Centrophenoxine HCl, ≥98%

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Procholinergic with nootropic properties. Mild cerebral activator.

Chemical Name2-dimethylaminoethyl (4-chlorophenoxy)acetate hydrochloride
SynonymsMeclofenoxate hydrochloride, Cerutil, Lucidril
CAS #3685-84-5
FormWhite powder
Molecular FormulaC12H16ClNO3•HCl
Molecular Weight294.18 g/mol
SolubilitySoluble in water. Sparingly soluble in cold isopropyl alcohol, acetone. Practically insoluble in benzene, ether, chloroform.

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Precaution and Disclaimer:

This Material is Sold For Research Use Only. Terms of Sale Apply. Not for Human Consumption, nor Medical, Veterinary, or Household Uses.

Chemical Information:

CAS Number:3685-84-5
Molecular Weight:294.18 g/mol
Melting Point:135-139°C
Molecular Formula:C12H16ClNO3•HCl
Synonyms:Meclofenoxate hydrochloride, Cerutil, Lucidril, Centrophenoxine hydrochloride, Centrophenoxine, Helfergin, Marucotol, Acefen, Atsefen, Brenal, Centrofenoxin, Amipolen, Cellative, Proserout, 3685-84-5, Meclophenoxate hydrochloride, Methoxynal, Lutiaron, Lucidryl hydrochloride, Dimethylaminoethyl p-chlorophenoxyacetate hydrochloride, NSC 4268, EINECS 222-975-3, Dimethylaminoethyl 4-chlorophenoxyacetate hydrochloride, 2-(dimethylamino)ethyl (4-chlorophenoxy)acetate hydrochloride, 2-(Dimethylamino)ethyl (p-chlorophenoxy)acetate hydrochloride, (p-Chlorophenoxy)acetic acid 2-(dimethylamino)ethyl ester hydrochloride, 4-chlorophenoxy-acetic acid 2-(dimethylamino)ethyl ester hydrochloride, Dimethylaminoethyl ester of p-chlorophenoxyacetic acid hydrochloride, CAS-3685-84-5, Methocynal, Centrophenoxine HCl, 2-dimethylaminoethyl (4-chlorophenoxy)acetate hydrochloride
PubChem CID:19379


Technical Information:

Application:Meclofenoxate (Lucidril, centrophenoxine) is a procholinergic clinically shown to aid memory, increase cellular membrane phospholipids, and improve general cognition in the elderly. It is used in neuroscience research into the cholinergic signaling system.
Appearance:White or off-white powder
Physical State:Solid
Solubility:Soluble in water. Sparingly soluble in cold isopropyl alcohol, acetone. Practically insoluble in benzene, ether, chloroform.
Storage:Store at room temperature or cooler, in a sealed airtight container, protected from heat, light and humidity.
Stability:Stable for at least two years when stored as above.



Centrophenoxine (Meclofenoxate, Lucidril) is a cholinergic research compound that has been marketed as a pharmaceutical and is used in the treatment of cognitive symptoms of dementia and Alzheimer’s disease. [1] Centrophenoxine is a derivative of dimethylethanolamine (DMAE) and is an ester of DMAE and 4-chlorophenoxyacetic acid (pCPA).

DMAE is a choline-like molecule with the ability to reduce buildup of the ‘age pigment’ and increase acetylcholine levels. DMAE occurs naturally in many food sources. The binding of DMAE to pCPA enhances its absorption and creates a much more effective cognition-enhancing compound. [2]

In elderly patients, studies on Centrophenoxine (meclofenoxate) have shown clinically significant improvements in memory and cognition, along with a mental stimulation effect.[3] In many European countries and some countries in Asia, Centrophenoxine is sold as a prescription drug. In other parts of the world, it is available either as a dietary supplement or a research chemical. Centrophenoxine was reported developed in 1959 at the French National Scientific Research Center. [4]



Apart from a 2008 Chinese study comparing the pharmacokinetics and bioequivalence of Centrophenoxine capsules and a references formulation of the drug, there is very limited data on the pharmacokinetics of this compound. As a prodrug, Centrophenoxine is hydrolyzed into 4-chlorophenoxyacetic acid and DMAE and is not detected in plasma. [5]

