Evidence-based·Last reviewed May 31, 2026·How we grade evidence

Centrophenoxine

PhytochemicalCholinergic

Centrophenoxine (meclofenoxate) is a 1950s-era prescription drug in some European countries for age-related cognitive decline. The human evidence is mostly small RCTs from the 1970s–90s in dementia and stroke recovery, with modest effect sizes that haven't been replicated in modern trials. Not FDA-approved in the US. Marketed as a 'nootropic' for healthy adults, but no controlled trials support that use.

Research compound — not an approved drug or dietary supplement

This compound is sold for research and is not FDA-approved for human use or as a dietary supplement. Human evidence is limited; purity and dosing of consumer products are unverified. The data below is an evidence review for education only — talk to a clinician before considering it.

Quick decision guide

May help most

Older adults with mild-to-moderate cognitive impairment whose clinician (in a country where it's prescribed) considers it as an adjunct — not a primary therapy for dementia.

Common dosing range

1,000–2,000 mg per day in 2–3 divided doses; older clinical trials typically used 2 g/day.

When to expect effects

8 weeks in the clinical trials; effects on healthy adults are not established.

Watch out for

Old, limited evidence base; long-term safety not characterized; many products are unregulated 'research chemicals' with unverified purity.

Evidence snapshot

Age-related cognitive decline (mild–moderate)Emerging (older trials)
Stroke / vascular cognitive recoveryEmerging (older trials)
Lipofuscin reduction (anti-aging)Low (animal only)
Cognitive enhancement in healthy adultsLow (no RCTs)

What is it

Centrophenoxine (meclofenoxate) is a synthetic compound consisting of DMAE (dimethylaminoethanol) bound to a chlorinated phenoxyacetic acid carrier. Developed in France in the 1950s, it has been used as a prescription medication for cognitive impairment and age-related cognitive decline in several European countries.

Is it worth it for you?

Use this as a quick fit check, not a diagnosis.

Worth considering if

You're an older adult with documented mild-to-moderate cognitive impairment AND it's prescribed by a clinician in a country where it's a registered medicine
Your clinician suggests it as an adjunct alongside (not replacing) modern dementia therapy
You can source a verified pharmaceutical-grade product (Lucidril, Cerutil) rather than an unregulated 'research chemical'
You accept that the evidence is old, modest, and limited to specific patient populations

Probably skip if

You're a healthy adult looking for a 'smart drug' — there are no controlled trials in healthy adults
You're being sold consumer 'nootropic' products of unknown purity and dose accuracy
You expect dramatic or transformative cognitive effects — even the positive trials showed only modest improvements on psychometric tests
You're already on a cholinesterase inhibitor (donepezil, rivastigmine, galantamine) — discuss with neurologist; not a replacement for proven AD therapy
You're using it during pregnancy or breastfeeding — no human safety data
You're prone to anxiety, insomnia, or hyperactivity — these side effects are common, especially at higher doses

Evidence at a glance

Age-related cognitive decline (mild-to-moderate)

Limited Evidence
Effect
Modest improvement on memory/attention psychometric tests at 2 g/day for 4–8 weeks; no validated functional or biomarker endpoint
Best fit
Older adults with mild-to-moderate cognitive impairment under clinician supervision
Time
8 weeks in trials

Stroke / vascular cognitive recovery

Limited Evidence
Effect
Modest cognitive improvement in a combination trial; effect not separable from CDP-choline component
Best fit
Post-stroke patients under specialist supervision who want to explore adjuncts
Time
Months

Lipofuscin reduction / anti-aging

Mixed Evidence
Effect
Reduction in neuronal lipofuscin in aged animal studies; no validated human translation
Best fit
Researchers interested in aging biology — not a consumer recommendation
Time
Not established in humans

Cognitive enhancement in healthy adults

Mixed Evidence
Effect
No reliable effect demonstrated in healthy adults
Best fit
Not applicable — no evidence supports use in healthy adults
Time
Not established

Evidence for 4 uses

AI-assisted evidence assessment — talk to your doctor before relying on any single supplement.

