Pinealon Research: What the EDR Studies Show
Dr. Sieglinde Klaus
Scientific Editorial Team · Bergdorf Bioscience
Table of Contents
- 01What Is Pinealon, and What Do EDR Studies Measure?
- 02What Did the Work on Human Induced Neurons Show?
- 03What Changed at the Dendrites in the 5xFAD Model?
- 04What Did the Prenatal Hyperhomocysteinemia Model Show?
- 05How Does EDR Affect Oxidative Stress and Cell Death?
- 06Which Molecular Findings Support the Gene Regulation Hypothesis?
- 07What Did Aged Rats Show Under Hypoxia and Mild Hypothermia?
- 08What Do Human Reports Say About Pinealon?
- 09How Does Pinealon Differ From Related Short Peptides?
- 10What Do the Studies Support, and How Is the Material Positioned?
- 11Which Questions About Pinealon Are Asked Most Often?
- What Benefits Do the EDR Studies Show?
- Is Pinealon an Antioxidant?
- Are There Human Studies of Pinealon?
- Is Dendrite Growth Proof of Neuroprotection?
- Where Can I Find the Research Material?
- 12Which Original Papers Underpin This Article?
Pinealon is a synthetic tripeptide composed of glutamic acid, aspartic acid and arginine, sequence Glu-Asp-Arg or EDR. The most informative findings: human nerve cells derived from skin fibroblasts of older donors formed 28 percent more primary neurites and 46 percent more total length under EDR. In the 5xFAD mouse model, spine density increased. Offspring of methionine-loaded rats found the platform in the water maze sooner, and in hypoxia models EDR altered caspase-3 and cytokines. Four human reports add to this, including studies with 150 professional drivers and 110 patients. The data come from cell cultures, animals and human cells. Pinealon as an EDR research peptide
Key findings at a glance:
- Human induced neurons (2024): 28 percent more primary neurites (p=0.0208) and 46 percent more total dendrite length (p=0.0332) after ten days of EDR.
- 5xFAD mouse model (2021): spine density at CA1 rose from 11.31 to 12.64 (p=0.039); LTP did not change significantly.
- Rat offspring after prenatal hyperhomocysteinemia (2012): search time in the first trial 137 instead of 170 seconds (p<0.05); no group difference remained by the fifth trial.
- Cell and molecular studies (2008 to 2019): EDR bound to DNA, altered ROS and cell death markers and stimulated serotonin expression in aging cortical cell cultures.
- Human reports (2012 to 2016): four observations, including 150 professional drivers and 110 patients; several tested combinations of Pinealon and Vesugen, none an isolated placebo-controlled EDR study.
What Is Pinealon, and What Do EDR Studies Measure?
In the experimental literature, Pinealon refers to the tripeptide Glu-Asp-Arg. E, D and R are the one-letter symbols for glutamic acid, aspartic acid and arginine; EDR is the shorthand for the sequence. The 28 original papers with EDR-specific data measure ROS, cell death, DNA binding, serotonin expression, neurite length, dendritic spines, LTP, swimming times, caspase-3, cytokines and biological aging parameters. A short definition and the classification of the substance are in the Pinealon lexicon.
The levels stay separate: a cell assay answers a different question than a water maze, and spine density is not a memory test. The following list sorts the endpoints and the models:
- Cell stress, cell death and proliferation: ROS, propidium iodide, ERK1/2, cell cycle, Ki-67 and p53 in cell and tissue cultures.
- Neurite morphology: primary neurites and total dendrite length in human cortical neurons reprogrammed from fibroblasts.
- Synapse structure and function: spine density and LTP in hippocampal slices from 5xFAD mice.
- Behavior and ex vivo oxidative stress: Morris water maze and isolated cerebellar neurons in offspring of methionine-loaded rats, plus learning tests in young and old rats.
- Hypoxia and neurochemistry: adrenergic mediators, serotonin, cytokines and caspase-3 in rats under hypoxia, hypothermia or carotid occlusion.
- Human parameters: biological aging parameters, adaptation, chemiluminescence and CD34-positive blood cells in four observations.