With regards to DMAE – once absorbed, it is rapidly transported to the liver where a large portion of it is metabolized. In mice receiving 300 mg/kg bodyweight DMAE, around 25.2 µg/g plasma was detected. Furthermore, in rats, DMAE is rapidly oxidized to the N-oxide of DMAE – the primary metabolite. Only around 13.5% of the administered dose was eliminated by the 24-hour mark, indicating that most of the DMAE was routed towards phospholipid biosynthetic pathways. [6]


Modes of action:

Centrophenoxine has been labeled a “brain metabolic stimulant” and a “neuro-energizer”. Research into its mechanisms of action has pointed to its ability to stimulate glucose uptake, oxygen consumption, and carbon dioxide production in vivo and also in vitro in brain slices. [7] The chemical’s ability to increase the resistance of cerebral cells to various forms of oxygen deprivation has prompted researchers to suggest that it operates through the enhancement of alternative pathways of glucose metabolism. [8]

Centrophenoxine exerts similar effects to those produced by DMAE since it is really just a DMAE prodrug. In the liver, DMAE may serve as a precursor to choline. However, it is not yet clear to what extent DMAE is methylated and substituted into acetylcholine. In terms of its effects on cognition, this is definitely the most important aspect of Centrophenoxine and DMAE’s mechanisms of action. 

It is assumed that DMAE, once it has crossed the blood barrier, is methylated to form choline and is then incorporated into acetylcholine. However, some research shows that neither acute nor chronic in vivo administration of DMAE altered acetylcholine levels in the brain. These tests were not conducted on Centrophenoxine, however, which is known to have a better ability to cross the blood-brain barrier. [7]

In a 1982 study, researchers found that Meclofenoxate dramatically elevated choline levels in the rat central nervous system (CNS). In the hippocampus, this was coupled with an elevated steady-state level of Acetylcholine (ACh). The researchers also tested the effects of DMAE, which was around half as potent as Centrophenoxine in improving choline levels. [9]

Studies indicate that Centrophenoxine has the ability to reverse lipofuscin/beta-amyloid pigmentation build-up and also to act as an antioxidant against lipid peroxidation. Further studies suggest that Centrophenoxine can increase RNA synthesis, protein synthesis, and glucose uptake in neurons and glial cells. However, these effects appear to be dependant on the reduction of lipofuscin build-up and may only be relevant to the elderly. [10]


Further Scientific research:

A number of clinical trials have been conducted to examine the potential future applications of Centrophenoxine. We’ve included a brief selection of some important studies below.


Clinical Reviews:

Centrophenoxine (Meclofenoxate) was included in a systematic review in the Archives of Gerontology and Geriatrics, in 1989. The purpose of the review was to explore the mechanisms by which Centrophenoxine was able to increase longevity in a number of animal models. The review focussed on the membrane hypothesis of aging, which proposes that the reduction in the speed of gene expression in aging occurs as a result of membrane damage over time. Membranes are severely damaged through chronic exposure to free radicals, especially OH*. [11]

The researchers’ findings pointed towards the longevity-enhancing and Nootropic effects of Centrophenoxine as being heavily dependent on the antioxidant (free-radical scavenging) properties of DMAE. Basically, by protecting membranes from OH* damage, Centrophenoxine is able to slow the age-dependent deteriorations of intracellular membranes. [12]


Human studies:

In 1990, a clinical study was conducted on 50 elderly people (25 men, 25 women) suffering from dementia on a medium level. Patients were treated first with placebo and then with either an 8-week long treatment of Centrophenoxine at a dosage of 2 grams/day or with placebo. The key results were a significant increase in psychometric tests (enhanced cognition) and a significant increase in intracellular water content. The researchers suggest that the increase in intracellular water content is consistent with the OH* free radical scavenger properties of Meclofenoxate and the predictions of the membrane hypothesis of aging. [13]

In 1986, a clinical trial evaluated the efficacy of Centrophenoxine in treating Tardive dyskinesia, which is thought to occur as a result of diminished cholinergic activity and enhanced dopamine levels in the brain. The trial used a dosage of 600-1200 mg/day for 6-12 weeks. Among the 11 participants, 4 improved markedly, 1 moderately, 2 slightly, and 4 did not improve. [14]

