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RecruitingNCT06269627Updated Nov 2, 2026

Temporally-Resolved Electrophysiology of Acamprosate Treatment of Alcohol Use Disorder

A Phase 4 interventional study of Acamprosate calcium and Placebo in Alcohol Use Disorder, sponsored by National Institute on Alcohol Abuse and Alcoholism (NIAAA). Recruiting at 1 site in United States. Open to participants aged 21 Years to 65 Years. Per ClinicalTrials.gov, last updated 2026-11-02.

Sponsored by National Institute on Alcohol Abuse and Alcoholism (NIAAA) · Phase 4, Interventional, and Basic science

From the registry’s dates

  • Started May 2025; still recruiting 1 year 6 months later.
Phase
Phase 4
Study type
Interventional
Enrollment
48
Allocation
Randomized
Ages
21 Years to 65 Years
Sex
All
01

Study summary

Background:

Chronic heavy drinking can cause alcohol use disorder (AUD). AUD changes how the brain works. People with AUD may drink compulsively or feel like they cannot control their alcohol use. Acamprosate is an FDA-approved drug that reduces anxiety and craving in some, but not all, people with AUD.

Objective:

To learn more about how acamprosate affects brain function in people with AUD.

Eligibility:

People aged 21 to 65 years with moderate to severe AUD.

Design:

Participants will stay in the clinic for 21 days after a detoxification period of approximately 7 days.

Acamprosate is a capsule taken by mouth. Half of participants will take this drug 3 times a day with meals. The other half will take a placebo. The placebo looks like the study drug but does not contain any medicine. Participants will not know which capsules they are taking.

Participants will have a procedure called electroencephalography (EEG): A gel will be applied to certain locations on their scalp, and a snug cap will be placed on their head. The cap has sensors with wires. The sensors detect electrical activity in the brain. Participants will lie still and perform 2 tasks: they will look at different shapes and press a button when they see a specific one; and they will listen to tones and press dedicated buttons when they hear the corresponding tones.

Participants will have 2 EEGs: 1 on day 2 and 1 on day 23 of their study participation. They may opt to have up to 4 more EEG studies (one on day 13 and one on each of the three follow-up visits) and 2 sleep studies, in which they would have sensors attached to their scalp while they sleep.

Participants may have up to three follow-up visits for 6 months.

Read the detailed description

Study Description:

This double-blind placebo-controlled study will focus on electrophysiological changes in brains of alcohol use disorder (AUD)inpatients resulting from a post-withdrawal 21-day acamprosate/placebo treatment. Known and established electroencephalogram (EEG) markers of AUD as well as anxiety and alcohol craving levels will be assessed pre- and post-treatment. We hypothesize that acamprosate normalizes EEG markers associated with AUD beyond placebo, specifically, reduces beta power, increases alpha power, does not change slow band (delta and theta) power in resting EEG; and reduces theta event-related synchronization (ERS), and amplifies and hastens P300 waveforms in event-related potentials (ERPs).

Objectives:

Primary Objective: To test, via within-subject comparisons, whether a 21-day acamprosate treatment regimen normalizes the EEG of AUD inpatients beyond placebo in reducing beta power, increasing alpha power, and changing slow band (delta and theta) power in resting EEG; and reducing theta event-related synchronization (ERS), and amplifying and hastening P300 waveforms in event-related potentials (ERPs).

Secondary Objectives: 1) To correlate EEG changes with clinical changes, such as anxiety and alcohol craving. 2) To determine polysomnographic markers of response to acamprosate. 3) To correlate polysomnographic markers with clinical changes, such as anxiety and alcohol craving.

Endpoints:

Primary Endpoint: The said markers of EEG power and higher order EEG patterns will be measured before and after the 21-day treatment to compare the active-medication and placebo groups.

Secondary Endpoints: 1) Acamprosate-induced changes in EEG power and higher order EEG patterns will be correlated to changes in anxiety and alcohol craving. 2) Acamprosate-induced changes in EEG power will be correlated to changes in polysomnographic markers such as total sleep time, slow wave sleep duration, sleep efficiency, and total wake duration after sleep onset. 3) Changes in polysomnographic markers will be correlated to changes in anxiety and alcohol craving.

