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Pinealon 10 mg
Peptide Library · Profile
Pinealon 10 mg
The name says pineal gland. We searched PubMed for anything connecting this peptide to melatonin, sleep or circadian rhythm and found no study at all. There is exactly one experiment in which it was put on pineal tissue, and in that experiment it did nothing — while a different peptide, the one Epitalon is made of, worked. The literature that does exist is about neurons, and it is worth reading. It just has nothing to do with the gland in the name.
Molecular weight418.41Da · free acid · Glu-Asp-Arg
PubMed records naming it22one of which is a false match
Randomised controlled trialsNone foundno registration, no control group reported
PharmacokineticsNone foundin any species, by any route
The short version
Plain English first. Everything below this section is the same material with the sources, the numbers and the caveats attached.
What it is
A three-amino-acid peptide — glutamate, aspartate, arginine — from the Russian bioregulator programme. In the scientific literature it is almost never called Pinealon. It is called EDR, and that is the only name you can find it under.
What has actually been measured
More than you might expect, and it is all in neurons. Rat brain cortex cultures, rat learning in a water maze, rats under low oxygen, and — the best of it — human neurons grown from the skin cells of elderly donors, where it lengthened the dendritic tree by 46%. That last result is real and statistically significant. Several of the other claims made for the same study are not.
What has not been measured
Anything about where it goes or how long it lasts: no pharmacokinetic study exists in any species. No randomised controlled trial. And nothing about the pineal gland — zero papers link it to melatonin, sleep or circadian rhythm. The human reports that do exist are three Russian-language papers in a single journal, none with a DOI, and in all of them it was given together with a second peptide, so no result belongs to this one alone.
What most people get wrong
Two things, and they point in opposite directions. The first is the name: this is not a pineal or sleep compound, and no evidence says it is. The second is more awkward for us than for the marketing — the one human study that looked for safety signals found two: prooxidant activity rather than antioxidant, and suppressed CD34+ haematopoietic markers. The authors recommended it anyway. Almost nobody quotes those findings.
What Pinealon is
A synthetic tripeptide: glutamate, aspartate, arginine. Three residues, 418 daltons. “Pinealon” is a trade name and it is nearly absent from the primary literature — the papers are indexed under the sequence code.
You need two names to find it, and one of them is three letters
| Designation | Where it is used |
|---|---|
| EDR | The dominant form in the primary literature — used bare, as a three-letter sequence code, in titles and figure legends. This is what to search |
| Glu-Asp-Arg | The expanded sequence, at first mention in most papers |
| Pinealon | The trade name. Appears mainly in the Russian clinical and geroprotection papers and in vendor copy — rarely in the cell and molecular work |
A search for the trade name across PubMed returns 22 records, and one of those is a false match — a paper about an unrelated tetrapeptide isolated from a distillery by-product, pulled in by sequence-string overlap. So the real figure is 21. For comparison, that is a smaller literature than most approved drugs generate in a year.
| Sequence | Glu-Asp-Arg · H-Glu-Asp-Arg-OH |
| Formula | C15H26N6O8 |
| Molecular weight | 418.41 Da, free acid |
| Net charge at pH 7 | about −1 — three carboxylic acids against an arginine and one amine |
| ChEBI identifier | Registered, and the formula above matches it |
The molecular weight is our own calculation from the three residue masses less two waters: 418.41 Da, which agrees to two decimals with the registered chemical entry. We calculate rather than copy because vendor-published weights for short bioregulators in this family are inconsistent, and because a weight is meaningless without the salt form — see below.
It is not a relative of Epitalon, and that is the point
This peptide gets shelved next to Epitalon and sold as part of the same family, so it is worth being exact. Epitalon is Ala-Glu-Asp-Gly. Cartalax is Ala-Glu-Asp — Epitalon minus one glycine, a genuine structural near-twin. Pinealon is Glu-Asp-Arg, which shares two residues with neither in the same positions.
