Other compounds

Pinealon

Updated · 27 sources · Editorial policy

Pinealon is the trade name for a synthetic tripeptide, a chain of three amino acids: glutamic acid, aspartic acid and arginine. In the scientific literature it is usually called EDR (Glu-Asp-Arg). It comes from Vladimir Khavinson’s group at the St. Petersburg Institute of Bioregulation and Gerontology in Russia, which describes it as a “neuroprotective” peptide bioregulator for the brain. Online it is marketed for memory, cognition and “brain aging.”

The single most important fact: no randomized, placebo-controlled trial of pinealon has been published in the indexed literature, and nearly all of the research involves one research group and its collaborators. The evidence consists of cell-culture work, rodent studies and a handful of small, mostly Russian-language human reports whose abstracts do not describe randomization, blinding or a placebo group. Pinealon is not an FDA-approved drug.

This page summarizes what the published laboratory, animal and human reports show. It is for education only and is not medical advice.

Property Detail
Class Synthetic tripeptide (Glu-Asp-Arg); one of the Khavinson “peptide bioregulators”
Other names EDR, EDR peptide, H-Glu-Asp-Arg-OH, L-glutamyl-L-aspartyl-L-arginine
Formula and weight C₁₅H₂₆N₆O₈, 418.40 g/mol (PubChem)
CAS number 175175-23-2 (PubChem synonym list)
Origin Described by its developers as a tripeptide isolated from Cortexin, a polypeptide extract of calf brain cortex
Human data A few small Russian reports in older adults, workers and patients after brain injury; no randomized, placebo-controlled trial found
Studied doses 100 µg capsule twice daily for 2 weeks in one occupational study; 10–400 µg/kg by injection into the abdomen in rodents
Half-life Unknown. We found no published pharmacokinetic study in humans or animals
US status Not an FDA-approved drug; two bulk-ingredient listings exist in FDA’s NDC directory, which does not imply approval
WADA Not named on the 2026 list; class S0 covers substances with no government approval for human therapeutic use

What it is

EDR is the tripeptide L-glutamyl-L-aspartyl-L-arginine. PubChem lists “pinealon” and “Pinealon acetate salt form” as synonyms of the same compound (PubChem).

The name suggests a link to the pineal gland, but the developers describe a different origin. A 2020 review by Khavinson and colleagues calls EDR “a tripeptide isolated from the polypeptide neuroprotective drug Cortexin” (Khavinson et al., Molecules 2020). A 2019 paper from the same circle describes EDR as a synthesized derivative of Cortexin, which it calls a clinically approved calf cerebral cortex polypeptide complex (Kuznik et al., Mol Biol (Mosk) 2019). Pinealon should not be confused with epitalon (Ala-Glu-Asp-Gly), the group’s pineal tetrapeptide.

Pinealon belongs to a family of short peptides the group promotes as tissue-specific bioregulators. Others in the library include epitalon, cartalax, thymalin, thymagen and vilon. In Russian reports pinealon is often given together with vesugen, a related tripeptide (Lys-Glu-Asp) promoted for blood vessels.

How it works in the body

Nobody has shown how EDR acts in people. The group proposes that short peptides enter cells, reach the nucleus and bind DNA or histone proteins, switching genes on or off (Khavinson et al., Molecules 2020). The evidence offered for this includes:

  • Cell entry. A fluorescent-labeled version of pinealon was seen in the cytoplasm, nucleus and nucleolus of HeLa cells (a human cancer cell line), and in test tubes it changed the fluorescence of short DNA strands in a sequence-dependent way (Fedoreyeva et al., Biochemistry (Mosc) 2011).
  • DNA binding in solution. A physics group at St. Petersburg State University reported, using spectroscopy, NMR and computer simulation, that EDR can partly enter the major groove of DNA, an effect helped by magnesium ions (Silanteva et al., J Phys Chem B 2019).
  • Computer docking. Docking models predicted EDR binding sites in the promoter regions of genes such as CASP3, APOE, SOD2 and GAP43 (Khavinson et al., Pharmaceuticals 2021), and binding to the histone H1.3 protein (Kuznik et al., Mol Biol (Mosk) 2019).

Docking models and test-tube binding predict what might happen; they do not show that EDR binds these genes inside living brain cells or changes their activity in people.

Pharmacokinetics

We found no published study measuring EDR’s absorption, distribution, half-life or excretion, in people or in animals. The only work on how it might enter cells is a computer modeling study suggesting it could fit into the binding sites of the LAT1, LAT2 and PEPT1 transporters (Khavinson et al., Biomolecules 2023). Whether intact EDR survives digestion after oral use, or reaches the brain after any route, has not been reported. Half-life figures quoted online are not based on published measurements.

