Pinealon (EDR): what the evidence shows and what it does not

Why is a peptide called Pinealon not from the pineal gland?

The mapping, from two papers: the 2020 Molecules review introduces EDR as a tripeptide isolated from the polypeptide neuroprotective drug Cortexin, which is a cerebral cortex preparation (Khavinson, 2020). A 2024 paper sets out the whole family mapping: KED from vessels, EDR from cerebral cortexes, AEDG from pineal glands, all of them from calves (Kraskovskaya, 2024).

What that does to the trade name: the pineal peptide in this family is AEDG, which reaches the market as epitalon. Someone who meets the name Pinealon and infers a pineal origin has been misled by the label rather than by the literature, because both papers state the cortex origin without hedging it.

Why this page opens there: the origin sentence is not buried. It sits in the opening paragraph of the 2020 review, before any result, which makes it the cheapest check available on anything written about this compound: a page that has the gland wrong has not opened the source it is standing on.

The whole published record, on one screen

The scope: eleven documents carry every substantive claim below. The column that matters is the second one, because this literature mixes solution chemistry, cell culture, rats and small uncontrolled human cohorts, and a result does not travel from one of those rows to another.

The count, and how to reproduce it: on 4 August 2026 the Europe PMC search string pinealon returns 29 records, and the same endpoint returns nothing at all for a nonsense control string, which is what makes the first number worth printing rather than repeating.

What did the independent DNA study measure?

The finding: EDR can partly penetrate the major groove of DNA and affect the base atoms, mainly the N7 and O6 of guanine, and magnesium ions promote the interaction by screening the negative charge on the DNA phosphate groups (Silanteva, 2019). The methods named are spectral measurement, NMR, viscosimetry and molecular dynamics.

Why we single this paper out: its five authors are all at the Faculty of Physics, Saint Petersburg State University. Six of the eleven papers in the reference list below name Khavinson as an author, and a seventh lists the St Petersburg Institute of Bioregulation and Gerontology among its affiliations. That institute both produces this research and is tied to the commercial peptide line, which is a conflict to state rather than bury. The DNA paper is the one result here that does not carry it.

What it does not establish: anything happening inside a person. A peptide reaching a groove in a DNA duplex in a cuvette is a physical-chemistry result, and the distance from there to a clinical effect is the whole distance this page is about. We read the abstract in full and verified the record; the full text sits behind a paywall and nothing beyond the abstract is claimed here.

How does Pinealon differ from the other peptides in the same experiment?

The one measurement that separates them: Fedoreyeva and colleagues labeled several of these peptides with fluorescein, watched them enter HeLa cells, and then measured Stern-Volmer quenching constants against synthetic oligonucleotides of known sequence (Fedoreyeva, 2011). The constants came out different for different peptides, which is the paper's evidence that the binding is sequence-specific rather than general stickiness.

The split it reports: epithalon, pinealon and bronchogen bound preferentially to oligonucleotides containing CNG, which the paper notes are the targets for cytosine DNA methylation in eukaryotes. Within that, it reports that epithalon, testagen and pinealon appear to prefer CAG-containing sequences while bronchogen prefers CTG-containing ones. Those are per-compound results out of one shared experiment, which is what makes the passage a comparison rather than a list, and the paper hedges the second half with the word seem.

The layer above it is a prediction, not a measurement: a 2014 paper reports that Glu-Asp-Arg and Lys-Glu-Asp raise serotonin expression in aging brain cortex cultures, and identifies a CCTGCC sequence in the tryptophan hydroxylase gene as complementary to those peptides by molecular docking (Khavinson, 2014). Docking is a computed prediction of fit. It is a hypothesis about a mechanism, and the paper presents it as one.

What happened in neurons grown from elderly donors?

The model: dermal fibroblasts taken from elderly donors were transdifferentiated into induced cortical neurons, and EDR, KED or AEDG were applied at 10 ug per mL daily for ten days (Kraskovskaya, 2024). Human-derived cells in a dish, not a human trial, and the paper is explicit about which of those two it is.

The dendrite numbers, per peptide: primary process counts rose 34 percent with AEDG, 32 percent with KED and 28 percent with EDR. Total dendrite length rose 32 percent with AEDG, 42 percent with KED and 46 percent with EDR. On primary process count, EDR came last of the three; on total length it came first. Branching points are a separate measure in the same figure of that paper, and there the order changes with EDR highest, but the paper calls all three of those branching increases slight or insignificant.