So the family resemblance that lets Cartalax borrow Epitalon's reputation — see our Cartalax profile for why that borrowing fails anyway — is not available here at all. Pinealon is a different sequence with a different charge and a different literature. Any claim that transfers an Epitalon finding to this peptide is transferring it across a bigger gap than usual, and there is no structural argument for doing so.
The counterion problem, and the exact opposite of LL-37
No vendor we checked discloses the salt form. On 418 daltons that is not a rounding error. This peptide has two sites that can hold an acid counterion — the arginine side chain and the N-terminal amine — and trifluoroacetate weighs 114 daltons:
| Form | Peptide content | In a nominal 10 mg vial |
|---|---|---|
| Free acid | 100% | 10.00 mg |
| Mono-acetate | 87.4% | 8.74 mg |
| Mono-TFA | 78.6% | 7.86 mg |
| Di-TFA | 64.7% | 6.47 mg |
One trifluoroacetate costs 21.4% of the mass here. On LL-37, a 4,493-dalton peptide, the same counterion costs 2.5% — but LL-37 has twelve places to put one, so it can reach a similar worst case by accumulation. Short peptides are penalised per counterion; long ones are penalised by count. Anyone reasoning about a tripeptide's mass by analogy with a larger peptide is wrong by about a fifth before they start, and nothing on any label tells you which form is in the vial.
Our arithmetic from the published formula, not a finding from any source. No source we found performs it.
The name is the weakest claim on the page
This section exists because the product name does the most work in the marketing and has the least behind it. We checked it directly rather than assuming either way.
Zero papers connect it to melatonin, sleep or circadian rhythm
We searched PubMed for this peptide under both its names together with melatonin, sleep, circadian rhythm and the pineal gland. The search returned two records in total. Neither supports the name:
| A 2011 rat pineal study | Four peptides tested on organotypic pineal culture. Ala-Glu-Asp-Gly — the Epitalon sequence — stimulated pinealocyte proliferation and secretion. EDR did not affect the apoptosis marker, and was not among the peptides that stimulated Ki-67. The paper's conclusion names only AEDG as tissue-specifically active on the pineal |
| A 2026 orthopaedic review | States in passing that epitalon, DSIP and pinealon “target circadian and mitochondrial regulators.” It cites no primary circadian study for pinealon, and the same review states plainly that for this class “there is a current lack of clinical trials” |
So the only primary experiment in which this peptide met pineal tissue is one where a different peptide worked and this one did not, and the only paper asserting a circadian role is a narrative review with nothing under it.
What the literature pairs it with instead
Three of the rat studies run this peptide head-to-head against Cortexin, a cerebral cortex extract — not against a pineal extract. The cell work is in brain cortex cultures and in cortical neurons. Its documented effects are on serotonin synthesis, caspase-3, dendrites and learning.
Read without the name, this is a cortical neuron peptide with a small but coherent preclinical literature. Read with the name, it is a pineal and sleep compound with no evidence whatsoever. We could not find any paper identifying this sequence inside pineal tissue — the isolation-and-identification study that would justify the name. Searched and not found.
For contrast, Epitalon's programme did publish the equivalent work for its own tetrapeptide. The asymmetry is the same one we flagged on the Cartalax page: where a bioregulator's name claims an organ, sometimes the identification paper exists and sometimes it does not, and it is worth checking which.
What has actually been measured
The preclinical work is the real substance of this compound, and some of it is decent. We have separated the results that carry a p-value from the ones that do not, because the gap between them is where most of the marketing lives.
The best study, and the claim it overstates
A 2024 paper in International Journal of Molecular Sciences built human cortical neurons by transdifferentiating skin fibroblasts from elderly donors — a genuinely clever model — and applied this peptide for ten days. We read the full text rather than the abstract, and the two do not agree.
