Skeletal formula of acamprosate
Ball-and-stick model of the acamprosate molecule
Clinical data
Trade namesCampral EC
Other namesN-Acetyl homotaurine, Acamprosate calcium (JAN JP), Acamprosate calcium (USAN US)
Routes of
ATC code
Legal status
Legal status
  • AU: S4 (Prescription only)
  • UK: POM (Prescription only)
  • US: ℞-only
Pharmacokinetic data
Protein bindingNegligible[1]
Elimination half-life20 h to 33 h[1]
  • 3-Acetamidopropane-1-sulfonic acid
CAS Number
PubChem CID
CompTox Dashboard (EPA)
ECHA InfoCard100.071.495 Edit this at Wikidata
Chemical and physical data
Molar mass181.21 g·mol−1
3D model (JSmol)
  • [Ca+2].O=C(NCCCS(=O)(=O)[O-])C.[O-]S(=O)(=O)CCCNC(=O)C
  • 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 checkY
 ☒NcheckY (what is this?)  (verify)

Acamprosate, sold under the brand name Campral, is a medication used along with counseling to treat alcohol use disorder.[1][2]

Acamprosate is thought to stabilize chemical signaling in the brain that would otherwise be disrupted by alcohol withdrawal.[3] When used alone, acamprosate is not an effective therapy for alcohol use disorder in most individuals;[4] studies have found that acamprosate works best when used in combination with psychosocial support since the drug facilitates a reduction in alcohol consumption as well as full abstinence.[2][5][6]

Serious side effects include allergic reactions, abnormal heart rhythms, and low or high blood pressure, while less serious side effects include headaches, insomnia, and impotence.[7] Diarrhea is the most common side-effect.[8] It is unclear if use is safe during pregnancy.[9][10]

It is on the World Health Organization's List of Essential Medicines.[11]

Medical uses

Acamprosate is useful when used along with counseling in the treatment of alcohol use disorder.[2] Over three to twelve months it increases the number of people who do not drink at all and the number of days without alcohol.[2] It appears to work as well as naltrexone for maintenance of abstinence from alcohol,[12] however naltrexone works slightly better for reducing alcohol cravings and heavy drinking,[13] and acamprosate tends to work more poorly outside of Europe where treatment services are less robust.[14]


Acamprosate is primarily removed by the kidneys. A dose reduction is suggested in those with moderately impaired kidneys (creatinine clearance between 30 mL/min and 50 mL/min).[1][15] It is also contraindicated in those who have a strong allergic reaction to acamprosate calcium or any of its components.[15]

Adverse effects

The US label carries warnings about increases of suicidal behavior, major depressive disorder, and kidney failure.[1]

Adverse effects that caused people to stop taking the drug in clinical trials included diarrhea, nausea, depression, and anxiety.[1]

Potential adverse effects include headache, stomach pain, back pain, muscle pain, joint pain, chest pain, infections, flu-like symptoms, chills, heart palpitations, high blood pressure, fainting, vomiting, upset stomach, constipation, increased appetite, weight gain, edema, sleepiness, decreased sex drive, impotence, forgetfulness, abnormal thinking, abnormal vision, distorted sense of taste, tremors, runny nose, coughing, difficulty breathing, sore throat, bronchitis, and rashes.[1]


Acamprosate calcium


The pharmacodynamics of acamprosate are complex and not fully understood;[16][17][18] however, it is believed to act as an NMDA receptor antagonist and positive allosteric modulator of GABAA receptors.[17][18]

Its activity on those receptors is indirect, unlike that of most other agents used in this context.[19] An inhibition of the GABA-B system is believed to cause indirect enhancement of GABAA receptors.[19] The effects on the NMDA complex are dose-dependent; the product appears to enhance receptor activation at low concentrations, while inhibiting it when consumed in higher amounts, which counters the excessive activation of NMDA receptors in the context of alcohol withdrawal.[20]

The product also increases the endogenous production of taurine.[20]