Regulatory status

  • Not an approved drug in the US. A search of FDA’s drug approvals database (Drugs@FDA, via openFDA) returned no product containing pinealon. We found no FDA or EMA approval.
  • Bulk-ingredient listings. FDA’s National Drug Code (NDC) directory contains two “bulk ingredient” entries named pinealon and pinealon acetate, submitted by chemical suppliers (openFDA NDC query). FDA states that inclusion in the directory “does not indicate that FDA has verified the information provided or that the products are FDA-approved” (FDA NDC Directory).
  • Compounding. Pinealon was not named on FDA’s page of bulk substances that may present significant safety risks when we checked; that page does name the related peptide epitalon (FDA, 2026). Absence from that page does not mean pinealon has been reviewed or found safe.
  • Sport. Pinealon is not named on the 2026 WADA Prohibited List. Class S0 bans, at all times, any pharmacological substance “with no current approval by any governmental regulatory health authority for human therapeutic use” (WADA 2026 Prohibited List). We found no WADA ruling specific to pinealon.

What the research shows

Almost every study below has Khavinson or staff of his St. Petersburg institute as authors, or used peptide supplied through that network. A few human reports come from other Russian clinical and occupational-health groups, such as one in Ekaterinburg. We found no replication by a group outside Russia. Many papers are short Russian-language articles for which only an abstract is available.

Human evidence

We found no randomized, placebo-controlled trial of pinealon. The human reports we found are summarized below. None of the abstracts describes randomization or blinding, and most do not report effect sizes.

Study Who and how many Peptide and dose Reported result
Nazimko et al., Adv Gerontol 2012 Locomotive crew workers; number not given in abstract Pinealon, 100 µg capsule twice daily, 2 weeks “Improved parameters of biological age” and adaptation markers; no figures given
Bashkireva and Artamonova, Adv Gerontol 2012 150 male truck drivers vs 150 metal workers (survey of neurotic symptoms) Several peptides; best effect with pinealon plus vesugen; dose not given Improved psychoemotional scores; how many received peptides, and against what comparison, is not stated
Meshchaninov et al., Adv Gerontol 2015 32 people aged 41–83 with several chronic diseases and organic brain syndrome in remission Pinealon and vesugen; dose not given Slower “biological age” by the authors’ indicators; vesugen had the larger effect. Also found pro-oxidant activity and a fall in blood CD34+ cells, which the authors read as inhibition of blood-cell production
Myakotnykh et al., Adv Gerontol 2016 110 people of different ages, comparing several “geroprotective” methods Vesugen and pinealon; dose not given Largest effect on biological-age indicators with the two peptides combined; massage and the peptides were judged the safest methods

A 2020 review by the group adds that oral pinealon, given with standard therapy to 72 patients with long-term effects of traumatic brain injury, improved memory and reduced headaches (Khavinson et al., Molecules 2020). It cites for this a Russian-language review (Umnov et al., Adv Gerontol 2013) and a patent, not a peer-reviewed trial report, so the design, dose, controls and outcome measures cannot be checked.

“Biological age” in these studies is a composite score built by the researchers from several clinical and lab measurements. It is not a validated endpoint for any drug approval, and changes in it do not show that a person will stay healthier or live longer.

Nerve cells in culture

Study Model Reported finding
Khavinson et al., Rejuvenation Res 2011 Rat cerebellar neurons, immune cells (neutrophils) and PC12 cells under oxidative stress Dose-dependent reduction in reactive oxygen species (ROS) and fewer necrotic (dying) cells; delayed activation of the ERK1/2 signaling pathway
Kraskovskaya et al., Bull Exp Biol Med 2017 Mouse hippocampal neurons exposed to amyloid (an in-vitro model of Alzheimer’s disease) EDR at 200 ng/mL raised the number of “mushroom” dendritic spines (mature synapse sites) by 71%, back to normal levels
Kraskovskaya et al., Int J Mol Sci 2024 Neurons made from skin cells of elderly human donors EDR, KED and AEDG increased dendrite branching; EDR reduced oxidative DNA damage; no effect on mitochondria, lysosomes or the aging marker p16
Khavinson et al., Bull Exp Biol Med 2014 Aging brain cortex cell cultures EDR and KED increased serotonin expression

Not every laboratory result fits the “antioxidant” label. In a 2008 Russian study, pinealon and related peptides showed no direct antioxidant activity and raised the resting level of reactive oxygen species inside neurons, while lowering the share of dead cells (Kozina et al., Adv Gerontol 2008). In rat pineal gland cultures, EDR did not change the apoptosis marker AIF, and only epitalon stimulated the secretory marker the authors measured (Khavinson et al., Bull Exp Biol Med 2011).

