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Details

Stereochemistry ACHIRAL
Molecular Formula 2C5H10NO4S.Ca
Molecular Weight 400.482
Optical Activity NONE
Defined Stereocenters 0 / 0
E/Z Centers 0
Charge 0

SHOW SMILES / InChI
Structure of ACAMPROSATE CALCIUM

SMILES

[Ca++].CC(=O)NCCCS([O-])(=O)=O.CC(=O)NCCCS([O-])(=O)=O

InChI

InChIKey=BUVGWDNTAWHSKI-UHFFFAOYSA-L
InChI=1S/2C5H11NO4S.Ca/c2*1-5(7)6-3-2-4-11(8,9)10;/h2*2-4H2,1H3,(H,6,7)(H,8,9,10);/q;;+2/p-2

HIDE SMILES / InChI

Molecular Formula Ca
Molecular Weight 40.078
Charge 2
Count
MOL RATIO 1 MOL RATIO (average)
Stereochemistry ACHIRAL
Additional Stereochemistry No
Defined Stereocenters 0 / 0
E/Z Centers 0
Optical Activity NONE

Molecular Formula C5H10NO4S
Molecular Weight 180.202
Charge -1
Count
MOL RATIO 2 MOL RATIO (average)
Stereochemistry ACHIRAL
Additional Stereochemistry No
Defined Stereocenters 0 / 0
E/Z Centers 0
Optical Activity NONE

Description

Acamprosate was the third medication, after disulfiram and naltrexone, to receive U.S. Food and Drug Administration (FDA) approval for postwithdrawal maintenance of alcohol abstinence. The French pharmaceutical company Laboratoires Meram began clinical development and testing of acamprosate in 1982. From 1982 to 1988, acamprosate was tested for safety and for efficacy as a treatment for alcohol dependence. Based on these studies, in 1989 Laboratoires Meram was granted marketing authorization for acamprosate in France under the trade name Aotal®. Since then, acamprosate has been extensively used and studied throughout Europe and, subsequently, in the United States. Although acamprosate has been used in Europe for more than 20 years, it was not approved by FDA until July 2004. Acamprosate became available for use in the United States in January 2005, under the trade name Campral® Delayed-Release Tablets (Merck Santé, a subsidiary of Merck KGaA, Darmstadt, Germany). Campral is currently marketed in the United States by Forest Pharmaceuticals. 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.

CNS Activity

Originator

Approval Year

Targets

Primary TargetPharmacologyConditionPotency
120.0 µM [Kd]

Conditions

ConditionModalityTargetsHighest PhaseProduct
Primary
Acamprosate

Cmax

ValueDoseCo-administeredAnalytePopulation
244.64 ng/mL
666 mg single, oral
ACAMPROSATE plasma
Homo sapiens

AUC

ValueDoseCo-administeredAnalytePopulation
3829.56 ng × h/mL
666 mg single, oral
ACAMPROSATE plasma
Homo sapiens

T1/2

ValueDoseCo-administeredAnalytePopulation
10.26 h
666 mg single, oral
ACAMPROSATE plasma
Homo sapiens

Doses

AEs

OverviewOther

Other InhibitorOther SubstrateOther Inducer






Drug as perpetrator​

Drug as victim

Tox targets

PubMed

Sample Use Guides

In Vivo Use Guide
The recommended dose of CAMPRAL (Acamprosate) is two 333 mg tablets (each dose should total 666 mg) taken three times daily. Although dosing may be done without regard to meals, dosing with meals was employed during clinical trials and is suggested as an aid to compliance in those patients who regularly eat three meals daily. A lower dose may be effective in some patients. Treatment with CAMPRAL should be initiated as soon as possible after the period of alcohol withdrawal, when the patient has achieved abstinence, and should be maintained if the patient relapses. CAMPRAL should be used as part of a comprehensive psychosocial treatment program.
Route of Administration: Oral
In Vitro Use Guide
Acamprosate (0.1-1 mM) added to the perfusion fluid in vitro reduced excitatory and inhibitory postsynaptic potentials and the depolarizing responses evoked by iontophoretic application of the excitatory amino acids, L-glutamate, L-aspartate, L-homocysteate and N-methyl-D-aspartate, but did not alter the responses to gamma-aminobutyric acid in rat neocortical neurons.
Substance Class Chemical
Record UNII
59375N1D0U
Record Status Validated (UNII)
Record Version