02

Conditions studied

  • Alcohol Use Disorder

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Keywords

  • Multimodal
  • Neuroscience
  • Resting State
  • Event-Related Potentials
  • Artificial Intelligence
  • Machine Learning
  • ELECTROENCEPHALOGRAPHY
  • Acamprosate
03

In context

Alcoholism

1,674 studies on the registry are indexed under Alcoholism; 331 are open to participants now.

This study's planned enrollment of 48 is below the median of 88 across 1,428 interventional studies indexed under Alcoholism.

Browse Alcoholism studies →

Lead sponsor

National Institute on Alcohol Abuse and Alcoholism (NIAAA) is the lead sponsor of 102 studies on the registry; 14 are open to participants now.

Of its 13 completed or terminated interventional studies of FDA-regulated products, 9 (69%) have results posted.

Counted across the registry records on this site, refreshed daily.

04

Who can participate

Ages eligible
21 Years to 65 Years
Sexes eligible
All
Accepts healthy volunteers
No

Go through the criteria one by one — yes, no or not sure — and take the list to your doctor or the study team. Kept in this browser only.

Inclusion criteria

In order to be eligible to participate in this study, an individual must meet all of the following criteria:

  1. Age 21-65. In younger participants, the central nervous system has not sufficiently developed, whereas in older participants, degenerative changes may confound the studied measures. Moreover, the minimum legal drinking age is 21 years.
  2. Enrolled in NIAAA natural history protocol 14-AA-0181.
  3. Admitted to alcohol treatment program of NIAAA with moderate to severe alcohol use disorder by a clinician at the time of admission.
  4. Determination by the attending physician or licensed practitioner caring for the patient that the patient's current clinical status is stable enough to provide for research.

Exclusion criteria

EXCLUSION CRITERIA:

An individual who meets any of the following criteria will be excluded from participation in this study:

  1. Use of naltrexone, disulfiram, benzodiazepines (except Oxazepam), antiepileptic compounds, antidepressants, neuroleptics, or acamprosate within a time sufficient for the medication to be eliminated from the body (five half-lives from last use).
  2. Pregnancy at admission (negative urine pregnancy test required).
  3. History of head trauma associated with an unconscious state lasting more than 30 minutes, persistent sequelae, and/or cranial surgery.
  4. History of epilepsy.
  5. History of non-substance related psychotic disorders.
  6. for acamprosate (previously exhibited to acamprosate calcium or any of its compounds; and/or severe renal impairment, manifested as (GFR) \<= 60 ml/min/1.73 m2).
  7. Positive screens for alcohol or any illicit drugs (except THC) after admission and alcohol detoxification via breathanalysis and urine drug screen.
Terms in these criteria, in plain language(4)

Underlined terms in the criteria open these too. Explained by clinicaltrials.gg, not part of the registry record. The study team decides who can take part.

Informed consent

Before you join, the study team explains what taking part involves — its purpose, what happens, the risks and possible benefits — and answers your questions, so you can decide freely. Consent is usually recorded on a form (the informed consent form, ICF) signed by you or, where the law allows, by someone legally authorised to decide for you.

You can keep asking questions during the study, you are told of new information that matters, and you can choose to leave at any time.

Contraindication

A reason a treatment, test or procedure should not be given to a particular person, such as an allergy, another illness or a medicine they take.

Hypersensitivity

An allergy, or another reaction of the immune system, to a substance. “Hypersensitivity to the study drug” means a known allergic reaction to it — not every side effect a medicine can have.

GFR and eGFR (kidney filtering)

GFR (glomerular filtration rate) is how much blood the kidneys filter each minute. It is usually estimated from a blood test — eGFR, by formulas such as CKD-EPI or MDRD — and some studies ask for it to be measured directly instead. Usually given in mL/min/1.73 m².

Check the method, the units and the minimum the study states. A value of 90 or above is in the normal-or-high range, but kidney damage can show in other tests too.

05

Study design

Phase
Phase 4
Primary purpose
Basic science
Allocation
Randomized
Intervention model
Parallel assignment
Masking
Triple (Participant, Investigator, Outcomes assessor)
Enrollment
48 participants (estimated)

Study arms

  • Active comparator
    Active

    This arm has participants receiving acamprosate for 21 day as inpatients.