| Measure | Change | Reported p | Status |
|---|---|---|---|
| Total dendrite length | +46% | 0.0332 | Significant |
| Primary processes | +28% | 0.0208 | Significant |
| Branching points | +65% | none given | Paper calls the increase “slight” |
| Terminal processes | +51% | none given | Paper calls it “statistically insignificant” |
| Oxidative DNA damage (8-OHdG) | −23% | 0.0566 | Above the paper's own α of 0.05 |
| Mitochondrial activity | −12% | none given | No significant effect |
| Lysosomal activity | −8% | none given | No significant effect |
| p16 (senescence marker) | +12% | none given | No significant effect. Note the direction |
| LaminB1 | values fall | none given | No significant effect — and the text says “slightly increased” while its own numbers decrease |
The antioxidant claim does not survive its own statistics
The paper's abstract states that this peptide “reduces oxidative DNA damage” in neurons from elderly donors. In the body of the paper, that result is p = 0.0566, which the authors themselves describe as “very close to significant” — against their own stated threshold of 0.05.
Both statements are in the same document. The abstract is what gets quoted; the body is what the experiment found. We are flagging this rather than repeating the abstract, because the antioxidant claim is one of the two most common things said about this compound and it rests on this single number.
On what we can stand behind from that paper: the dendrite results are significant and they were obtained in human neurons, which is unusual for anything in this family. The model used three donor lines, from donors aged 61, 66 and 68 — a small sample, and worth knowing before the finding is described as established. The authors of this one are at the Institute of Cytology and a St Petersburg research institute; the bioregulator institute is also represented on the author list, so it is a collaboration rather than an independent replication.
The animal and culture work
| Study | What it found | The caveat worth carrying |
|---|---|---|
| Serotonin in cortex culture 2014, aging rat brain cortex cells | Stimulated serotonin expression; a molecular docking argument that the peptide matches a six-base sequence in the tryptophan hydroxylase gene | The gene-regulation half is docking, not measurement — no DNA was mixed with peptide in that experiment |
| Learning in a water maze 2013, young and old rats | Outperformed Cortexin on learning in both age groups; regional changes in brain caspase-3 | Russian-language, no DOI, group sizes and dosing not available to us |
| Acute hypoxic hypoxia 2014, old rats | Moved IL-6 and TNF toward reference levels; interpreted as increased neurogenesis and reduced neuroinflammation | Interpretation, not measurement, of neurogenesis. Russian-language, no DOI |
| Hypoxia and hypothermia 2015, 18-month rats | Both peptide preparations shifted brain neurotransmitters | Cortexin beat it on free-radical processes and caspase-3 — the paper says so explicitly |
Two of these four studies report this peptide losing a head-to-head comparison to a crude cortex extract on the measures the extract was better at, and winning on learning. That is a more interesting and more honest picture than either the marketing or a blanket dismissal, and it is the same pattern we found on Cartalax, where the crude extract outperformed the purified tripeptide.
The human reports, and why we will not call them trials
Three papers describe giving this peptide to people. All three are in one journal, all three are in Russian, none has a DOI, and in all three it was given alongside a second peptide. That last point is the one that disqualifies the lot of them as evidence about this compound.
| Report | Population | What it actually says |
|---|---|---|
| 2015 · Advances in Gerontology 28(1):62–7 | 32 people, 41–83, with multiple chronic conditions and organic brain syndrome in remission | Anabolic effect and improved CNS indicators — but Vesugen, the other peptide, performed better; prooxidant activity found by chemiluminescence; CD34+ haematopoietic markers decreased, which the authors read as significant inhibition of haemopoiesis |
| 2016 · Advances in Gerontology 29(4):594–601 | 110 people across age groups | Compared against dry carbon dioxide baths, hyperbaric oxygen and massage. The headline result is the two peptides used together, not this one alone |
| 2015 · Advances in Gerontology 28(3):510–512 | Lorry drivers in an occupational health programme | Work ability index improved. Explicitly a “preventive medical nutrition” programme — so an oral preparation — and again combined peptide use |
Four reasons none of this is a result about Pinealon
No control group is reported in any of them, and no randomisation. No registration in any trial registry we could reach. Combination arms throughout — when two compounds are given together and the pair improves, you have learned about the pair. And in the one report where the two were compared, the other peptide did better.
Add the fourth: where a route is identifiable it is oral. We found no human report in which this peptide was injected. It is sold here as a vial for reconstitution, and nothing in the human literature describes that route.