Animal studies

Model Main reported result
5xFAD mice, a genetic Alzheimer’s model; 400 µg/kg by injection into the abdomen daily for 2 months; 10 mice per group in the plasticity experiment (Khavinson et al., Pharmaceuticals 2021) EDR raised dendritic spine density in the hippocampus by 11% (p = 0.039), to the level of control mice. It did not significantly change the number of mushroom spines, and its trend toward restoring long-term potentiation (a cellular basis of memory) was not statistically significant
Pregnant rats fed excess methionine to raise homocysteine; 10 µg/kg by abdominal injection for 5 days before loading; 23 offspring per group (Arutjunyan et al., Int J Clin Exp Med 2012) Offspring of treated mothers had better water-maze learning, normal 10-day weight (25.03 vs 17.86 g in untreated methionine-loaded litters) and cerebellar neurons more resistant to oxidative stress. Offspring homocysteine stayed high (10.5 vs 9.8 µM)
Animal model of low-pressure (hypobaric) hypoxia; species not given in the abstract (Kozina, Adv Gerontol 2008) Pinealon had the strongest anti-hypoxic effect of four peptides tested (vilon, epitalon, vesugen, pinealon)
Old rats with carotid artery occlusion (Mendzheritskii et al., Adv Gerontol 2011) Pinealon and Cortexin improved survival; pinealon reduced exploratory and motor behavior and moderately raised brain caspase-3 (an enzyme of programmed cell death)
Young and old rats under acute hypoxia (Mendzheritski et al., Adv Gerontol 2013; Mendzheritskii et al., Adv Gerontol 2014) Pinealon improved water-maze learning more than Cortexin and changed regional caspase-3 activity and blood cytokines; no figures in the abstracts

Doses, routes and group sizes are missing from most of the Russian abstracts. The rodent doses cannot be translated into human doses, and none of these studies tested safety.

Side effects and risks

No human safety data

No published study has systematically assessed pinealon’s safety in people. There are no reported toxicology studies (acute, repeat-dose, reproductive or genotoxicity), no dose-response data, and no drug interaction data. Its effects in pregnancy, breastfeeding, children and people with kidney, liver, psychiatric or neurological disease are unknown. Reviews by the developers describe peptide bioregulators as free of side effects (Khavinson et al., Molecules 2020), but none of the human reports was designed or large enough to detect them.

Signals worth noting

Two of the group’s own reports point in a less reassuring direction. One human study found pro-oxidant activity and a fall in circulating CD34+ blood stem cells, which the authors interpreted as “significant inhibition of hemopoiesis” (blood-cell formation) (Meshchaninov et al., Adv Gerontol 2015). A cell study found raised intracellular reactive oxygen species with pinealon and related peptides (Kozina et al., Adv Gerontol 2008). Neither finding has been followed up.

Product quality

Products sold online as pinealon are not regulated drugs in the US. Their identity, purity, dose per capsule or vial, and (for injectable forms) sterility are not independently verified. Injected peptides with impurities or aggregates can trigger immune reactions, a concern FDA has raised for similar research peptides such as epitalon (FDA, 2026).

Key takeaways

  • A three-amino-acid peptide. Pinealon is the trade name for EDR (Glu-Asp-Arg), developed by Khavinson’s group in St. Petersburg; despite the name, its developers describe it as derived from the calf brain extract Cortexin.
  • Not an approved drug. We found no FDA or EMA approval; NDC bulk-ingredient listings are not approvals, and WADA’s S0 class bans substances without any government approval for human therapy.
  • No controlled human trials. Human data are a few small Russian reports on “biological age,” mood scores and recovery after brain injury, without described randomization, blinding or placebo.
  • Evidence is from one research network. Nearly every study involves the same institute or its collaborators, often as abstract-only Russian papers, with no replication outside Russia.
  • Laboratory and rodent results only. EDR reduced oxidative stress in nerve cell cultures and modestly improved spine density and learning in rodent models, with mixed and sometimes non-significant results.
  • Pharmacokinetics and safety are unknown. No half-life, absorption or toxicology data have been published, and one human report noted reduced blood stem cells.

