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Purity: ≥98%
Acamprosate calcium (also known as Campral EC), a medication used in the treatment of alcohol dependence, is a GABA receptor agonist and modulator of glutamatergic systems; it reduces alcohol consumption in animal models of alcohol addiction. Acamprosate is thought to stabilize the chemical balance in the brain that would otherwise be disrupted by alcohol withdrawal. Reports indicate that acamprosate works to best advantage in combination with psychosocial support and can help facilitate reduced consumption as well as full abstinence. Until it became a generic in the United States, Campral was manufactured and marketed in the United States by Forest Laboratories, while Merck KGaA markets it outside the US.
| Targets |
Acamprosate acts as a partial coagonist/modulator of NMDA receptors, depending on concentration and receptor activity. It may also interact with GABA receptors, though recent studies indicate little direct effect on GABAA or glycine receptors. The drug modulates NMDA receptor subunit expression and regulates glutamatergic neurotransmission, helping to balance excitatory and inhibitory neurotransmitter systems disrupted by chronic alcohol use.[2]
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| ln Vitro |
In vitro activity: Acamprosate has low bioavailability, but also has an excellent
tolerability and safety profile. In comparison with naltrexone and disulfiram, which are the other FDA-approved treatments for alcohol dependence, acamprosate is unique in that it is not metabolized by the liver and is also not impacted by alcohol use, so can be administered to patients with hepatitis or liver disease (a common comorbid condition among individuals with alcohol dependence) and to patients who continue drinking alcohol. Acamprosate shows biphasic effects on NMDA receptors in isolated neonatal rat respiratory networks, enhancing low receptor activity at low concentrations and inhibiting highly activated receptors at high concentrations.[2] In Xenopus oocytes expressing neuronal receptors and ion channels, acamprosate modulates receptor activity, particularly affecting NMDA receptor function.[2] Studies using rat brain tissue identified a spermidine-sensitive binding site for acamprosate, suggesting a specific mechanism of action at NMDA receptors.[2] |
| ln Vivo |
Acamprosate calcium(Campral EC) is a GABA receptor agonist and modulator
of glutamatergic systems; reduces alcohol consumption in animal models of alcohol addiction. In alcohol-dependent patients, acamprosate significantly reduces the risk of returning to any drinking by 86% and increases cumulative abstinence duration by 11% compared to placebo, based on meta-analysis of 24 randomized controlled trials.[2] Acamprosate does not show superior efficacy over placebo in reducing heavy drinking days.[2] The drug also demonstrates sustained effects post-treatment, with a 9% lower risk of relapse and 9% higher abstinence duration compared to placebo after discontinuation.[2] |
| Enzyme Assay |
Acamprosate was studied for its binding to NMDA receptors using rat brain synaptosomal preparations. Binding assays characterized a spermidine-sensitive site, indicating modulation rather than direct antagonism.[2]
Receptor activity modulation was assessed using Xenopus oocytes expressing NMDA and GABA receptors, showing concentration-dependent effects on ion channel currents.[2] |
| Cell Assay |
In vitro studies using Caco-2 cell monolayers evaluated intestinal absorption of acamprosate, showing low permeability and paracellular absorption.[2]
Studies on chronically alcohol-exposed rat synaptosomes showed that acamprosate modulates GABA transmission, though recent evidence suggests minimal direct GABA receptor involvement.[2] |
| Animal Protocol |
Wild-type and ENT1 null mice (8–16 weeks old, male) were used. Chronic ethanol was administered via inhalation in a vapor chamber for 16 hours/day for 3 consecutive days, with an 8-hour withdrawal period between sessions. Prior to vapor exposure, mice received a single intraperitoneal (i.p.) injection of 1.5 g/kg ethanol (20% v/v in saline) and 68.1 mg/kg pyrazole to initiate and maintain intoxication. Blood ethanol concentrations were maintained around 150 mg/dL.[5] For acamprosate treatment, after an 8-hour withdrawal period following the last ethanol exposure, mice received acamprosate at 400 mg/kg/day (i.p.), administered as two injections of 200 mg/kg each, 12 hours apart, for 5 consecutive days. Control mice received saline at equivalent volumes.[5] In vivo 16.4T proton magnetic resonance spectroscopy ([1H] MRS) was performed to measure metabolite levels in the mPFC and NAc at baseline, after withdrawal, and after acamprosate treatment. An 8 µL volume of interest was placed in each region, and spectra were acquired using a PRESS sequence (TR=1768 ms, TE=10 ms, NA=3072). Metabolites were quantified using LCModel software relative to creatine as an internal standard.[5] |
| ADME/Pharmacokinetics |
Acampate calcium has low oral bioavailability (approximately 11%). It is absorbed via the paracellular pathway, reaching peak plasma concentrations 4.3–15.3 hours after acute administration, decreasing to steady-state concentrations 3.5–9.5 hours later. [2] Steady-state plasma concentrations are reached within 5–7 days after administration. [2] The drug is not metabolized by the liver and has no known active metabolites. It is primarily excreted unchanged in feces, with renal excretion being correlated with bioavailability. [2] Food intake further reduces its absorption. [2] Drug interaction studies have shown no significant interactions between acampate calcium and naltrexone, disulfiram, diazepam, or alcohol. [2]