The oxidative marker, and the caveat the abstract drops: staining for 8-hydroxydeoxyguanosine fell from 0.40 relative units in the untreated group to 0.36 with AEDG, 0.34 with KED and 0.31 with EDR, a fall of 23 percent for EDR. The results section calls that decrease statistically significant. Two sentences later the same paper gives the p value as 0.0566 and describes the effect as very close to significant, which is a different thing at the conventional threshold. The abstract carries only the positive sentence.

What the same experiment found nothing for: the paper reports no effect from these tripeptides on mitochondrial activity, on lysosomal activity, or on the level of p16 protein in the induced neurons. Reading the negative results is how a comparison stays a comparison instead of turning into a brochure.

Do the cell results and the human results agree?

What the cells said: pinealon restricted reactive oxygen species accumulation in a dose-dependent way in cerebellar granule cells, neutrophils and PC12 cells, cut necrotic cell death on a propidium iodide test, and delayed the time course of ERK 1/2 activation (Khavinson, 2011). The authors infer from the concentration behavior that the peptide also interacts directly with the cell genome.

What the people said: a Ural State Medical University group gave Pinealon and Vesugen to 32 people aged 41 to 83 with chronic polymorbidity and organic brain syndrome in remission, and reported prooxidant activity on chemiluminescence, plus a fall in CD34+ hematopoietic cells that they read as significant inhibition of hemopoiesis (Meshchaninov, 2015). Their own recommendation is that these peptides be used as geroprotectors of an anabolic neuroprotective and no antioxidant type.

The plain reading: the in vitro antioxidant story and the only human oxidative measurement point in opposite directions, in print, in two retrievable sources. That is not a hedge we are adding; it is the state of the record. The human report also found Vesugen the more visible of the two, and did not isolate what Pinealon contributed on its own.

Where the animal work sits: rats loaded with dietary methionine during pregnancy produced offspring whose spatial orientation and learning improved with pinealon, with fewer necrotic cerebellar neurons and less reactive oxygen species accumulation (Arutjunyan, 2012). Rats, in a prenatal model, which is the row on this page most likely to be quoted somewhere else as though it were a human result.

What have people been given, and what was measured?

The only single-compound human record: locomotive crew workers took the peptide for two weeks, and the report specifies one capsule containing 100 mkg of Pinealon twice a day (Nazimko, 2012). The spelling mkg is that paper's transliteration of microgram, and the microgram against milligram distinction is worth holding onto, because this figure is one ten-thousandth of a gram and reads nothing like the milligram amounts attached to injectable compounds. It is reported here as what that source administered, and for no other purpose.

What the report does not carry: a participant count, a control group, blinding, or any randomization. The outcome is a composite of biological-age parameters and adaptive-reaction indicators, which is an assessment framework rather than a clinical endpoint.

The record that looks like a trial and is not: PubMed tags one pinealon paper with the publication type Clinical Trial, and reading it disarms the tag. It compares 150 male lorry drivers with 150 male metal craftsmen on neurobehavioral measures, and reports that the best effect came from combined application of several cytogens, pinealon and vezugen together (Bashkireva, 2012). It is an occupational comparison with a peptide arm, not a randomized trial of this compound.

The format the human record specifies: the two documents that name a route both name an oral one. The workers study specifies a capsule, and the 2020 review describes oral administration. The two Ural and occupational reports do not state a route at all. Anyone reasoning from those reports to a reconstituted vial has changed the route of administration, and the questions that come with a freeze-dried powder in a vial were never part of what these papers measured.

Where does the 72-patient figure come from?

The claim in circulation: the 2020 Molecules review states that oral Pinealon added to standard therapy in 72 patients with traumatic brain injury consequences and cerebrasthenia improved memory and reduced the duration and intensity of headaches (Khavinson, 2020). It is a specific number attached to a named patient population, which is the shape of claim that travels furthest.

What is behind it: that sentence carries reference 11. Pulling the review's own reference list, entry 11 is a 2013 paper in Advances in Gerontology, PubMed identifier 24738258, whose publication types are Journal Article and Review, in Russian (Umnov, 2013). So the 72-patient figure reaches an English reader as a review citing a review.