Pinealon is not the same as Epitalon, Vesugen, Pineamin or Cortexin. In the literature Epitalon is referred to as AEDG and Vesugen as KED; both have different sequences. Pineamin is a pineal peptide preparation, Cortexin a preparation from bovine cerebral cortex. A PubMed hit on DREL from Jiuzao likewise concerns a different substance. Anyone who transfers data from one preparation to another loses the link to the substance that was actually studied.
What Did the Work on Human Induced Neurons Show?
In 2024, EDR increased primary neurites of human cortical neurons by 28 percent and total dendrite length by 46 percent. Kraskovskaya and colleagues worked with cells that had been reprogrammed directly into neurons from skin fibroblasts of three female donors (61, 66, 68 years). Exposure was 10 micrograms per milliliter daily for ten days after neuronal differentiation. Analysis used MAP2-stained confocal images with NeuronStudio. Kraskovskaya et al., 2024
Primary neurites rose from 4.59±0.3 to 5.87±0.5 (p=0.0208), total dendrite length by 46 percent (p=0.0332). EDR, KED and AEDG were tested separately against untreated cells. AEDG (+34 percent, p=0.0046) and KED (+32 percent, p=0.0093) were stronger than EDR for primary neurites.
Not every measurement in this study was positive. The DNA damage marker 8-OHdG/DAPI fell numerically from 0.40±0.04 to 0.31±0.03 but did not reach statistical significance at p=0.0566. The authors describe the reduction in places as significant; the p-value does not support that. This is a trend, not confirmed DNA protection. Mitochondrial and lysosomal activity and the cell aging markers p16 and Lamin B1 also did not change significantly. Kraskovskaya et al., 2024
Other cell and tissue models show how strongly the result depends on age and tissue. In organotypic skin explants from young rats, the tripeptide T-33, that is Glu-Asp-Arg, promoted proliferation; in explants from old rats this effect was not pronounced, and T-38, that is Lys-Glu-Asp, acted there. Proliferation rose through lower apoptosis, measured at p53. Voicekhovskaya et al., 2012 In an organotypic pineal culture, AEDG and KED stimulated the proliferation marker Ki-67; EDR influenced neither Ki-67 nor the apoptosis marker AIF. Khavinson et al., 2011
What Changed at the Dendrites in the 5xFAD Model?
In the 5xFAD mouse model, EDR increased total spine density on CA1 neurons from 11.31±0.36 to 12.64±0.31 per 10 micrometers of dendrite (p=0.039). Electrophysiological long-term potentiation (LTP), by contrast, did not change significantly. Khavinson and colleagues treated 5xFAD and 5xFAD-M mice for two months intraperitoneally with EDR or KED. Ten animals were examined per group, five per sex. Hippocampal slices were studied with electrophysiological LTP measurement and confocal morphometry of CA1 spines; the dose was 400 micrograms per kilogram daily. Khavinson et al., 2021 Two further spine models add to the picture: in an Aβ synaptotoxicity culture, EDR at 200 ng/ml increased mushroom spines by 71 percent, KED by 20 percent. Kraskovskaya et al., 2017 In the YAC128 Huntington model, spine density was reduced from 8.4±0.7 to 5.5±0.4 per 10 micrometers (−34 percent); EDR at 200 ng/ml raised it to wild-type level without statistical significance. Khavinson et al., 2017
The combination is revealing: a structural measure improved, a functional one did not. More spines do not automatically mean stronger synaptic transmission. Conversely, unchanged LTP does not rule out a structural effect. Anyone who infers better cognition from density alone skips exactly the step the study leaves open.
The in silico analysis yields a hypothesis, not a measurement of gene regulation. For the spine shape subgroups, the percentages in the text are not fully consistent; for classification, the robust total density and the clear null LTP result are the better basis.
In 2025, panels 5 and 8 of the paper were corrected. They had originally been identical but labeled differently. The authors state that the conclusions remain unchanged. This is an image correction, not a retraction of the study. Correction 2025
What Did the Prenatal Hyperhomocysteinemia Model Show?