We are relying on English abstracts for all three, because the full texts are Russian-language and we could not obtain them. That limitation cuts both ways and we are stating it rather than quietly treating the abstracts as the paper — which, as the 2024 neuron study above demonstrates, is exactly the mistake that produces wrong claims.
How it is said to work
The proposal is the one shared by the whole bioregulator programme: short peptides enter the cell, reach the nucleus, bind DNA sequence-specifically and change gene expression. For this compound, the evidence is better than for most of the family — and it comes from a physics department.
The DNA binding was measured, not just modelled
A 2019 paper in the Journal of Physical Chemistry B studied this peptide against DNA using spectroscopy, NMR, viscosimetry and molecular dynamics. The finding: the peptide can partly penetrate the major groove of DNA and interact with base atoms, chiefly the N7 and O6 positions of guanine, and magnesium ions promote the interaction by screening DNA's phosphate charges.
Two things make this the strongest mechanistic item in the whole family. It is physical measurement, not docking — actual peptide, actual DNA, in a tube. And the authors are at the Faculty of Physics, Saint Petersburg State University, not the bioregulator institute. It is the only independent group we found working on this molecule.
Three gaps between that result and the claim
- Binding DNA in a tube is not regulating a gene in a cell. The 2019 work shows an interaction exists and is magnesium-dependent. It does not show a transcriptional consequence, and it was not done in a cell.
- Nuclear delivery is still assumed. The programme's own 2021 review on this peptide says the peptide “is assumed to enter cells and bind to histone proteins and/or ribonucleic acids” — the word is theirs. Nothing we found measures how much of an administered tripeptide reaches a nucleus.
- The gene list is a review's list, not a measured one. The signalling pathways and proteins attributed to this peptide — MAPK/ERK, caspase-3, p53, SOD2, GPX1, PPARA, PPARG, calmodulin — come from a review assembling results across models and arms. They are not the output of one experiment that measured them.
That 2021 review is also where the frequently-repeated line about improved memory in elderly patients originates. It is a review by the programme's own principals; the underlying human material is the Russian combination-arm literature in the section above. We have left the claim attributed rather than repeated.
Reported protocols
There is no protocol with a defensible source, so this section does not contain one. What follows is an account of why the figures in circulation cannot be used, which is more useful than repeating them.
The figures that circulate carry no citation
We looked for a primary source behind every dose figure we could find for this compound and found none — not one of them traces to a study. The published figures also disagree with each other about the route, which is the tell: a quantity that is the same whether it is swallowed or injected was never derived from anything.
We are not printing them. Our view is that reproducing an uncited number next to a product is how an uncited number becomes a convention, and this family of compounds has enough of those already.
Why the one real concentration cannot be converted
The figures that do have an experiment behind them are culture concentrations — the 2024 neuron study applied this peptide at a defined concentration in a dish, daily, for ten days. A reader might try to scale that to a body. Here is why it fails.
A dish is held at a fixed concentration continuously. A free tripeptide in a body is not: it would be expected to be degraded by serum and tissue peptidases in minutes, and no pharmacokinetic study of this compound exists in any species to say how fast. Any conversion from a culture concentration to an administered quantity assumes instant uniform distribution and zero clearance, and both assumptions are wrong by an unknown margin. That is not a calculation with a wide error bar; it is a calculation with no basis.
The claim that effects from this family of peptides “persist for weeks to months” — the claim that justifies intermittent use — has no source we could find for this compound. No washout study, no durability study, no epigenetic persistence study. Searched and not found.