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| Toxicity/Toxicokinetics |
Effects During Pregnancy and Lactation
◉ Overview of use during lactation There is currently no information on the clinical use of calcium acampanol during lactation. Based on its chemical properties, it is likely to enter breast milk. However, the oral bioavailability of calcium acampanol is only 11%, so it is unlikely to have a systemic effect on breastfed infants. If the mother needs to take calcium acampanol, there is no need to stop breastfeeding. Breastfed infants should be monitored for diarrhea. ◉ Effects on breastfed infants As of the revision date, no relevant published information was found. ◉ Effects on lactation and breast milk As of the revision date, no relevant published information was found. Calcium acampanol is generally well tolerated and has an excellent safety profile. The most common side effect is diarrhea (16% vs. 10% in the placebo group). [2] Other reported side effects include abdominal pain, constipation, nausea, vomiting, gastrointestinal symptoms, and itching, but these side effects occur at a low rate. [2] The withdrawal rate due to side effects was slightly higher in the calcium acamprate group (7-8%) than in the placebo group (6-7%), but the difference was not statistically significant. [2] Serious adverse events were rare and there was no significant difference between the two groups. [2] Because the drug is excreted by the kidneys, it is contraindicated in patients with severe renal insufficiency. [2] |
| References |
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| Additional Infomation |
Calcium acampanate is an organic calcium salt containing the acampanate group (1-). It is a structural analog of taurine and is used to prevent relapse in patients with alcohol dependence. See also: acampanate (containing the active moiety).
Acampanate has been approved by the U.S. Food and Drug Administration (FDA) for the treatment of alcohol dependence. Unlike other approved drugs, acampanate is not metabolized by the liver and is safe for patients with liver disease or those who continue to drink alcohol. [2] It has no potential for abuse and has very few drug interactions. [2] Its efficacy is moderate compared to placebo and is not always superior to naltrexone or disulfiram. [2] Patient adherence is crucial; patients taking ≥80% of the prescribed dose have better efficacy. [2] Genetic factors (e.g., GABRA6, DRD2, GATA4 polymorphisms) may affect treatment response. [2] This drug may reduce alcohol cravings and stabilize the function of the hypothalamic-pituitary-adrenal (HPA) axis. [2] |
| Molecular Formula |
C10H20CAN2O8S2
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| Molecular Weight |
400.47
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| Exact Mass |
400.028
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| CAS # |
77337-73-6
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| Related CAS # |
Acamprosate-d3 calcium;1225580-94-8;Acamprosate;77337-76-9
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| PubChem CID |
155434
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| Appearance |
White to off-white solid powder
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| Melting Point |
>300ºC
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| LogP |
1.059
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| Hydrogen Bond Donor Count |
2
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| Hydrogen Bond Acceptor Count |
8
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| Rotatable Bond Count |
6
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| Heavy Atom Count |
23
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| Complexity |
202
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| Defined Atom Stereocenter Count |
0
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| SMILES |
CC(=O)NCCCS(=O)(=O)[O-].CC(=O)NCCCS(=O)(=O)[O-].[Ca+2]
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| InChi Key |
BUVGWDNTAWHSKI-UHFFFAOYSA-L
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| InChi Code |
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
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| Chemical Name |
Calcium 3-(acetylamino)propane-1-sulfonate
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| Synonyms |
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: Please store this product in a sealed and protected environment, avoid exposure to moisture. |
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| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
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| Solubility (In Vivo) |
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| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.4971 mL | 12.4853 mL | 24.9707 mL | |
| 5 mM | 0.4994 mL | 2.4971 mL | 4.9941 mL | |
| 10 mM | 0.2497 mL | 1.2485 mL | 2.4971 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
Link: https://clinicaltrials.gov/ct2/show/NCT07204977
Conditions:Amyotrophic Lateral Sclerosis|Motor Neuron DiseaseLink: https://clinicaltrials.gov/ct2/show/NCT06269627
Conditions:Alcohol Use DisorderLink: https://clinicaltrials.gov/ct2/show/NCT03634917
Conditions:Alcoholism
Ethanol exposure in a vapor chamber and ethanol withdrawal experiment.Neuropharmacology. 2012 Jun;62(8):2480-8. |
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Simplified illustration of the cortical-striatal circuit in ENT1 null mice.Neuropharmacology. 2012 Jun;62(8):2480-8. |
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