In 2012, offspring of methionine-loaded mothers found the platform faster on the second training day if they had received maternal Pinealon: 137 seconds compared with 170 seconds (p<0.05). The control group needed 112 seconds. By the fifth learning trial the group difference was gone. Arutjunyan and colleagues gave Pinealon on five days before methionine loading at 10 µg/kg i.p.; they studied six litters per group and 23 young animals per group in the Morris water maze. Behavioral testing took place at 45 days of age, and the isolated cerebellar neurons came from 10-day-old offspring. Arutjunyan et al., 2012
The second part of the study concerns oxidative stress. After an additional H2O2 challenge, propidium iodide-positive cells were 7.0±0.9 percent instead of 17.7±2.1 percent, and DCF fluorescence as an indicator of oxidative stress was 108.6±4.1 instead of 158.7±3.8 (p<0.05 in each case). The basal DCF signal, by contrast, did not differ substantially (54.2 versus 51.6). The positive finding concerns the response to an added stimulus, not the resting value.
Two limitations: first, homocysteine remained elevated in plasma. In this model Pinealon did not change the trigger but part of its consequences. Second, swimming speed is a possible confounder of search time; a difference in swimming behavior can mimic or amplify a learning deficit. The early trials show an advantage in finding the platform, the fifth trial no longer does. That pattern speaks for faster early adaptation, not for persistently better learning.
A second hypoxia experiment adds to this finding. In a model of hypobaric hypoxia, Pinealon showed the strongest antihypoxic effect among four short peptides. The authors attribute it less to direct inhibition of the ROS rise than to stimulation of the body's own antioxidant systems and a possible limitation of NMDA excitotoxicity. Kozina, 2008 In female rats with methionine loading, Pinealon also corrected the disturbed diurnal rhythm of norepinephrine in the medial preoptic hypothalamus. Korenevskii et al., 2014
How Does EDR Affect Oxidative Stress and Cell Death?
The cell studies do not show a uniform antioxidant picture: in one model EDR limited ROS and necrotic cell death, in another it raised intracellular ROS levels but lowered the share of dead neurons. The 2011 paper studied Pinealon in cerebellar granule cells, neutrophils and PC12 cells under oxidative stress. The measurements covered the accumulation of reactive oxygen species, propidium iodide as a marker of necrotic cell death, the time course of ERK1/2 activation and the cell cycle distribution. Pinealon limited ROS and necrotic cell death in a concentration-dependent manner. ERK1/2 activation began with a delay. The cell cycle changes persisted at concentrations where the ROS and cell death effects were already saturated. Khavinson et al., 2011
The temporal separation argues for at least two processes: with a nonspecific stress response, the fall in ROS, the protection from cell death and ERK1/2 activation would saturate at the same time; yet the cell cycle effect keeps increasing. It does not, however, establish a DNA mechanism; the genomic explanation is an inference from the findings, not a directly measured target.
The second paper from 2008 challenges the picture of a pure antioxidant. Pinealon, Vesugen, Vilon and Epitalon showed no direct antioxidant activity in vitro. They did, however, limit lipid peroxidation of human lipoproteins, presumably by changing their structure, and increased the stability of red blood cells against osmotic hemolysis. At the same time the steady-state intracellular ROS level rose, while the share of dead cells in the neuronal population fell; Epitalon was the exception. Kozina et al., 2008
Pinealon is not a classical antioxidant. The data argue for a modulation of stress and survival pathways; a raised ROS level can be an adaptation signal in cell culture. That explains the opposing ROS findings. The study is accessible only as an abstract; concentrations and cell origin cannot be checked from it.
Which Molecular Findings Support the Gene Regulation Hypothesis?