    Drug: Acamprosate calcium

  • Placebo comparator
    Placebo

    This arm has participants receiving placebo for 21 day as inpatients.

    Other: Placebo

Interventions

  • Two oral capsules (packaged as one) containing 666 mg of acamprosate calcium will be given three times a day (total daily dose: 1998 mg/day) for a total of 21 days.

  • OtherPlacebo

    Two oral capsules (packaged as one) containing 666 mg of inactive substance (e.g., sugar) will be given three times a day (total daily dose: 1998 mg/day) for a total of 21 days.

06

What researchers measure

Primary outcomes

  1. Reduction of beta power

    Spectral power of EEG signals will be calculated in the beta frequency band (beta power). We expect a reduction of beta power to be greater in participants receiving acamprosate for 21 days than participants receiving placebo.

    Time frame: 21 day period as inpatients

Secondary outcomes

  1. Promotion of alpha power in active group compared to placebo group.

    Spectral power of EEG signals will be calculated in the alpha frequency band (alpha power). We expect a promotion of alpha power to be greater in participants receiving acamprosate for 21 days than participants receiving placebo.

    Time frame: 21 day period as inpatients

  2. No change in slow band (delta and theta) power in active group compared to placebo group.

    Spectral power of EEG signals will be calculated in the delta and theta frequency bands (slow band power). We do not expect a significant difference in change in slow band power between the active and placebo groups over the course of 21 days.

    Time frame: 21 day period as inpatients

  3. Reduction of theta event-related synchronization in active group compared to placebo group.

    Immediate brain activity, recorded via EEG, in response to task-related stimuli is termed as event-related potentials (ERPs). Spectral power of such ERPs in theta frequency band is called theta event-related synchronization (ERS).We expect a reduction of theta ERS to be greater in participants receiving acamprosate for 21 days than participants receiving placebo.

    Time frame: 21 day period as inpatients

  4. Amplification and hastening of P300 in active group compared to placebo group.

    Immediate brain activity, recorded via EEG, in response to task-related stimuli is termed as event-related potentials (ERPs). These ERPs have stereotypical peaks, e.g., P300. We expect amplification and hastening of P300 peaks in ERPs among participants receiving acamprosate for 21 days in comparison to participants receiving placebo.

    Time frame: 21 day period as inpatients

  5. Correlation of EEG markers of acamprosate treatment with clinical measures of anxiety and alcohol craving

    The above EEG measures that are found to be associated with acamprosate treatment will be tested for correlation with clinical measures of anxiety and alcohol craving.

    Time frame: 21 day period as inpatients

  6. Correlation of EEG markers of acamprosate treatment with polysomnography markers

    The above EEG measures that are found to be associated with acamprosate treatment will be tested for correlation with polysomnography markers such as total sleep time, slow wave sleep duration, sleep efficiency, and total wake duration after sleep onset.

    Time frame: 21 day period as inpatients

  7. Correlation of polysomnography markers of acamprosate treatment with clinical measures of anxiety and alcohol craving

    The above polysomnography measures that are found to be associated with acamprosate treatment will be tested for correlation with clinical measures of anxiety and alcohol craving.

    Time frame: 21 day period as inpatients

07

Study locations

1 of 1 sites recruiting
  • National Institutes of Health Clinical Center
    Bethesda, Maryland 20892, United States
    Recruiting
    • NIH Clinical Center Office of Patient Recruitment (OPR) · Contactccopr@nih.gov · 800-411-1222
08