Where the vendor claims come from
| Claim | What it is actually based on |
|---|---|
| “Supports the pineal gland / sleep / melatonin” | Nothing. Zero papers. The one pineal-tissue experiment found this peptide inactive while the Epitalon sequence worked |
| “Antioxidant, reduces oxidative DNA damage” | One result, at p = 0.0566, which is above the paper's own threshold. And a human report found the opposite — prooxidant activity |
| “Protects neurons, improves memory” | Partly supported. Rat learning and human dendrite outgrowth are real findings. The human memory claim comes from a programme review resting on combination-arm reports |
| “Regulates gene expression / binds DNA” | The best-supported claim on the page — major-groove interaction measured by an independent physics group. But measured in a tube, not in a cell |
| “Mitochondrial support” | Contradicted. The one study that measured mitochondrial activity found a 12% decrease, not significant |
| “Senolytic / anti-senescence” | Contradicted. The same study measured p16, the senescence marker, and found a 12% increase — not significant, but the wrong direction |
| Studies in traumatic brain injury patients | We could not trace this to any paper and are not repeating it. Searched and not found |
Published side-effect lists and stacking guidance for this compound are uncited, on a molecule with no toxicology study and no pharmacokinetics. A side-effect list assembled without a safety study behind it is a genre convention, not a safety profile — and in this case it also manages to omit the two findings a human report actually produced.
Storage
No stability or storage study specific to this compound was found in any primary source — not in solution, not lyophilised, at any temperature, over any time course. What exists is generic peptide handling guidance from suppliers.
Freeze the lyophilised solid, keep it dry and dark. Our general conventions are in the storage guide.
On the 28 days: our guide recommends 28 days for a reconstituted peptide in bacteriostatic water, and that figure is half a sterility rule and half a stability convention. The sterility half transfers here unchanged — benzyl alcohol behaves the same regardless of what is dissolved in it. The stability half has never been measured for this molecule. The 28 days is always recommended, never a deadline, and on this compound it carries no compound-specific evidence at all.
Anyone presenting “stable for 28 days once reconstituted” as a finding about this peptide is importing generic guidance. It is a house convention, and we would rather say so than let it look like data.
Reported effects
There is no toxicology for this compound — no lethal dose study, no acute or repeat-dose study, no genotoxicity, no reproductive toxicity, no immunogenicity assessment. What there is, unusually, is two safety signals from the one human report that looked, and almost nobody quotes them.
The two findings from the 32-person report
Prooxidant activity. Measured by chemiluminescence. The authors' own conclusion recommends these peptides as geroprotectors of an “anabolic neuroprotective and no antioxidant type” — which is them saying, in their own words, that this is not an antioxidant. That is in direct conflict with how the compound is usually sold.
Suppressed haematopoietic markers. CD34+ polypotent haematopoietic cells in blood decreased, which the authors describe as significant inhibition of haemopoiesis. They suggest the cells were simply not recruited into adaptive responses. Either way it is a measured decrease in a blood-cell precursor marker, in people, and it was reported as significant.
Two things to hold alongside that. It is a combination report, so neither finding can be assigned to this peptide alone. And the same report found no effect on chromatin condensation, which the authors read as reassuring at the nuclear-genetic level, while noting the property should be studied further. We are reporting all three findings from that paper, not the convenient one.
No adverse event literature
No case reports, no pharmacovigilance signal, and no regulatory communication describing harm from this compound were found. That is not reassurance and must not be read as any: there is no registered trial collecting events, no post-market surveillance covering a research vial, and — as above — no report at all of this peptide being injected into a person. An empty adverse-event record for a route nobody has formally used is a measure of absent observation.
Nobody has opened a vial
We found no published analysis of the contents of Pinealon vials sold online — no mass spectrometry, no chromatography, by any regulator, academic group or independent laboratory.
One identity risk worth stating plainly, because it is specific to this compound's shelf position. Pinealon, Epitalon and Cartalax sit adjacent in catalogues and in inventories, and at 418, 390 and 333 daltons they are all small and all within a hundred daltons of each other. The risk is not analytical — any competent mass spectrometer separates them easily, and their sequences share no two residues in the same order. The risk is picking and labelling, which is an argument for lot-specific certificates rather than against them. Ours are on the certificate register.