Age-related cognitive decline (mild-to-moderate)

Supplement benefit
Limited Evidence

Older European RCTs in elderly patients with mild-to-moderate cognitive impairment or early dementia have shown modest improvements on psychometric tests of memory and attention vs placebo at 1,5002,000 mg/day for 48 weeks (Marcer 1977, Pek 1989). Effect sizes were small and the trials are dated by modern standards (small samples, limited blinding rigor, no biomarker endpoints, pre-current diagnostic criteria for AD). No modern large RCT has confirmed clinically meaningful benefit on validated dementia outcomes. Not a substitute for cholinesterase inhibitors or other proven AD therapies.

Effect size
Modest improvement on memory/attention psychometric tests at 2 g/day for 4–8 weeks; no validated functional or biomarker endpoint
Time to effect
8 weeks in trials
Best fit
Older adults with mild-to-moderate cognitive impairment under clinician supervision
Less likely
Severe/advanced dementia (trials show no benefit); healthy adults; people with anxiety or insomnia (side effects)

Bottom line: Old evidence with small effects in a narrow population. Don't expect modern-AD-level rigor.

Evidence is mixed

Positive trials are old (1970s–1990s), small (n=50), conducted in European clinical practice with pre-modern diagnostic criteria. No modern replication exists. Cochrane-style systematic reviews of meclofenoxate for dementia are absent or note insufficient evidence.

Stroke / vascular cognitive recovery

Supplement benefit
Limited Evidence

A 1996 multi-centre European RCT (Fischhof) combined CDP-choline + meclofenoxate vs placebo in patients with cerebrovascular insufficiency and mild cognitive decline, with modest cognitive improvement vs placebo. The CDP-choline component now has its own (modest, mixed) stroke evidence base independent of meclofenoxate. Hard to attribute benefit to centrophenoxine specifically. Modern post-stroke rehabilitation evidence focuses on antiplatelet therapy, BP control, and structured rehab.

Effect size
Modest cognitive improvement in a combination trial; effect not separable from CDP-choline component
Time to effect
Months
Best fit
Post-stroke patients under specialist supervision who want to explore adjuncts
Less likely
Anyone hoping for a substitute for established post-stroke rehab and secondary-prevention therapy

Bottom line: Not a stroke treatment. Standard post-stroke care is the priority.

Lipofuscin reduction / anti-aging

Mechanism only
Mixed Evidence

In aged guinea pigs and rats, centrophenoxine reduced neuronal lipofuscin (the brown pigment that accumulates with age) over weeks of treatment. The proposed mechanism is enhanced membrane lipid turnover and antioxidant action of the DMAE moiety. There's no human evidence that lipofuscin reduction translates to clinically meaningful anti-aging effects; lipofuscin itself isn't a validated target for any age-related disease.

Effect size
Reduction in neuronal lipofuscin in aged animal studies; no validated human translation
Time to effect
Not established in humans
Best fit
Researchers interested in aging biology — not a consumer recommendation
Less likely
Anyone hoping to reverse aging or 'detoxify the brain' through supplementation

Bottom line: Animal mechanism, not a human anti-aging claim.

Cognitive enhancement in healthy adults

Mechanism only
Mixed Evidence

There are essentially no controlled trials of centrophenoxine in healthy adults for cognitive enhancement. The compound is widely sold and discussed in 'nootropic' communities based on its mechanism (cholinergic precursor, membrane fluidization) and on subjective user reports. Side effects (headache, insomnia, irritability, muscle tension) are common at the doses people self-administer. The risk-benefit balance for healthy users isn't supported by evidence.

Effect size
No reliable effect demonstrated in healthy adults
Time to effect
Not established
Best fit
Not applicable — no evidence supports use in healthy adults
Less likely
Anyone hoping for clinical-trial-grade cognitive enhancement

Bottom line: Skip it for general 'smart drug' use; the evidence isn't there and side effects are common.

