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Acamprosate Calcium GABA Receptor agonist

Cat.No.S3748

Acamprosate (N-Acetylhomotaurine, Calcium acetylhomotaurinate,N-acetylhomotaurinate) is a synthetic compound with a chemical structure similar to the amino acid neurotransmitter gamma-aminobutyric acid (GABA) and the amino acid neuromodulator taurine.
Acamprosate Calcium GABA Receptor agonist Chemical Structure

Chemical Structure

Molecular Weight: 200.24

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Quality Control

Batch: S374801 Water]40 mg/mL]false]DMSO]Insoluble]false]Ethanol]Insoluble]false Purity: 99.73%
99.73

Solubility

In vitro
Batch:

Water : 40 mg/mL

DMSO : Insoluble
(Moisture-contaminated DMSO may reduce solubility. Use fresh, anhydrous DMSO.)

Ethanol : Insoluble

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In vivo
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Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.

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Chemical Information, Storage & Stability

Molecular Weight 200.24 Formula

C5H11NO4S.1/2Ca

Storage (From the date of receipt)
CAS No. 77337-73-6 Download SDF Storage of Stock Solutions

Synonyms N-Acetylhomotaurine Calcium, calcium acetylhomotaurinate,N-acetylhomotaurinate Smiles CC(=O)NCCCS(=O)(=O)[O-].CC(=O)NCCCS(=O)(=O)[O-].[Ca+2]

Mechanism of Action

In vitro

Acamprosate binds to a specific spermidine-sensitive site that modulates the NMDA receptor in a complex way.

In vivo

Acamprosate is absorbed via the gastrointestinal tract, with pharmacokinetic linearity in terms of dose and time. Absolute bioavailability of acamprosate under fasting conditions is approximately 11%. After food intake, bioavailability decreases by approximately 20%, but this decrease lacks clinical significance. Steady-state plasma concentrations of acamprosate are reached within 5 days of dosing and the terminal half-life ranges from 20–33 hours following the standard 2 × 333 dosing regime. Plasma protein binding is negligible. Acamprosate is not metabolized in the liver and is excreted unchanged in the urine. Acamprosate may have neuroprotective effects. Acamprosate appears to work by normalizing the dysregulation of NMDA-mediated glutamatergic neurotransmission that occurs during chronic alcohol consumption and withdrawal, and thus attenuates one of the physiological mechanisms that may prompt relapse.

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