Regulatory status
Pinealon is named explicitly by Health Canada and is absent from the FDA's compounding lists. Both of those are facts about its legal position, and neither is a safety verdict.
| Body | Pinealon named? | What it says |
|---|---|---|
| Health Canada, 1 Aug 2025 | Yes — by name | Listed among unauthorised injectable peptide drugs seized from a Canadian seller, alongside 43 others including Epitalon, Cortagen, Livagen, Ovagen, Vilon, Prostamax, Bronchogen and LL-37 |
| FDA, updated 22 Apr 2026 | No — not under any of its names | Neither Pinealon, EDR nor Glu-Asp-Arg appears on the compounding page. Epitalon does, as a nomination that was withdrawn; so does Cathelicidin LL-37 |
| Approved medicine anywhere | Not that we could establish | We found no marketing authorisation for this peptide as a medicine in any jurisdiction. Where a route is documented in the human literature it is oral, in supplement or medical-nutrition programmes |
| WADA 2026 Prohibited List | Not named — S0 applies | S0 covers substances with no current approval by any governmental regulatory health authority for human therapeutic use. Prohibited at all times on that definition |
| Australia | Not checked. We make no claim | |
Being on Health Canada's list means this is an unauthorised drug in Canada, full stop. Note the direction of the asymmetry with the FDA: Canada names it and America does not, which is the reverse of what obscurity would predict and is worth knowing rather than glossing. Absence from a list measures attention, not permission.
Sentient Biogenix supplies Pinealon for laboratory research use only. It is not for human or veterinary use.
Questions we actually get
What is it?
A synthetic tripeptide — glutamate, aspartate, arginine. In the literature it is written EDR, which is the only name worth searching. It is one of the Khavinson bioregulators, a family of short peptides developed from the 1970s at a St Petersburg institute.
Does it help sleep?
There is no evidence that it does. We searched for any paper connecting this peptide to melatonin, sleep or circadian rhythm and found none. The single experiment in which it was applied to pineal tissue found it inactive, while the Epitalon sequence in the same experiment was active. If you want the sleep-adjacent compound in this family, the evidence points at Epitalon — and our profile on that one is not uncritical either.
Then why is it called Pinealon?
We do not know, and we could not find an isolation paper identifying this sequence in pineal tissue. What the literature does is pair it repeatedly with Cortexin, a cortex extract, and study it in cortical neurons. Read without the name it is a cortical neuron peptide with a small, coherent preclinical literature.
Is it an antioxidant?
The evidence runs both ways and the stronger reading is no. The cell paper's abstract says it reduces oxidative DNA damage, but the paper's own number for that result is p = 0.0566, above its stated threshold. And the 32-person human report found prooxidant activity, with its authors concluding the peptides act in an “anabolic neuroprotective and no antioxidant” way. Those are their words.
Is there any human data?
Three reports, all in one Russian-language journal, none with a DOI, none randomised or controlled, and in all three it was given together with a second peptide. In the one report that compared them, the other peptide did better. And where a route is identifiable it is oral — no human report describes injecting it.
What does it actually do, then?
The two things we would stand behind: in human neurons grown from elderly donors' skin cells it lengthened the dendritic tree by 46%, significantly; and in rats it improved water-maze learning, outperforming a cortex extract. Both are small studies. Neither is a human outcome.
What's the half-life?
Unknown. No pharmacokinetic study of this compound exists in any species. A free tripeptide would be expected to survive minutes in serum, but that has not been measured here and we will not print a number for it.
Is it related to Epitalon or Cartalax?
Not structurally. Epitalon is Ala-Glu-Asp-Gly and Cartalax is Ala-Glu-Asp — those two are one glycine apart. This is Glu-Asp-Arg, a different sequence with a different charge. It is sold as part of the same family and shares the same programme, but no Epitalon finding transfers to it.
So why do you sell it?
Because it is a legitimate research compound, the DNA-interaction work on it is the best in its family and comes from an independent group, and the human neuron result is interesting. What we will not do is sell it as a sleep or pineal compound, or as an antioxidant. The name is wrong and the antioxidant claim does not survive its own statistics, and you should know that before you buy anything from us.