Sources

  1. National Center for Biotechnology Information. PubChem compound summary for CID 10273502, Glu-Asp-Arg (pinealon). PubChem.
  2. Khavinson V, Linkova N, Kozhevnikova E, et al. EDR Peptide: Possible Mechanism of Gene Expression and Protein Synthesis Regulation Involved in the Pathogenesis of Alzheimer’s Disease. Molecules. 2020;26(1):159. PubMed.
  3. Kuznik BI, Davydov SO, Popravka ES, et al. Epigenetic mechanisms of peptide-driven regulation and neuroprotective protein FKBP1b. In Russian. Mol Biol (Mosk). 2019;53(2):339–348. PubMed.
  4. Fedoreyeva LI, Kireev II, Khavinson VKh, et al. 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. PubMed.
  5. Silanteva IA, Komolkin AV, Morozova EA, et al. Role of Mono- and Divalent Ions in Peptide Glu-Asp-Arg-DNA Interaction. J Phys Chem B. 2019;123(9):1896–1902. PubMed.
  6. Khavinson V, Ilina A, Kraskovskaya N, et al. Neuroprotective Effects of Tripeptides-Epigenetic Regulators in Mouse Model of Alzheimer’s Disease. Pharmaceuticals (Basel). 2021;14(6):515. PubMed.
  7. Khavinson VK, Linkova NS, Rudskoy AI, et al. Feasibility of Transport of 26 Biologically Active Ultrashort Peptides via LAT and PEPT Family Transporters. Biomolecules. 2023;13(3):552. PubMed.
  8. Food and Drug Administration. openFDA NDC directory query: pinealon. Accessed October 2026. openFDA.
  9. Food and Drug Administration. National Drug Code Directory. Content current as of March 4, 2026. FDA.
  10. Food and Drug Administration. Certain bulk drug substances for use in compounding that may present significant safety risks. Content current as of April 22, 2026. FDA.
  11. World Anti-Doping Agency. The 2026 Prohibited List. In effect January 1, 2026. WADA.
  12. Nazimko VA, Morgul’ EV, Petrova OA, et al. Analysis of some parameters of biological age and adaptation possibilities of workers of locomotive brigades. In Russian. Adv Gerontol. 2012;25(1):57–62. PubMed.
  13. Bashkireva AS, Artamonova VG. The peptide correction of neurotic disorders among professional truck-drivers. In Russian. Adv Gerontol. 2012;25(4):718–728. PubMed.
  14. Meshchaninov VN, Tkachenko EL, Zharkov SV, et al. Effect of synthetic peptides on aging of patients with chronic polymorbidity and organic brain syndrome of the central nervous system in remission. In Russian. Adv Gerontol. 2015;28(1):62–67. PubMed.
  15. Myakotnykh VS, Torgashov MN, Egorin KV, et al. Comparative analysis of different methods of geroprotective. In Russian. Adv Gerontol. 2016;29(4):594–601. PubMed.
  16. Umnov RS, Lin’kova NS, Khavinson VKh. Neuroprotective effects of peptides bioregulators in people of various age. In Russian. Adv Gerontol. 2013;26(4):671–678. PubMed.
  17. Khavinson V, Ribakova Y, Kulebiakin K, et al. Pinealon increases cell viability by suppression of free radical levels and activating proliferative processes. Rejuvenation Res. 2011;14(5):535–541. PubMed.
  18. Kraskovskaya NA, Kukanova EO, Lin’kova NS, et al. Tripeptides Restore the Number of Neuronal Spines under Conditions of In Vitro Modeled Alzheimer’s Disease. Bull Exp Biol Med. 2017;163(4):550–553. PubMed.
  19. Kraskovskaya N, Linkova N, Sakhenberg E, et al. Short Peptides Protect Fibroblast-Derived Induced Neurons from Age-Related Changes. Int J Mol Sci. 2024;25(21):11363. PubMed.
  20. Khavinson VKh, Lin’kova NS, Tarnovskaya SI, et al. Short peptides stimulate serotonin expression in cells of brain cortex. Bull Exp Biol Med. 2014;157(1):77–80. PubMed.
  21. Kozina LS, Arutiunian AV, Stvolinskiĭ SL, et al. Biological activity of regulatory peptides in model experiments in vitro. In Russian. Adv Gerontol. 2008;21(1):68–73. PubMed.
  22. Khavinson VKh, Linkova NS, Chalisova NI, et al. Effect of short peptides on expression of signaling molecules in organotypic pineal cell culture. Bull Exp Biol Med. 2011;152(1):138–141. PubMed.
  23. Arutjunyan A, Kozina L, Stvolinskiy S, et al. Pinealon protects the rat offspring from prenatal hyperhomocysteinemia. Int J Clin Exp Med. 2012;5(2):179–185. PubMed.
  24. Kozina LS. Investigation of antihypoxic properties of short peptides. In Russian. Adv Gerontol. 2008;21(1):61–67. PubMed.
  25. Mendzheritskiĭ AM, Karantysh GV, Ivonina KO. Effects of introduction of short peptides before carotid artery occlusion on behaviour and caspase-3 activity in the brain of old rats. In Russian. Adv Gerontol. 2011;24(1):74–79. PubMed.
  26. Mendzheritski AM, Karantysh GV, Abramchuk VA, et al. Effect of peptide geroprotectors on the navigation system learning and caspase-3 in brain structures in rats of different age. In Russian. Adv Gerontol. 2013;26(2):252–257. PubMed.
  27. Mendzheritskiĭ AM, Karantysh GV, Ryzhak GA, et al. 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. In Russian. Adv Gerontol. 2014;27(1):94–97. PubMed.