In 2012, a study was published in the Journal of Alzheimer’s Disease about the potential uses of DMAE for Alzheimer’s patients. Although this study pertains to DMAE, it is important to remember that Centrophenoxine is a prodrug of DMAE and is metabolized to DMAE in the liver. The study’s objective was to assess the clinical efficacy and safety of DMAE in 242 patients with Alzheimer’s Disease. Unfortunately, although the drug was well-tolerated, no statistically significant improvement was seen after 12 weeks of treatment. [15]


Animal studies:

In a 1993 study, researchers examined the changes in lipid peroxidation, lipofuscin concentration, and multiple unit activity (MUA) recorded in the CA3 region of the hippocampus in live rats. With age, lipid peroxidation and lipofuscin concentrations increased, while MUA declined. In rats ages 4- to 8-months, Centrophenoxine had no effects on the three parameters. However, in rats aged 16- to 24-months, the drug significantly increased the MUA while decreasing lipid peroxidation and liofuscin concentration. [16]

 Age-related changes in acetylcholinesterase activity were measured in the hippocampus, brain stem, and cerebellum of rats aged 4 to 24 months. Age-dependent decreases in enzyme activity were first noticeable in the hippocampus, followed by the brain stem. Centrophenoxine significantly increased acetylcholinesterase activity in the hippocampus and brain stem. The cerebellum was not affected by age-related decreases in enzyme activity, nor was the enzyme activity influenced by Centrophenoxine. [17]

With regards to longevity, studies have shown that both DMAE and Centrophenoxine increase life-span of rats by between 30% and 50%. These results have been correlated in similar studies. In one such study, daily treatment of 100 mg/kg Centrophenoxine resulted in a 40% survival rate over 30 days, compared to 8% of the control rats. [18]

In a 1998 study, the effects of Centrophenoxine were compared to those of ginkgo biloba extract and zinc on lipid peroxide, free radical scavenging, and the cardiovascular system of aged rats. Rats were treated with 100 mg/kg meclofenoxate daily, for 4 weeks, either alone or in combination with either zinc (10.5 mg/kg) or ginkgo biloba extract (150 mg/kg). Aged rats treated with either Cetrophenoxine alone or in combination with either of zinc or ginkgo biloba showed improvements in free radical scavengers, especially in heart and brain tissues. Both zinc and Ginkgo potentiated Centrophenoxine’s effects on blood pressure and heart rate. [19]


Toxicology cases:

In a book entitled ‘Reviving the Broken Marionette: Treatments for CFS/ME and Fibromyalgia’, the potential toxicity of Centrophenoxine is discussed. It is said to be very safe and low of side effects. Rare side effects noted include insomnia, dizziness, tremor, restlessness, depression, nausea, muscle tension, and headaches. [20]

 Preliminary evidence points to possible teratogenic effects for DMAE (causing defects in unborn infants). This is thought to be linked to DMAE’s effects on choline uptake during the first few days of neural tube formation. Centrophenoxine may exhibit these same effects and may be toxic to embryo growth during the first few days after impregnation. [21]

  • Centrophenoxine is often misspelled as: centrophenoxin, centrophinoxine, centrophinoxine, sentrophenoxine, sentrophenoxin.