References
- Kraskovskaya N, Linkova N, Sakhenberg E, et al. Short peptides protect fibroblast-derived induced neurons from age-related changes. International Journal of Molecular Sciences 2024;25(21):11363. DOI 10.3390/ijms252111363. PMID 39518916. — read in full, not from the abstract, and that is why this page disagrees with the usual summary of it. Source of the dendrite results (+46%, p = 0.0332; +28% primary processes, p = 0.0208) and of the 8-OHdG result the abstract calls significant and the body reports at p = 0.0566. Also the source of the non-significant mitochondrial, lysosomal, p16 and LaminB1 results, two of which point the wrong way. Three donor lines, aged 61, 66 and 68.
- Silanteva IA, Komolkin AV, Morozova EA, Vorontsov-Velyaminov PN, Kasyanenko NA. Role of mono- and divalent ions in peptide Glu-Asp-Arg–DNA interaction. The Journal of Physical Chemistry B 2019;123(9):1896–1902. DOI 10.1021/acs.jpcb.8b10359. PMID 30762356. — the strongest item in the file and the only independent group we found. Faculty of Physics, Saint Petersburg State University, no bioregulator-institute author. Spectroscopy, NMR, viscosimetry and molecular dynamics: partial major-groove penetration, interaction at guanine N7 and O6, promoted by Mg²⁺. Measured, not docked — and in a tube, not a cell.
- Khavinson V, Linkova N, Chalisova N, Dudkov A, Koncevaya E. Effect of short peptides on expression of signaling molecules in organotypic pineal cell culture. Bulletin of Experimental Biology and Medicine 2011;152(1):138–41. DOI 10.1007/s10517-011-1473-y. PMID 22803060. — the only experiment in which this peptide met pineal tissue. Ala-Glu-Asp-Gly, the Epitalon sequence, stimulated pinealocyte proliferation and CGRP secretion. EDR did not, and the paper's conclusion names only AEDG as tissue-specifically active. This is the single most important citation on the page, and it is from the programme's own group.
- Khavinson VKh, Lin'kova NS, Tarnovskaya SI, Umnov RS, Elashkina EV, Durnova AO. Short peptides stimulate serotonin expression in cells of brain cortex. Bulletin of Experimental Biology and Medicine 2014;157(1):77–80. DOI 10.1007/s10517-014-2496-y. PMID 24909721. — the serotonin result, in aging rat brain cortex culture. The gene-regulation half of the paper is a molecular docking argument about a six-base sequence in the tryptophan hydroxylase gene, not a measurement.
- Khavinson V, Linkova N, Kozhevnikova E, Trofimova S. EDR peptide: possible mechanism of gene expression and protein synthesis regulation involved in the pathogenesis of Alzheimer's disease. Molecules 2021;26(1):159. DOI 10.3390/molecules26010159. PMID 33396470. — the programme's own review, and the origin of most of the pathway list attributed to this peptide. Note its own hedge, verbatim: the peptide “is assumed to enter cells and bind to histone proteins and/or ribonucleic acids.” Also the origin of the frequently repeated memory claim. Written by the programme's principals; not an independent appraisal.
- Meshchaninov VN, Tkachenko EL, Zharkov SV, Gavrilov IV, Katyreva IuE. Effect of synthetic peptides on aging of patients with chronic polymorbidity and organic brain syndrome of the central nervous system in remission. Advances in Gerontology 2015;28(1):62–7. PMID 26390612. Russian-language; no DOI. — the 32-person report, and the only human source with a safety observation. Source of the prooxidant finding, the decreased CD34+ haematopoietic markers read as inhibition of haemopoiesis, the absence of an effect on chromatin condensation, and the authors' own description of these peptides as “no antioxidant type.” Also records that Vesugen outperformed Pinealon. Combination arms; read via English abstract.
- Myakotnykh VS, Torgashov MN, Egorin KV, et al. Comparative analysis of different methods of geroprotective. Advances in Gerontology 2016;29(4):594–601. PMID 28539017. Russian-language; no DOI. — 110 people, against dry carbon dioxide baths, hyperbaric oxygen and massage. The headline finding is the two peptides used together, not this one alone. Read via English abstract.