Three independent methods support a direct interaction of EDR with DNA: nuclear localization in HeLa cells, physical binding to the major groove and a docking model for serotonin synthesis. That does not prove regulation of genes in the living brain. Fedoreyeva and colleagues labeled EDR with FITC and found the fluorescence also in the nucleus of HeLa cells. Unlabeled peptides quenched the fluorescence of oligonucleotides in a sequence- and methylation-dependent manner; for Pinealon the authors describe a preference for CAG-containing sequences. Fedoreyeva et al., 2011
The biophysics of 2019 goes a step further. Silanteva and colleagues studied the EDR-DNA interaction with spectroscopy, NMR, viscometry and molecular dynamics. According to that work, EDR partly penetrates the major groove of DNA and mainly influences atoms N7 and O6 of guanine. Magnesium ions promote binding by shielding the negatively charged phosphate groups of DNA; this effect persists in saline solution. Silanteva et al., 2019
The work comes from an independent physics group at St. Petersburg State University, not from the gerontological network. It shows a physical binding, not a biological consequence. Whether it takes place in the nucleus under physiological conditions and which genes are affected remains open. A third binding study showed sequence-specific binding to FITC-labeled wheat histones. Fedoreyeva et al., 2013 In an in silico comparison of 26 short peptides, EDR also had the best ICM score at LAT1 (−45.32). Khavinson et al., 2023
A third component concerns serotonin. In aging cultures of brain cortex cells, EDR and KED stimulated the expression of serotonin. By molecular docking the authors found a complementary CCTGCC sequence in the gene of 5-tryptophan hydroxylase, the key enzyme of serotonin synthesis. They interpret the finding as epigenetic regulation of serotonin synthesis and as a hint of neuro- and geroprotective activity. Khavinson et al., 2014
Cell culture and docking remain two levels: increased serotonin expression does not replace a measurement in the living animal. Between binding and effect lie uptake, distribution, concentration at the target site, chromatin binding and transcriptional change; none of these steps is fully measured for Pinealon in the brain.
What Did Aged Rats Show Under Hypoxia and Mild Hypothermia?
In hypoxia and hypothermia models Pinealon changes neurotransmitters, cytokines and caspase-3; the findings are positive but mixed. In 18-month-old rats, Pinealon and Cortexin raised adrenergic mediators under acute hypobaric hypoxia; under mild hypothermia serotonin rose in the cortex. Cortexin acted more strongly than Pinealon on radical processes and caspase-3. Mendzheritsky and colleagues compared the two preparations in a stress model, not in a memory test. Mendzheritsky et al., 2015 In metabolic models Pinealon influenced the expression of Grin1, Grin2b and Grin2d in diabetic rats; 100 ng/kg was the most favorable. Karantysh et al., 2020 A conference paper reports similar advantages for SOD1, GPX4 and GSR. Fomenko et al., 2020
A follow-up study examined old rats under acute hypoxic hypoxia. Pinealon was associated with a reduction in neuroinflammatory responses and with support for neurogenesis; Cortexin lowered apoptotic activity but left interleukin-6 elevated. The authors describe the Pinealon findings as approaching a reference level. Mendzheritsky et al., 2014 A third paper compared young and old: under hypoxia Pinealon improved learning performance in the Morris maze in young and old rats more than Cortexin, accompanied by regional changes in caspase-3 activity in cortex and brainstem. Mendzheritsky et al., 2013
A fourth experiment shows the limits. Before a carotid occlusion, Pinealon improved the survival rate of old rats. Behavioral parameters were mixed, and caspase-3 activity rose moderately, both in sham-operated animals and in the occlusion model. Mendzheritsky et al., 2011 Caspase-3 is not an unambiguous protective marker: depending on the region, activity rises or falls; a single value does not establish neuroprotection.
Together, Pinealon shifts neurotransmitters, cytokines and apoptotic markers. Effect sizes are missing from the abstracts, group sizes are not consistently reported, and several papers come from the same group. The positive learning finding in old rats nevertheless goes beyond cell culture.
What Do Human Reports Say About Pinealon?
