2598 Disulfiram A carbamate derivative used as an alcohol deterrent. It is a relatively nontoxic substance when administered alone, but markedly alters the intermediary metabolism of alcohol. When alcohol is ingested after administration of disulfiram, blood acetaldehyde concentrations are increased, followed by flushing, systemic vasodilation, respiratory difficulties, nausea, hypotension, and other symptoms (acetaldehyde syndrome). It acts by inhibiting aldehyde dehydrogenase. [PubChem] 97-77-8 3117 C10H20N2S4 296.050930 White powder. 71.5°C 117°C at 1.70E+01 mm Hg 4.09 mg/L (at 25°C) Inhalation (MSDS, A308); ingestion (MSDS, A308); dermal (MSDS, A308) ; eye contact (MSDS, A308) Disulfiram is absorbed slowly from the gastrointestinal tract (80 to 90% of oral dose). Disulfiram blocks the oxidation of alcohol at the acetaldehyde stage during alcohol metabolism following disulfiram intake causing an accumulation of acetaldehyde in the blood producing highly unpleasant symptoms. Disulfiram blocks the oxidation of alcohol through its irreversible inactivation of aldehyde dehydrogenase, which acts in the second step of ethanol utilization. In addition, disulfiram competitively binds and inhibits the peripheral benzodiazepine receptor, which may indicate some value in the treatment of the symptoms of alcohol withdrawal, however this activity has not been extensively studied. Disulfiram is completely absorbed from the human GI tract. However, a period of 12 hr is required for its full action, perhaps because, being highly sol in lipid, it is initially localized in fat. It is slowly metabolized in the liver to diethyldithiocarbamate, diethylamine, and carbon disulfide. Six hr after oral administration of the drug, one third of plasma disulfiram is in the form of diethyldithiocarbamate. Elimination is relatively slow, and about 1/5 still remains in body at end of a week. The greater part of the absorbed drug is excreted in the urine as the sulfate, partly free and partly esterified (A620, A622). LD50: 8.6g/kg (oral, rat). 3, not classifiable as to its carcinogenicity to humans. (L135) For the treatment and management of chronic alcoholism (A308). Occasionally implicated in producing psychosis, optic neuritis, and encephalopathy. Hematologic, neuromuscular, and gastrointestinal toxicity and hepatotoxicity may occur 10 days to 12 months after therapy is begun (T36). Symptoms of overdose include irritation, slight drowsiness, unpleasant taste, mild GI disturbances, and orthostatic hypotension. 2009-07-05T02:56:35Z 2014-12-24T20:25:42Z Disulfiram C01692 4659 DISULFIRAM D004221 Disulfiram DB00822 1353 true CCN(CC)C(=S)SSC(=S)N(CC)CC C10H20N2S4 InChI=1S/C10H20N2S4/c1-5-11(6-2)9(13)15-16-10(14)12(7-3)8-4/h5-8H2,1-4H3 InChIKey=AUZONCFQVSMFAP-UHFFFAOYSA-N 296.539 296.05093141 Exogenous Solid 3.88 HMDB14960 CHEMBL964 3005 <p>Adams, H.S. and Meuser, L.; US.Patent 1,782,111; November 18,1930; assigned to The<br /> Naugatuck Chemical Company.<br /> Bailey, G.C.; U.S.Patent 1,796,977; March 17,1931; assigned to The Roessler &amp; Hasslacher<br /> Chemical Company.</p>