What follows from that: the number may well trace to a real study further back, and we could not retrieve one. Until somebody does, it is not a trial result and must not be quoted as one, which is why it appears on this page as a provenance trace rather than as a row in the record table above.

What the record does not settle

The open items, stated as gaps rather than as absences of effect: where a document could close one of these we name the document, and for anything held in a container that document is a certificate of analysis rather than a paper.

• Anything isolated. Two of the three human reports gave a second peptide at the same time, so the contribution of EDR by itself has not been measured in a person.
• Registered trials. On 4 August 2026 the ClinicalTrials.gov version 2 API returned an empty study list for the trade name, and an empty study list for the sequence queried as a quoted phrase, against a control query that returned 757 studies. The bare unquoted sequence returns amino acid and protein nutrition studies with no record of this tripeptide among them, which is why the phrase query is the one reported here.
• Approval status. No marketing authorization turned up in the records we could query, and two registries we would have wanted, the Russian supplement registry and the European agency search, could not be read at all, so this page makes no claim about either.
• Dose relationships. One human report gives one amount for two weeks. Nothing in the record compares amounts, durations or schedules against each other.
• Identity of any given powder. A sequence in PubChem is not a statement about what is inside an unlabeled container, and a purity figure is not an identity check.
• Long-term safety. The one human oxidative and hematological measurement is a single uncontrolled cohort of 32 people, which is far too little to characterize anything.

How this page is sourced

What was retrieved before it was written: the full text of the two open-access papers, retrieved from the PubMed Central archive, and the complete abstract of every other paper, retrieved from the PubMed record. Every identifier below was pulled independently before it was printed, and the metadata beside it is what the record returned rather than what a summary of it said.

Where a source was checked against itself: the 23 percent oxidative-marker figure is stated as significant in one sentence of its paper and given as p equal to 0.0566 two sentences later. Both appear above because printing only the first would have reproduced the paper's own abstract instead of reading it. The 72-patient figure was traced through the citing review's reference list to the document it actually rests on.

What is deliberately absent: a granted European patent exists on this sequence, and it is not cited here, because a patent means a novelty examination rather than a safety or efficacy review and this page had no way to link the document within its own sourcing rules. Two registries also went unread, so no claim is made about Russian or European Union registration in either direction. This is the same discipline applied on other compounds whose literature is this thin.

Fourteen sources: eleven papers cited by PubMed identifier, six of which also carry a DOI, plus one chemical database record and two dated registry and regulator queries with their controls.

The standard: the full sourcing and citation-verification standard for this site, including who checks a page before it ships, lives on the methodology page.

Last reviewed: 4 August 2026.

1. 1

   Silanteva IA, Komolkin AV, Morozova EA, Vorontsov-Velyaminov PN, Kasyanenko NA. Role of Mono- and Divalent Ions in Peptide Glu-Asp-Arg-DNA Interaction. J Phys Chem B. 2019;123(9):1896-1902. doi:10.1021/acs.jpcb.8b10359. PMID 30762356. Abstract retrieved 4 August 2026; full text paywalled and not read.

2. 2

   Fedoreyeva LI, Kireev II, Khavinson VKh, Vanyushin BF. Penetration of short fluorescence-labeled peptides into the nucleus in HeLa cells and in vitro specific interaction of the peptides with deoxyribooligonucleotides and DNA. Biochemistry (Mosc). 2011;76(11):1210-1219. doi:10.1134/S0006297911110022. PMID 22117547.

3. 3

   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. 2020;26(1):159. doi:10.3390/molecules26010159. PMID 33396470. A narrative review, not a study. Full text read via PMC7795577.

4. 4

   Kraskovskaya N, Linkova N, Sakhenberg E, Krieger D, Polyakova V, Medvedev D, Krasichkov A, Khotin M, Ryzhak G. Short Peptides Protect Fibroblast-Derived Induced Neurons from Age-Related Changes. Int J Mol Sci. 2024;25(21):11363. doi:10.3390/ijms252111363. PMID 39518916. Full text read via PMC11546785.