How it works

Centrophenoxine functions as a carrier delivering DMAE to the brain more effectively than oral DMAE alone. DMAE is a precursor or analog of choline involved in acetylcholine synthesis. Centrophenoxine has been shown in animal studies to reduce accumulation of lipofuscin (the 'age pigment') in neurons, increase brain glucose and oxygen uptake, and have antioxidant effects. In human clinical studies, primarily from Europe, centrophenoxine has been used in elderly patients with cognitive impairment, including Alzheimer's disease and stroke recovery, with reports of modest cognitive improvements. Western clinical evidence by modern standards is limited.

How to take it

1. Typical dose
• Clinical-trial dose: 1,000–2,000 mg per day in 2–3 divided doses • Common supplement label: 250–500 mg per capsule, 2–4 capsules per day • Start low (250 mg morning) and titrate over a week to assess tolerance • Avoid evening doses (insomnia is the most common side effect)
2. Higher studied dose
Up to 2,000 mg/day is the trial maximum. Higher doses don't have clinical support and side effects (headache, insomnia, hyperactivity, muscle tension) scale up.
3. Timing
Take with breakfast and lunch — never after early afternoon, because the stimulant-like effect commonly disrupts sleep. Some users tolerate a third dose mid-afternoon (≤2 pm).
4. With food
With food — reduces GI upset and headache.
5. Split dosing
Split into 2–3 daily doses to keep blood levels steadier and to avoid an evening dose. A 1500 mg/d regimen might be 500 mg with breakfast, 500 mg at noon, 500 mg at 2 pm.
6. How long to try
Trials run 4–8 weeks. If you're going to evaluate effect, give it at least 4–8 weeks at full dose. Don't continue indefinitely without clear benefit and clinician oversight — long-term safety data is essentially absent.

What to track

Sleep quality — insomnia is the most common reason people stop
Mood — irritability and rare paradoxical depression with prolonged use
Muscle tension, jaw clenching
Cognitive symptoms — keep a brief journal so you can compare before/after honestly

Bottom line: If you're going to try it, start at 250 mg in the morning, build up to 1–2 g/d split before 2 pm, and stop at 8 weeks if no clear benefit. Don't take it after early afternoon.

4 commercial forms

Compare the main delivery options and what they’re best suited for.

Meclofenoxate HCl (pharmaceutical, e.g. Lucidril, Cerutil)

Regulated medicine (Europe)

Tablet form sold as a prescription drug in some European countries (formerly more widely available; now restricted). The most verifiable purity and dose.

Standard pharmaceutical absorption.

Centrophenoxine capsules (US supplement market)

Unregulated import

Sold in the US as a research chemical or unregulated nootropic. Purity, dose accuracy, and contaminants vary widely between brands. No FDA approval as a drug or supplement.

Assumed similar to pharmaceutical form when pure; quality control is the wildcard.

Centrophenoxine bulk powder

Highest risk

Loose powder marketed for 'research only' to enthusiasts. No quality control, no dosing accuracy, no contamination assurance. Highest risk and not advisable.

Dose accuracy depends entirely on user-supplied scales and the powder's purity.

DMAE (related compound, supplement)

Lower-potency precursor

DMAE alone is sold as a supplement in the US. Crosses the blood-brain barrier less efficiently than centrophenoxine (which uses the chlorinated phenoxyacetic acid as a carrier). MSKCC monograph notes inconsistent cognitive effects.

Less efficient brain delivery than the carrier-bound centrophenoxine.

Safety

Know the common side effects, key cautions, and who should avoid it.

Common side effects

headacheinsomniairritability / hyperactivitymuscle tension / jaw clenchingnauseastomach upset

Serious risks

Who should avoid it

Pregnancy & breastfeeding

Avoid in pregnancy and breastfeeding. There's no human safety data; the parent compound DMAE has shown teratogenic effects in animal studies and is contraindicated in pregnancy. The compound is not worth the unknowns when pregnant.

Bottom line: An unregulated import in the US with limited long-term safety data. If you proceed, source from a country where it's a registered medicine and use it under medical supervision.