Ethanol and benzodiazepines act on the central nervous system by binding to the GABAA receptor, increasing the effects of the inhibitory neurotransmitter GABA (i.e., they act as positive allosteric modulators at these receptors).[17][4] In alcohol use disorder, one of the main mechanisms of tolerance is attributed to GABAA receptors becoming downregulated (i.e. these receptors become less sensitive to GABA).[4] When alcohol is no longer consumed, these down-regulated GABAA receptor complexes are so insensitive to GABA that the typical amount of GABA produced has little effect, leading to physical withdrawal symptoms;[4] since GABA normally inhibits neural firing, GABAA receptor desensitization results in unopposed excitatory neurotransmission (i.e., fewer inhibitory postsynaptic potentials occur through GABAA receptors), leading to neuronal over-excitation (i.e., more action potentials in the postsynaptic neuron). One of acamprosate's mechanisms of action is the enhancement of GABA signaling at GABAA receptors via positive allosteric receptor modulation.[17][18] It has been purported to open the chloride ion channel in a novel way as it does not require GABA as a cofactor, making it less liable for dependence than benzodiazepines. Acamprosate has been successfully used to control tinnitus, hyperacusis, ear pain, and inner ear pressure during alcohol use due to spasms of the tensor tympani muscle.[medical citation needed]

In addition, alcohol also inhibits the activity of N-methyl-D-aspartate receptors (NMDARs).[21][22] Chronic alcohol consumption leads to the overproduction (upregulation) of these receptors. Thereafter, sudden alcohol abstinence causes the excessive numbers of NMDARs to be more active than normal and to contribute to the symptoms of delirium tremens and excitotoxic neuronal death.[23] Withdrawal from alcohol induces a surge in release of excitatory neurotransmitters like glutamate, which activates NMDARs.[24] Acamprosate reduces this glutamate surge.[25] The drug also protects cultured cells from excitotoxicity induced by ethanol withdrawal[26] and from glutamate exposure combined with ethanol withdrawal.[27]

The substance also helps re-establish a standard sleep architecture by normalizing stage 3 and REM sleep phases, which is believed to be an important aspect of its pharmacological activity.[20]


Acamprosate is not metabolized by the human body.[18] Acamprosate's absolute bioavailability from oral administration is approximately 11%,[18] and its bioavailability is decreased when taken with food.[28] Following administration and absorption of acamprosate, it is excreted unchanged (i.e., as acamprosate) via the kidneys.[18]

Its absorption and elimination are very slow, with a Tmax of 6 hours and an elimination half life of over 30 hours.[19]


Acamprosate was developed by Lipha, a subsidiary of Merck KGaA.[29] and was approved for marketing in Europe in 1989.[citation needed]

In October 2001 Forest Laboratories acquired the rights to market the drug in the US.[29][30]

It was approved by the FDA in July 2004.[31]

The first generic versions of acamprosate were launched in the US in 2013.[32]

As of 2015 acamprosate was in development by Confluence Pharmaceuticals as a potential treatment for fragile X syndrome. The drug was granted orphan status for this use by the FDA in 2013 and by the EMA in 2014.[33]

Society and culture

"Acamprosate" is the INN and BAN for this substance. "Acamprosate calcium" is the USAN and JAN. It is also technically known as N-acetylhomotaurine or as calcium acetylhomotaurinate.

It is sold under the brand name Campral.[1]


In addition to its apparent ability to help patients refrain from drinking, some evidence suggests that acamprosate is neuroprotective (that is, it protects neurons from damage and death caused by the effects of alcohol withdrawal, and possibly other causes of neurotoxicity).[25][34]


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  2. ^ a b c d Plosker GL (July 2015). "Acamprosate: A Review of Its Use in Alcohol Dependence". Drugs. 75 (11): 1255–1268. doi:10.1007/s40265-015-0423-9. PMID 26084940. S2CID 19119078.
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  4. ^ a b c d Malenka RC, Nestler EJ, Hyman SE, Holtzman DM (2015). "Chapter 16: Reinforcement and Addictive Disorders". Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (3rd ed.). New York: McGraw-Hill Medical. ISBN 9780071827706. It has been hypothesized that long-term ethanol exposure alters the expression or activity of specific GABAA receptor subunits in discrete brain regions. Regardless of the underlying mechanism, ethanol-induced decreases in GABAA receptor sensitivity are believed to contribute to ethanol tolerance, and also may mediate some aspects of physical dependence on ethanol. ... Detoxification from ethanol typically involves the administration of benzodiazepines such as chlordiazepoxide, which exhibit cross-dependence with ethanol at GABAA receptors (Chapters 5 and 15). A dose that will prevent the physical symptoms associated with withdrawal from ethanol, including tachycardia, hypertension, tremor, agitation, and seizures, is given and is slowly tapered. Benzodiazepines are used because they are less reinforcing than ethanol among alcoholics. Moreover, the tapered use of a benzodiazepine with a long half-life makes the emergence of withdrawal symptoms less likely than direct withdrawal from ethanol. ... Unfortunately, acamprosate is not adequately effective for most alcoholics.
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    Marketed formulations contain acamprosate calcium
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