Four human reports between 2012 and 2016 examined Pinealon-containing preparations in professional drivers, locomotive workers and older patients. They report more favorable adaptation and aging parameters but do not isolate EDR. The largest study covered 150 male professional drivers and 150 male metal workers as a comparison group. Among the drivers, occupationally unstable psychological adaptation patterns and borderline disorders predominated. The use of bioregulating peptides improved psychoemotional indices and stress resistance and lowered the risk of occupation-related borderline disorders (p<0.001 to 0.05). The best effect occurred with combined administration of several cytogenes, especially Pinealon plus Vesugen. Bashkireva and Artamonova, 2012
The second larger study examined 110 people of different age groups and compared several geroprotective methods: dry carbon dioxide baths, hyperbaric oxygenation, therapeutic massage and oligopeptide preparations with Vesugen and Pinealon. The strongest positive effect on biological aging parameters came from the combined use of the two oligopeptide complexes. Massage and oligopeptides were the safest with regard to biochemical and immunological parameters; the carbon dioxide baths and hyperbaric oxygenation had limitations and contraindications. Myakotnykh et al., 2016
The two smaller reports add to the picture. Nazimko and colleagues described employees of locomotive crews who received an oral capsule preparation labeled Pinealon for two weeks; they reported more favorable biological age parameters and adaptive responses, without information on group size, randomization or control. Nazimko et al., 2012 Meshchaninov and colleagues examined people aged 41 to 83 years with chronic multimorbidity and organic brain syndrome in remission. Biological age parameters were more favorable, more so for Vesugen; at the same time there was prooxidative activity and fewer CD34-positive blood cells. The abstract names 32 people but lists 18 men and 12 women. Meshchaninov et al., 2015
The four papers are human observations with limited power; none describes a placebo-controlled administration of Pinealon alone. Effect sizes, randomization and the identity of the administered material are not consistently documented in the abstracts. The CD34 decrease is a notable laboratory finding; from an abstract it does not establish clinically confirmed bone marrow toxicity. A primate report and a preprint add to the picture: in two rhesus monkeys Pinealon shortened learning and reaction time; Kuznetsova et al., 2019 a preprint with five mice per group found a nonsignificant trend toward better working memory. Marín-Jerez et al., 2026
A ClinicalTrials.gov search on 25 October 2026 for “Pinealon” and “EDR peptide” returned no matching registered intervention. The search for “Glu-Asp-Arg” produced one unrelated hit on amino acid mixtures. A name search is not proof that no human research exists; it does show that, as of this data cut, no registered controlled EDR study can be found.
How Does Pinealon Differ From Related Short Peptides?
Pinealon is the tripeptide Glu-Asp-Arg. Related preparations differ in sequence, length or origin; that decides which studies belong to the substance. A single different amino acid changes charge, binding behavior and stability. The following list sorts the main distinctions:
- Pinealon (EDR): Glu-Asp-Arg, three amino acids; the subject of the cell, animal and human reports evaluated here.
- Epitalon/Epithalon (AEDG): Ala-Glu-Asp-Gly, a tetrapeptide; its own body of evidence, not to be equated with EDR.
- Vesugen (KED): Lys-Glu-Asp, a different tripeptide; named separately in several human papers.
- Pineamin: a pineal peptide preparation, not isolated EDR; clinical data on this preparation do not belong to Pinealon.
- Cortexin: a polypeptide preparation from bovine cerebral cortex; the comparator in the rat experiments, not an EDR formulation.
- DREL: a different peptide from Jiuzao; one PubMed hit, not a Pinealon dataset.
- DSIP: a different short peptide with its own research question; the conceptual distinction is set out in the DSIP guide.
For classification, the sequence counts, not the shared discussion. The 2021 and 2024 papers tested EDR, KED and AEDG separately; that is a good example of how related peptides are kept cleanly apart. A similar length does not imply a shared effect, and a shared discussion does not imply that data can be transferred.
What Do the Studies Support, and How Is the Material Positioned?
Across the models a consistent direction emerges: under experimental stress EDR limits cell death, promotes the formation of neuronal processes, raises spine density in an Alzheimer mouse model and binds to DNA. The functional human level is missing. That wording is deliberately positive and precise at the same time: the preclinical findings are consistent, but they are not proof of efficacy in humans.
Three points matter: a large share of the papers comes from the St. Petersburg network around Khavinson and Mendzheritsky; the DNA biophysics of 2019 comes from an independent physics group. