Centrophenoxine (Meclofenoxate).
DMAE that works. Choline donor with anti-aging angle. Centrophenoxine is a synthetic ester that carries dimethylaminoethanol in and releases it, feeding the tissue choline pool your brain draws on for acetylcholine and membrane phospholipid.
Reviewed March 2026
- Category
- Nootropic
- Also filed under
- CholineCognitionAnti aging
What Centrophenoxine (Meclofenoxate) is, and what it does.
- Does it work
- This suits people already exploring choline-pool nootropics and older adults thinking about recall. The human record is small, so it sits in the early corner rather than the settled one.
- How much to take
- Start with 250 to 750mg a day, often split between morning and midday since it can feel activating late on. The 1,000mg in studies is a research condition.
- Time to feel it
- Reports describe changes across two to six weeks of daily use rather than the same day. The human record is small: four records at Europe PMC.
- The first dose
- Day one is usually uneventful, though some people report a mild lift and some a headache. A change in the choline pool is not something you register within a day.
- With regular use
- Reports of clearer recall cluster around two to six weeks of daily use. With four records at Europe PMC, that timeline rests on user accounts more than on measured trials.
- How well tolerated
- Headache is the commonly reported effect and often eases at a lower amount. Not for pregnancy or nursing. On prescribed medicines, especially cholinergic ones, ask your clinician.
- How it feels
- People describe mild clarity and a slightly brighter head rather than stimulation. For others it registers only as fewer foggy stretches through the afternoon.
- The overlooked benefit
- The ester bond is the whole delivery idea, and it is moisture-sensitive, so a dry sealed bottle keeps the molecule together instead of splitting back into halves.
250 to 750mg a day is where Centrophenoxine (Meclofenoxate) works.
Source: Mech Ageing Dev. 1977;6(6):445-457. Centrophenoxine anti-aging research.
The proof, claim by claim.
These words describe the research, not the molecule's worth. Research strength is how much work stands behind one claim, and it is never a product score.
Based on 20 human trials with 55% consistency.
- Supply of substrate to the tissue choline poolNarrative review
- Acetylcholine and phosphatidylcholine synthesis substrateNarrative review
- Memory and recall in older adultsRandomised trial
- Lipofuscin accumulation in aged tissueAnimal study
- Ester hydrolysis to dimethylaminoethanol after absorptionNarrative review
Questions people ask about Centrophenoxine (Meclofenoxate).
- When should I take it?
- Timing matters less than consistency. Pick a time that works for you and take it daily.
- Can I take it with other supplements?
- Usually fine. The main thing to watch is not doubling up on the same ingredient from different products. If you're on prescription meds, check with your pharmacist first.
- Any side effects to watch for?
- Most people tolerate it well at recommended doses. GI upset is the most common complaint with any supplement. Start with a lower dose and work up. If something feels off, stop and reassess.
- Who benefits most from this?
- Honestly, most people would benefit more from the basics. But if you've got a specific reason to try it, the risk is generally low.
Why these belong in the same formula. Each row says what the basis is, from settled biochemistry through to a trial that measured the pair.
Centrophenoxine is an ester that releases DMAE after hydrolysis, so the two deliver the same amine and their effects are additive rather than complementary. Running both at full dose doubles one input instead of covering two.
Alpha-GPC supplies free choline that crosses into the brain, while centrophenoxine works through a DMAE route into the same phospholipid and acetylcholine pool.
Acetylcholine synthesis is limited by choline availability, and the DMAE released by centrophenoxine feeds a related but narrower part of that pool. Added dietary choline covers the shortfall.
Phosphatidylcholine is both a choline reservoir and a membrane component, matching the membrane register centrophenoxine is used for.
Pantothenic acid becomes coenzyme A, which carries the acetyl group that choline acetyltransferase attaches to choline. Choline without acetyl-CoA leaves the second half of the reaction short.
ALCAR donates acetyl groups into the mitochondrial acetyl-CoA pool that supplies acetylcholine synthesis, so it works on the acetyl side while centrophenoxine works on the amine side.
Huperzine A slows acetylcholinesterase breakdown while centrophenoxine feeds the synthesis side, so the two raise synaptic acetylcholine additively. That additivity is why huperzine is usually cycled in such a stack.
Racetams raise cholinergic demand at the synapse without supplying choline, and centrophenoxine is one of the donors paired with them for that reason.
Noopept acts on cholinergic and BDNF signalling without adding substrate, so a choline-side donor is the conventional partner.
Centrophenoxine is hydrolysed to dimethylaminoethanol, which feeds the ethanolamine and choline pool, while citicoline delivers cytidine plus choline directly into the CDP-choline pathway. The two therefore arrive at the same membrane phospholipid synthesis route from different points. No combination study supports an added effect.
Converting an ethanolamine-type head group to a choline head group is a three-step methylation that consumes S-adenosylmethionine at each step. Anything that raises the ethanolamine load therefore draws on methyl donors. This is established one-carbon biochemistry rather than a measured pair.
Betaine regenerates methionine from homocysteine and so helps keep S-adenosylmethionine available for the methylation steps that build phosphatidylcholine. The relationship is upstream pathway support, not a direct interaction with centrophenoxine. Reported as plasma markers where it is measured at all.
The folate cycle supplies methyl groups for methionine regeneration, which in turn supports the SAM-dependent methylation of ethanolamine head groups. It is a supporting pathway rather than a partner acting on the same target. No combination evidence exists.
Methionine synthase needs methylcobalamin to complete the folate-dependent remethylation step, so B12 status gates the same methyl pool. The link to centrophenoxine runs entirely through that shared pathway. Pathway logic, not a trial.
A phosphatidylcholine molecule needs a choline head group and two fatty acyl chains, and DHA is the long-chain fatty acid most enriched in neuronal membrane phospholipids. Supplying head group precursors without acyl chain substrate addresses only half the molecule. Mechanistic pairing with no combination data.
The rodent literature on centrophenoxine centres on oxidative-stress and lipofuscin markers in ageing brain tissue, and lipofuscin forms from oxidised lipid and protein. Alpha-tocopherol is the membrane-resident antioxidant that limits lipid peroxidation. The overlap is on markers in animals, not human outcomes.
Lipoic acid participates in the recycling network that regenerates other antioxidants, so it sits on the same oxidative-marker axis the animal centrophenoxine work reports. Nothing links the two directly. Marker-level and preclinical.
Ubiquinol is a lipid-phase antioxidant and an electron carrier, both relevant to the lipid peroxidation markers reported in ageing rodent brain tissue. There is no study of the two together. This is a mechanistic neighbourhood, not a measured synergy.
Ginkgo and centrophenoxine appear together in older nootropic stacks built around cerebral blood flow and membrane hypotheses. Neither the pairing nor the rationale has been tested in the candidate literature. It is included so the combination is documented rather than endorsed.
Bacopa is used for its own cholinergic and antioxidant rationale, which overlaps with the mechanisms attributed to centrophenoxine. No study examines them together. Documented as a common pairing at its true confidence.
Theanine acts on glutamatergic and GABAergic signalling rather than on the choline pool, so it modifies the subjective texture of a cholinergic stack rather than adding to it. The pairing is common in consumer formulas. No combination data.
Caffeine antagonises adenosine receptors, an entirely different target from the choline pool, so any combined effect on alertness is additive rather than mechanistic. Cholinergic and adenosinergic stimulation together can also add to jitteriness and raise heart rate. Worth flagging as an additive stack rather than a designed pair.
Talk to a doctor before taking Centrophenoxine (Meclofenoxate) if any of these apply to you: bipolar, seizure. These are flags to check first, not effects Centrophenoxine (Meclofenoxate) is known to cause.
Not medical advice. Show the label to your pharmacist.What Centrophenoxine (Meclofenoxate) actually does.
Centrophenoxine, also named meclofenoxate, is an ester formed from 4-chlorophenoxyacetic acid and dimethylaminoethanol. Its behaviour in the body follows from that structure: it is a delivery vehicle for the amine half.
Non-specific esterases hydrolyse the ester bond after absorption, releasing dimethylaminoethanol and 4-chlorophenoxyacetate, so the two halves then follow separate routes.
Dimethylaminoethanol is an ethanolamine bearing two methyl groups on the nitrogen, one methylation short of choline, and it enters the tissue ethanolamine and choline pool rather than acting as a receptor ligand.
Choline drawn from that pool is the substrate both for acetylcholine synthesis by choline acetyltransferase and for phosphatidylcholine synthesis through the CDP-choline pathway, which is the biochemical basis for describing this molecule as a choline-pool agent.
Where Centrophenoxine (Meclofenoxate) comes from.
There is no plant or animal source. Two industrial chemicals are joined into one molecule, then turned into a salt and recrystallised so it can be weighed and capsuled. Because the join is an ester, moisture slowly pulls it back apart into its two halves.
Chemically synthesised. The molecule is identical to the one a plant or an animal makes, and building it deliberately means a known purity, a fixed dose and no crop contaminants. For several nutrients this is the only route that reaches a usable amount.
Both are bulk industrial chemicals; the amine half, dimethylaminoethanol, is itself a commercial ingredient known as DMAE.
4-chlorophenol is alkylated with a chloroacetic acid derivative to give the phenoxyacetic acid, a well-known plant growth regulator chemistry.
The acid is activated and esterified with dimethylaminoethanol, forming the amino ester that is the molecule itself.
Treatment with hydrogen chloride gives the hydrochloride, which is recrystallised from an alcohol or alcohol and ether mixture to remove unreacted acid and amine.
Lots are specified on assay by titration or chromatography, water content, residual 4-chlorophenoxyacetic acid and free dimethylaminoethanol, and residual solvent.
The dry salt is blended with a flow aid and filled, with moisture protection because the ester hydrolyses in damp conditions.
Supply rarely discloses the assay method, water content, or residual free dimethylaminoethanol and 4-chlorophenoxyacetic acid, which are the specification points that matter for an ester salt.
Getting Centrophenoxine (Meclofenoxate) from food.
The whole-food sources on file. A supplement closes the gap, it does not replace dinner.
A gram-for-gram figure (how much of each you would eat to match a dose) will appear here once it is sourced and reviewed. This page will not print a number it cannot cite.
The forms it comes in.
The essence, in one line each.
- Reports region-specific changes in antioxidant enzyme and lipid peroxidation markers in the brains of ageing rats given centrophenoxine; the authors frame these as modulatory marker effects.Animal study. Bhalla et al., 2005 (Experimental Gerontology). PMID 16137852 ↗
These are the studies our verdict leans on, chosen from the 1 we read for Centrophenoxine (Meclofenoxate). The full linked list is below.
FDA Disclaimer: These statements have not been evaluated by the Food and Drug Administration. This information is for educational purposes only and is not intended to diagnose, treat, cure, or prevent any disease. Consult your healthcare provider before starting any supplement regimen.