  • [1]  Index Nominum 2000: International Drug Directory. (2000). Taylor & Francis, pp. 636–. ISBN 978-3-88763-075-1.
  • [2] Centrophenoxine, Examine.com. (2018). Available online from https://examine.com/supplements/centrophenoxine/ [Accessed November 1, 2017]
  • [3] Marcer D, Hopkins SM. (1977). The differential effects of meclofenoxate on memory loss in the elderly. Age and ageing. 6(2):123–31.
  • [4] Freeman B. (2003). Centrophenoxine – The Neuroenergizer, posted on WorldHealth.net, available online from https://www.worldhealth.net/news/centrophenoxine-_the_neuroenergizer/ [Accessed November 2, 2017]
  • [5] Zou JJ, Ji HJ, Wu DW, Yao J, Hu Q, Xiao DW, Wang GJ. (2008). Bioequivalence and pharmacokinetic comparison of a single 200-mg dose of meclofenoxate hydrochloride capsule and tablet formulations in healthy Chinese adult male volunteers: a randomized sequence, open-label, two-period crossover study. Clin Ther, 30(9):1651-7.
  • [6] Karen E. Haneke MS. (2002). Dimethylethanolamine (DMAE) [108-01-0] and Selected Salts and Esters. Review of Toxicological Literature. Available online from https://ntp.niehs.nih.gov/ntp/htdocs/chem_background/exsumpdf/dmae_update_110002_508.pdf [Accessed November 2, 2017]
  • [7] Zs-Nagy I. (1994). A survey of the available data on a new nootropic drug, BCE-001. Ann N Y Acad Sci, 717:102-14.
  • [8] Marcer D, Hopkins SM. (1977). The differential effects of meclofenoxate on memory loss in the elderly. Age Ageing, 6(2):123-31.
  • [9] Wood PL, Péloquin A. Increases in choline levels in rat brain elicited by meclofenoxate. Neuropharmacology, 21(4):349-54.
  • [10] Ludwig-Festl, M., Gräter, B., Bayreuther, K. (1983). [Increase in cell metabolism in normal, diploid human glial cells in stationary cell cultures induced by meclofenoxate]. (Article in German). Arzneimittelforschung, 33(4):495-501.
  • [11] Zs-Nagy I. (1997) The membrane hypothesis of aging: its relevance to recent progress in genetic research. J Mol Med (Berl), 75(10):703-14.
  • [12] Zs-Nagy I. (1989). On the role of intracellular physicochemistry in quantitative gene expression during aging and the effect of centrophenoxine. A review. Arch Gerontol Geriatr, 9(3):215-29.
  • [13] Fülöp T, Wórum I, Csongor J, Leövey A, Szabó T, Pék G, Zs -Nagy I. (1990). Effects of centrophenoxine on body composition and some biochemical parameters of demented elderly people as revealed in a double-blind clinical trial. Arch Gerontol Geriatr, 10(3):239-51.
  • [14] Izumi K, Tominaga H, Koja T, Nomoto M, Shimizu T, Sonoda H, Imamura K, Igata A, Fukuda T. (1986). Meclofenoxate therapy in tardive dyskinesia: a preliminary report. Biol Psychiatry, 21(2):151-60.
  • [15] Dubois B, Zaim M, Touchon J, Vellas B, Robert P, Murphy MF, Pujadas-Navinés F, Rainer M, Soininen H, Riordan HJ, Kanony-Truc C. (2012). Effect of six months of treatment with V0191 in patients with suspected prodromal Alzheimer's disease. J Alzheimers Dis, 29(3):527-35.
  • [16] Sharma D, Maurya AK, Singh R. (1993). Age-related decline in multiple unit action potentials of CA3 region of rat hippocampus: correlation with lipid peroxidation and lipofuscin concentration and the effect of centrophenoxine. Neurobiol Aging, 14(4):319-30.
  • [17] Sharma D, Singh R. (1995). Centrophenoxine activates acetylcholinesterase activity in hippocampus of aged rats. Indian J Exp Biol, 33(5):365-8.
  • [18] Klatz R, Goldman B. (2003). The Science of Anti-Aging Medicine, American Academy of Anti-Aging Med, Chicago. 268 pages pp. 66-67.
  • [19] al-Zuhair H, Abd el-Fattah A, el-Sayed MI. (1998). The effect of meclofenoxate with ginkgo biloba extract or zinc on lipid peroxide, some free radical scavengers and the cardiovascular system of aged rats. Pharmacol Res, 38(1):65-72.
  • [20] Haavisto M. (2008). Reviving the Broken Marionette:Treatments for CFS/ME and Fibromyalgia. Lulu.com. Science - 348 pages pp. 167-168
  • [21] Fisher MC, Zeisel SH, Mar MH, Sadler TW. (2002). Perturbations in choline metabolism cause neural tube defects in mouse embryos in vitro. FASEB J, 16(6):619-21.

Precaution and Disclaimer:

This Material is Sold For Research Use Only. Terms of Sale Apply. Not for Human Consumption, nor Medical, Veterinary, or Household Uses.

[Centrophenoxine Q4 2017] Centrophenoxine.2017018.pdf

[Centrophenoxine Q2 2015] Centrophenoxine.20140124.pdf