4-hydroxy-3-[1-(4-nitrophenyl)-3-oxobutyl]-2H-chromen-2-one acenocumarolo 152-72-7 CC(=O)CC(C1=CC=C(C=C1)[N+]([O-])=O)C1=C(O)C2=CC=CC=C2OC1=O InChI=1S/C19H15NO6/c1-11(21)10-15(12-6-8-13(9-7-12)20(24)25)17-18(22)14-4-2-3-5-16(14)26-19(17)23/h2-9,15,22H,10H2,1H3 VABCILAOYCMVPS-UHFFFAOYSA-N Organic compounds Phenylpropanoids and polyketides Coumarins and derivatives Hydroxycoumarins 4-hydroxycoumarins 1-benzopyrans Heteroaromatic compounds Hydrocarbon derivatives Ketones Lactones Nitroaromatic compounds Nitrobenzenes Organic oxides Organic oxoazanium compounds Organonitrogen compounds Organopnictogen compounds Oxacyclic compounds Propargyl-type 1,3-dipolar organic compounds Pyranones and derivatives Vinylogous acids 1-benzopyran 4-hydroxycoumarin Allyl-type 1,3-dipolar organic compound Aromatic heteropolycyclic compound Benzenoid Benzopyran C-nitro compound Carbonyl group Heteroaromatic compound Hydrocarbon derivative Ketone Lactone Monocyclic benzene moiety Nitroaromatic compound Nitrobenzene Organic 1,3-dipolar compound Organic nitro compound Organic nitrogen compound Organic oxide Organic oxoazanium Organic oxygen compound Organoheterocyclic compound Organonitrogen compound Organooxygen compound Organopnictogen compound Oxacycle Propargyl-type 1,3-dipolar organic compound Pyran Pyranone Vinylogous acid Aromatic heteropolycyclic compounds C-nitro compound hydroxycoumarin methyl ketone Detected and Not Quantified Exogenous Extracellular Membrane Acenocoumarol Action Pathway SMP0000269 Acenocoumarol Drug Metabolism Action Pathway SMP0143755 Acenocoumarol Predicted Metabolism Pathway SMP0174683 Solid White powder. melting_point 196-199°C solubility practically insoluble logp 1.98 logp 2.53 ALOGPS logs -4.52 ALOGPS solubility 1.06e-02 g/l ALOGPS logp 2.68 ChemAxon pka_strongest_acidic 5.79 ChemAxon pka_strongest_basic -6.8 ChemAxon iupac 4-hydroxy-3-[1-(4-nitrophenyl)-3-oxobutyl]-2H-chromen-2-one ChemAxon average_mass 353.3255 ChemAxon mono_mass 353.089937217 ChemAxon smiles CC(=O)CC(C1=CC=C(C=C1)[N+]([O-])=O)C1=C(O)C2=CC=CC=C2OC1=O ChemAxon formula C19H15NO6 ChemAxon inchi InChI=1S/C19H15NO6/c1-11(21)10-15(12-6-8-13(9-7-12)20(24)25)17-18(22)14-4-2-3-5-16(14)26-19(17)23/h2-9,15,22H,10H2,1H3 ChemAxon inchikey VABCILAOYCMVPS-UHFFFAOYSA-N ChemAxon polar_surface_area 109.42 ChemAxon refractivity 94.18 ChemAxon polarizability 34.35 ChemAxon rotatable_bond_count 5 ChemAxon acceptor_count 5 ChemAxon donor_count 1 ChemAxon physiological_charge -1 ChemAxon formal_charge 0 ChemAxon Ingestion (L1817) ; dermal (L1817). Rapidly absorbed orally with greater than 60% bioavailability. Peak plasma levels are attained 1 to 3 hours following oral administration. 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 proteins, this limits the gamma-carboxylation and subsequent activation of the vitamin K-dependent coagulant proteins. The synthesis of vitamin K-dependent coagulation factors II, VII, IX, and X and anticoagulant proteins C and S is inhibited. Depression of three of the four vitamin K-dependent coagulation factors (factors II, VII, and X) results in decresed prothrombin levels and a decrease in the amount of thrombin generated and bound to fibrin. This reduces the thrombogenicity of clots. (A308) 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. LD50: 1470 mg/kg (Oral, Mouse) (T14) LD50: 115 mg/kg (Intraperitoneal, Mouse) (T14) No indication of carcinogenicity to humans (not listed by IARC). Acenocoumarol is an anticoagulant drug derived from coumarin. (L1261) 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. #<HealthEffect::ActiveRecord_Associations_CollectionProxy:0x00007f3bcff34258> 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. The primary antidote to acenocoumarol poisoning is immediate administration of vitamin K1 (initially slow intravenous injections of 10-25 mg repeated all 3-6 hours until normalisation of the prothrombin time; then 10 mg orally four times daily as a "maintenance dose"). It is an extremely effective antidote, provided the poisoning is caught before too much damage has been done to the victim's circulatory system. At high doses acenocoumarol can affect the body for many months, and the antidote must be administered regularly for a long period of time. (L1257) DB01418 HMDB15487 54676537 CHEMBL397420 10443441 53766 Acenocoumarol Acenocoumarol 18048412 15613922 15724697 16372822 16611310 9684795 Lewis RJ (1996). Sax's Dangerous Properties of Industrial Materials. 9th ed. Volumes 1-3. New York, NY: Van Nostrand Reinhold. Wikipedia. Brodifacoum. Last Updated 22 June 2009. : http://en.wikipedia.org/wiki/Brodifacoum Wikipedia. Acenocoumarol. Last Updated 29 June 2009. : http://en.wikipedia.org/wiki/Acenocoumarol Wikipedia. Phytotoxin. Last Updated 7 August 2009.: http://en.wikipedia.org/wiki/Phytotoxin BE0000713 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 proteins, this limits the gamma-carboxylation and subsequent activation of the vitamin K-dependent coagulant proteins. The synthesis of vitamin K-dependent coagulation factors II, VII, IX, and X and anticoagulant proteins C and S is inhibited. Depression of three of the four vitamin K-dependent coagulation factors (factors II, VII, and X) results in decresed prothrombin levels and a decrease in the amount of thrombin generated and bound to fibrin. This reduces the thrombogenicity of clots. BE0000925 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 proteins, this limits the gamma-carboxylation and subsequent activation of the vitamin K-dependent coagulant proteins. The synthesis of vitamin K-dependent coagulation factors II, VII, IX, and X and anticoagulant proteins C and S is inhibited. Depression of three of the four vitamin K-dependent coagulation factors (factors II, VII, and X) results in decresed prothrombin levels and a decrease in the amount of thrombin generated and bound to fibrin. This reduces the thrombogenicity of clots. BE0000530 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 proteins, this limits the gamma-carboxylation and subsequent activation of the vitamin K-dependent coagulant proteins. The synthesis of vitamin K-dependent coagulation factors II, VII, IX, and X and anticoagulant proteins C and S is inhibited. Depression of three of the four vitamin K-dependent coagulation factors (factors II, VII, and X) results in decresed prothrombin levels and a decrease in the amount of thrombin generated and bound to fibrin. This reduces the thrombogenicity of clots.