Indication |
For the maintenance of abstinence from alcohol in patients with alcohol dependence who are abstinent at treatment initiation |
Pharmacodynamics |
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. |
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. |
Volume of distribution |
|
Protein binding |
Non detectable |
Metabolism |
Acamprosate does not undergo metabolism. |
Route of elimination |
Following oral administration of CAMPRAL®, the major route of excretion is via the kidneys as acamprosate. |
Half life |
20 - 33 hours |
Clearance |
Not Available |
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. |
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