References and documents

Publications

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  • Coutin-Churchman P, Moreno R, Anez Y, Vergara F. Clinical correlates of quantitative EEG alterations in alcoholic patients. Clin Neurophysiol. 2006 Apr;117(4):740-51. doi: 10.1016/j.clinph.2005.12.021. Epub 2006 Feb 21. PubMed 16495144 ↗
  • Nair Chaitanya M, Jayakkumar S, Chong E, Yeow CH. A wearable, EEG-based massage headband for anxiety alleviation. Annu Int Conf IEEE Eng Med Biol Soc. 2017 Jul;2017:3557-3560. doi: 10.1109/EMBC.2017.8037625. PubMed 29060666 ↗
  • Chen C, Yu X, Belkacem AN, Lu L, Li P, Zhang Z, Wang X, Tan W, Gao Q, Shin D, Wang C, Sha S, Zhao X, Ming D. EEG-Based Anxious States Classification Using Affective BCI-Based Closed Neurofeedback System. J Med Biol Eng. 2021;41(2):155-164. doi: 10.1007/s40846-020-00596-7. Epub 2021 Feb 5. PubMed 33564280 ↗
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  • Traub RD, Whittington MA, Colling SB, Buzsaki G, Jefferys JG. Analysis of gamma rhythms in the rat hippocampus in vitro and in vivo. J Physiol. 1996 Jun 1;493 ( Pt 2)(Pt 2):471-84. doi: 10.1113/jphysiol.1996.sp021397. PubMed 8782110 ↗
  • Whittington MA, Jefferys JG, Traub RD. Effects of intravenous anaesthetic agents on fast inhibitory oscillations in the rat hippocampus in vitro. Br J Pharmacol. 1996 Aug;118(8):1977-86. doi: 10.1111/j.1476-5381.1996.tb15633.x. PubMed 8864532 ↗
  • Porjesz B, Almasy L, Edenberg HJ, Wang K, Chorlian DB, Foroud T, Goate A, Rice JP, O'Connor SJ, Rohrbaugh J, Kuperman S, Bauer LO, Crowe RR, Schuckit MA, Hesselbrock V, Conneally PM, Tischfield JA, Li TK, Reich T, Begleiter H. Linkage disequilibrium between the beta frequency of the human EEG and a GABAA receptor gene locus. Proc Natl Acad Sci U S A. 2002 Mar 19;99(6):3729-33. doi: 10.1073/pnas.052716399. Epub 2002 Mar 12. PubMed 11891318 ↗
  • Faulkner HJ, Traub RD, Whittington MA. Disruption of synchronous gamma oscillations in the rat hippocampal slice: a common mechanism of anaesthetic drug action. Br J Pharmacol. 1998 Oct;125(3):483-92. doi: 10.1038/sj.bjp.0702113. PubMed 9806331 ↗
  • Saletu-Zyhlarz GM, Arnold O, Anderer P, Oberndorfer S, Walter H, Lesch OM, Boning J, Saletu B. Differences in brain function between relapsing and abstaining alcohol-dependent patients, evaluated by EEG mapping. Alcohol Alcohol. 2004 May-Jun;39(3):233-40. doi: 10.1093/alcalc/agh041. PubMed 15082461 ↗
  • Klimesch W. EEG alpha and theta oscillations reflect cognitive and memory performance: a review and analysis. Brain Res Brain Res Rev. 1999 Apr;29(2-3):169-95. doi: 10.1016/s0165-0173(98)00056-3. PubMed 10209231 ↗
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  • Hada M, Porjesz B, Begleiter H, Polich J. Auditory P3a assessment of male alcoholics. Biol Psychiatry. 2000 Aug 15;48(4):276-86. doi: 10.1016/s0006-3223(00)00236-5. PubMed 10960158 ↗
  • Maurage P, Campanella S, Philippot P, de Timary P, Constant E, Gauthier S, Micciche ML, Kornreich C, Hanak C, Noel X, Verbanck P. Alcoholism leads to early perceptive alterations, independently of comorbid depressed state: an ERP study. Neurophysiol Clin. 2008 Apr;38(2):83-97. doi: 10.1016/j.neucli.2008.02.001. Epub 2008 Mar 3. PubMed 18423329 ↗
  • Gilmore CS, Fein G. Theta event-related synchronization is a biomarker for a morbid effect of alcoholism on the brain that may partially resolve with extended abstinence. Brain Behav. 2012 Nov;2(6):796-805. doi: 10.1002/brb3.95. Epub 2012 Oct 5. PubMed 23170242 ↗
  • Boeijinga PH, Parot P, Soufflet L, Landron F, Danel T, Gendre I, Muzet M, Demazieres A, Luthringer R. Pharmacodynamic effects of acamprosate on markers of cerebral function in alcohol-dependent subjects administered as pretreatment and during alcohol abstinence. Neuropsychobiology. 2004;50(1):71-7. doi: 10.1159/000077944. PubMed 15179024 ↗
  • Bauer LO, Hesselbrock VM. Brain maturation and subtypes of conduct disorder: interactive effects on p300 amplitude and topography in male adolescents. J Am Acad Child Adolesc Psychiatry. 2003 Jan;42(1):106-15. doi: 10.1097/00004583-200301000-00017. PubMed 12500083 ↗
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  • Pietrzak B, Czarnecka E. Effect of the combined administration of ethanol and acamprosate on rabbit EEG. Pharmacol Rep. 2005 Jan-Feb;57(1):61-9. PubMed 15849378 ↗
  • Staner L, Boeijinga P, Danel T, Gendre I, Muzet M, Landron F, Luthringer R. Effects of acamprosate on sleep during alcohol withdrawal: A double-blind placebo-controlled polysomnographic study in alcohol-dependent subjects. Alcohol Clin Exp Res. 2006 Sep;30(9):1492-9. doi: 10.1111/j.1530-0277.2006.00180.x. PubMed 16930211 ↗