- Bashkireva AS, Kachan EYu. Assessment of work ability index in evaluation of small peptides geroprotective effect. Advances in Gerontology 2015;28(3):510–512. PMID 28509489. Russian-language; no DOI. — lorry drivers, occupational health. Explicitly a “preventive medical nutrition” programme, so oral, and again combined peptide use. Read via English abstract.
- Mendzheritski AM, Karantysh GV, Abramchuk VA, Ryzhak GA. Effect of peptide geroprotectors on the navigation system learning and caspase-3 in brain structures in rats of different age. Advances in Gerontology 2013;26(2):252–257. PMID 28976148. Russian-language; no DOI. — the water-maze result. Outperformed Cortexin on learning in both young and old rats. Group sizes, dose and route not available to us.
- Mendzheritskii AM, Karantysh GV, Ryzhak GA, Dem'ianenko SV. Regulation of content of cytokines in blood serum and of caspase-3 activity in brains of old rats in model of sharp hypoxic hypoxia with Cortexin and Pinealon. Advances in Gerontology 2014;27(1):94–7. PMID 25051764. Russian-language; no DOI. — IL-6 and TNF moved toward reference levels. The increased-neurogenesis reading is the authors' interpretation, not a measurement of neurogenesis.
- Mendzheritsky AM, Karantysh GV, Ryzhak GA, Prokofiev VN. Pinealon and Cortexin influence on behavior and neurochemical processes in 18-month aged rats within hypoxia and hypothermia. Advances in Gerontology 2015;28(3):532–539. PMID 28509493. Russian-language; no DOI. — the second head-to-head loss: “Cortexin shows a more pronounced effect on free radical processes and caspase 3 activity in brain than Pinealon.” The crude extract beat the purified tripeptide, which is the same pattern we found on Cartalax.
- Rahman OF, Lee SJ, Seeds WA. Therapeutic peptides in orthopaedics: applications, challenges, and future directions. Journal of the American Academy of Orthopaedic Surgeons Global Research & Reviews 2026;10(1). DOI 10.5435/JAAOSGlobal-D-25-00236. PMID 41490200. — included because it is the only paper we found asserting a circadian role for this peptide, and it does so in a single clause with no primary citation. The same review states for this whole class that “there is a current lack of clinical trials.”
- Health Canada. Unauthorized injectable peptide drugs seized and sold by Canada Peptide may pose serious health risks. Advisory, 1 August 2025. recalls-rappels.canada.ca — read in full this session. Pinealon appears by name in the affected-products table, among 44 entries. The lead-in is “Unauthorized injectable peptide drugs, including:”, so the list is not exhaustive.
- US Food and Drug Administration. Certain bulk drug substances for use in compounding that may present significant safety risks. Content current as of 22 April 2026. fda.gov — read in full this session. Pinealon, EDR and Glu-Asp-Arg are absent from the entire page. Epitalon and Cathelicidin LL-37 both appear in the nominated-but-withdrawn table.
- World Anti-Doping Agency. Prohibited List 2026, section S0. — Pinealon is not named. The application of S0 is ours, using the list's own definition of a substance with no current approval by any governmental regulatory health authority for human therapeutic use.
Listed rather than hidden, what we could not check. Searches for this page were run against PubMed, which was reachable throughout; the record count, identifiers and abstracts above come from it, and the DOI links go to the publishers. The three human reports are Russian-language full texts we could not obtain, so everything said about them comes from their English abstracts — a limitation that matters, because the 2024 neuron paper on this list is a worked example of an abstract disagreeing with its own body. We could not find: a paper identifying this sequence in pineal tissue; any paper linking it to melatonin, sleep or circadian rhythm; a pharmacokinetic study in any species; a stability study; a toxicology study; a registered trial; a primary source for any circulating dose figure; or an independent analysis of research-grade vials. Each of those is stated as searched and not found, never as does not exist — much of this literature is Russian-language and non-indexed, and that distinction carries more weight on this page than on most. The molecular weight, charge and all counterion figures are our own arithmetic from the published formula, flagged as such where they appear.
For laboratory research use only. Not for human or veterinary use. Nothing on this page is dosing guidance, and no figure here should be read as a recommendation.