[4] Fomepizole works by blocking the enzyme that converts methanol and ethylene glycol to their toxic breakdown products.

By competitively inhibiting the first enzyme, alcohol dehydrogenase, in the metabolism of ethylene glycol and methanol, fomepizole slows the production of the toxic metabolites.

It is, in essence, the antithesis of a disulfiram approach which tries to increase the buildup of acetaldehyde resulting in positive punishment for the patient.

Disulfiram also has a considerably longer half-life than that of fomepizole, requiring the person to not drink ethanol in order to avoid severe effects.

If the person is not adequately managed on a benzodiazepine, barbiturate, acamprosate, or another GABAA receptor agonist, the alcohol withdrawal syndrome, and its attendant, life-threatening risk of delirium tremens "DT", may occur.

Fomepizole treatment may be initiated while the DT de-titration sequence is still being calibrated based upon the person's withdrawal symptoms and psychological health.

[citation needed] Common side effects associated with fomepizole use include headache and nausea.

Peak concentration following single oral doses of 7 to 50 mg/kg of body weight occurred in 1 to 2 hours.

Following multiple doses, fomepizole rapidly induces its own metabolism via the cytochrome P450 mixed-function oxidase system.