5. 5

   Khavinson V, Ribakova Y, Kulebiakin K, Vladychenskaya E, Kozina L, Arutjunyan A, Boldyrev A. Pinealon increases cell viability by suppression of free radical levels and activating proliferative processes. Rejuvenation Res. 2011;14(5):535-541. doi:10.1089/rej.2011.1172. PMID 21978084.

6. 6

   Khavinson VKh, Lin'kova NS, Tarnovskaya SI, Umnov RS, Elashkina EV, Durnova AO. Short peptides stimulate serotonin expression in cells of brain cortex. Bull Exp Biol Med. 2014;157(1):77-80. doi:10.1007/s10517-014-2496-y. PMID 24909721.

7. 7

   Arutjunyan A, Kozina L, Stvolinskiy S, Bulygina Y, Mashkina A, Khavinson V. Pinealon protects the rat offspring from prenatal hyperhomocysteinemia. Int J Clin Exp Med. 2012;5(2):179-185. PMID 22567179. Animal study, rats. No DOI registered.

8. 8

   Nazimko VA, Morgul' EV, Petrova OA, Sheikhova RG, Kozina LS, Savenko MA, Lysenko DS. [Analysis of some parameters of biological age and adaptation possibilities of workers of locomotive brigades]. Adv Gerontol. 2012;25(1):57-62. PMID 22708445. Russian language, English abstract indexed in MEDLINE. No DOI registered.

9. 9

   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]. Adv Gerontol. 2015;28(1):62-67. PMID 26390612. Russian language, English abstract indexed in MEDLINE. No DOI registered.

10. 10

    Bashkireva AS, Artamonova VG. [The peptide correction of neurotic disorders among professional truck-drivers]. Adv Gerontol. 2012;25(4):718-728. PMID 23734521. Russian language, English abstract indexed in MEDLINE. Carries the PubMed publication type Clinical Trial; the abstract describes an occupational comparison. No DOI registered.

11. 11

    Umnov RS, Linkova NS, Khavinson VKh. [Neuroprotective effects of peptides bioregulators in people of various age]. Adv Gerontol. 2013;26(4):671-678. PMID 24738258. Reference 11 of the 2020 Molecules review, and the document its 72-patient statement rests on. Publication types Journal Article and Review, Russian language. No DOI registered.

12. 12

    PubChem Compound Summary CID 10273502, Glu-Asp-Arg. National Library of Medicine. Queried 4 August 2026 through the PUG REST interface: the names pinealon and Glu-Asp-Arg both resolve to this record, formula C15H26N6O8, molecular weight 418.40, CAS 175175-23-2. pubchem.ncbi.nlm.nih.gov, CID 10273502.

13. 13

    ClinicalTrials.gov, U.S. National Library of Medicine. Registry searched 4 August 2026 through the version 2 API. The query term pinealon returned a total count of zero. clinicaltrials.gov, pinealon query. The sequence returned a total count of zero when the query term was the quoted phrase Glu-Asp-Arg. clinicaltrials.gov, quoted sequence query. The same term unquoted returns a total count of 26, and reading all 26 records shows why the quoted form is the one reported: they match on the separate amino acid names, mostly in protein and nutrition studies, and not one of the 26 names this tripeptide or pinealon anywhere in its record. The same endpoint queried for semaglutide the same day returned 757 studies, which is the control showing it answers when there is something to find.

14. 14

    U.S. Food and Drug Administration, openFDA. Drugs@FDA endpoint queried on generic name pinealon and drug labeling endpoint queried on pinealon, both on 4 August 2026, both returning NOT_FOUND. api.fda.gov, Drugs@FDA query. The same labeling query run for semaglutide the same day returned 18 records, which is the control showing the endpoint answers when there is something to find.

Related pages

Around this page: five neighboring pages on reading a compound record, and on the paperwork that describes a powder.

• PE 22-28 explained: another compound whose entire literature fits on one screen, read the same way.
• How to read a COA: what a certificate settles about a container, and what it leaves open.
• What purity does not tell you: why a high percentage is not an answer to what the molecule is.
• What a lyophilized peptide is: the vial format, and the questions that arrive with it.
• Micrograms against milligrams: the unit gap that makes two numbers look comparable when they are not.

The evidence series: each new compound record we read end to end appears first in The Decadewise briefing.