Interactions

cholinesterase inhibitors (donepezil, rivastigmine, galantamine)Moderate

Both increase cholinergic tone; potential additive cholinergic side effects (nausea, salivation, bradycardia). Discuss with neurologist before stacking.

stimulants (caffeine, modafinil, ADHD medications)Moderate

Additive stimulant-like effects (insomnia, jitteriness, anxiety). Avoid evening combination.

antiepileptic medicationsModerate

Cholinergic effects may lower seizure threshold; centrophenoxine should generally be avoided in people on antiepileptics for seizure disorders.

anticholinergic medicationsMinor

Centrophenoxine's pro-cholinergic effect may oppose anticholinergic drugs' intended action.

antidepressants (SSRIs, SNRIs)Minor

Theoretical risk of additive activation or mood destabilization. Monitor mood when combining.

Choosing a product

What to look for on the label — and what to be skeptical of.

Look for

Pharmacy product from a country where centrophenoxine is a registered medicine (Lucidril, Cerutil) — these have at least had national regulatory review
Mg of meclofenoxate (the active) clearly listed per capsule
Third-party Certificate of Analysis (purity, identity, contaminant testing) if buying as a US 'research chemical'
Sealed pharmaceutical packaging with batch and expiration date
Manufacturer disclosed (avoid relabeled bulk powder of unknown origin)

Be skeptical of

'Anti-aging breakthrough' or 'reverse brain aging' marketing — the lipofuscin signal is animal-only
'FDA-approved nootropic' — false; centrophenoxine is not FDA-approved
'Better than racetams' / direct comparisons to other unapproved nootropics — no head-to-head trials
'Boosts IQ in healthy adults' — no controlled trial supports this
'Safe for daily long-term use' — long-term human safety data is essentially absent
Powder products of unknown origin without certificate of analysis — the supplement-grade market for this compound is poorly regulated

Frequently asked questions

How is centrophenoxine different from DMAE?

Centrophenoxine includes a carrier (chlorophenoxy acid) that helps DMAE cross the blood-brain barrier more efficiently. Oral DMAE alone has lower brain bioavailability.

Is centrophenoxine legal?

It is a prescription medication in several European countries. In the US, it is sold as a supplement but is not widely recognized as a legal dietary supplement ingredient.

Does centrophenoxine really reverse aging?

Animal studies show lipofuscin reduction, but human evidence for meaningful anti-aging effects is not established. Most claims rely on extrapolation from animal data.

Does centrophenoxine cause headaches?

Headaches are sometimes reported, possibly related to changes in cholinergic activity. Starting at lower doses may reduce this risk.

How long does it take to see effects?

Cognitive effects typically develop over days to weeks of regular use, not immediately.

References by claim

Age-related cognitive decline (mild-to-moderate)

Marcer & Hopkins, 1977PubMed — Age and Ageing (1977) link

Pek et al., 1989PubMed — Archives of Gerontology and Geriatrics (1989) link

Stroke / vascular cognitive recovery

Fischhof et al., 1996PubMed — European Neuropsychopharmacology (1996) link

Cognitive enhancement in healthy adults

Memorial Sloan Kettering — About Herbs (DMAE)Dimethylaminoethanol monograph (2024) link

Lipofuscin reduction / anti-aging

Nandy, 1978PubMed — Mechanisms of Ageing and Development (1978) link

Safety

Centrophenoxine on NIH DSLDNIH Dietary Supplement Label Database link

Other references

Meclofenoxate (PubChem CID 4039)PubChem link

Meclofenoxate (ChEBI:6712)ChEBI link

Centrophenoxine on WikidataWikidata link

Track Centrophenoxine with Pilora

Set up dose reminders, check interactions, and join the community in the Pilora iPhone app.

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Evidence-based·Last reviewed May 31, 2026·Evidence current as of May 31, 2026·How we grade evidence

Disclaimer: This compound is not approved by the FDA for human use and is not a dietary supplement. This page is an educational review of available research — much of it preclinical or early-stage — not a recommendation to use it. Consumer product quality is unregulated. Consult a qualified clinician.