Individual participant data

Plan to share: Undecided — Study participant research data will include but not be limited to cognitive responses, EEG and PSG recordings, and cardiac and ocular activities (electronic data); and clinical and study assessments, and behavioral interviews (paper data). Individual participants and their research data will be identified by a unique study identification number. The key to link participants with their research data will be limited to the participating investigators, including the PI, lead associate investigator, and CNIRC research coordinators. Access to study data will be restricted to authorized personnel. De-identified data may be shared with collaborating researchers for data analysis.

09

Timeline

1 registry update since Sep 25, 2026
ElapsedEstimatedEstimated, not yet reachedSimilar studies: half by the dot; the band is the middle halfHalf of similar studies reached it by the dot; the band is the middle half, from a quarter to three quarters

Started May 2025 (actual). Primary completion is estimated for Dec 2026, 19 months after the start.

Of 24 phase 4 interventional studies under Alcoholism, half reached primary completion within 58 months of starting (the median), counting those still running; a quarter within 49 and three quarters within 83. This study's planned 19 months is below that.

How these figures are worked out, and which studies are left out of them.

Registered
Feb 17, 2024
First posted
Feb 21, 2024
StartActual
May 7, 2025
Primary completionEst.
Dec 31, 2026
CompletionEst.
Dec 31, 2026
Last update
Nov 2, 2026
What these dates mean
Start.
When the first participant enrolled; while estimated, when the study expects to open to recruitment.
Primary completion.
When the last participant was examined or treated to collect data for the study's main question, its primary outcome. A study that stopped early gives the date its data collection stopped.
Completion.
When the last participant's last visit took place, for every outcome, secondary ones and side effects included: the end of the study. Often later than primary completion, sometimes the same day.
Actual and Est.
Actual means the registry says the date has happened. Est. (estimated) is a date the sponsor plans or expects. It can still move, and the sponsor is expected to change it to actual once it has passed.
Minor edits
Nothing that changes what the study is or who can join. Edited: verification date
1 update, last Nov 2, 2026
Show all 1 update
  1. Nov 2, 2026
    Minor edits only
    + 1 other change: verification date

From the registry record's own update history. This site started tracking changes on Sep 25, 2026; for anything earlier, see the record history on ClinicalTrials.gov ↗

10

Registry details

Key details

Study ID
NCT06269627
Responsible party
Sponsor
First posted
Feb 21, 2024
Start date
May 7, 2025
Primary completion
Dec 31, 2026 (estimated)
Completion
Dec 31, 2026 (estimated)
Last update
Nov 2, 2026

Study contacts

Beth A Lee, R.N.
Contact
beth.lee@nih.gov
(301) 451-6964
Nancy Diazgranados, M.D.
Contact
nancy.diazgranados@nih.gov
(301) 496-7515
Nancy Diazgranados, M.D.
principal investigator · National Institute on Alcohol Abuse and Alcoholism (NIAAA)

Oversight

FDA-regulated drug
Yes
FDA-regulated device
No
View the source record on ClinicalTrials.gov ↗

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