indication

For the maintenance of abstinence from alcohol in patients with alcohol dependence who are abstinent at treatment initiation

pharmacology

Pharmacodynamic studies have shown that acamprosate calcium reduces alcohol intake in alcohol-dependent animals in a dose-dependent manner and that this effect appears to be specific to alcohol and the mechanisms of alcohol dependence. Acamprosate calcium has negligible observable central nervous system (CNS) activity in animals outside of its effects on alcohol dependence, exhibiting no anticonvulsant, antidepressant, or anxiolytic activity.

mechanism of action

The mechanism of action of acamprosate in maintenance of alcohol abstinence is not completely understood. Chronic alcohol exposure is hypothesized to alter the normal balance between neuronal excitation and inhibition. in vitro and in vivo studies in animals have provided evidence to suggest acamprosate may interact with glutamate and GABA neurotransmitter systems centrally, and has led to the hypothesis that acamprosate restores this balance. It seems to inhibit NMDA receptors while activating GABA receptors.

toxicity

In all reported cases of acute overdosage with acamprosate (total reported doses of up to 56 grams of acamprosate calcium), the only symptom that could be reasonably associated with acamprosate was diarrhea.

biotransformation

Acamprosate does not undergo metabolism.

absorption

The absolute bioavailability of acamprosate after oral administration is about 11%. The food effect on absorption is not clinically significant and no adjustment of dose is necessary.

half life

20 - 33 hours

route of elimination

Following oral administration of CAMPRAL®, the major route of excretion is via the kidneys as acamprosate.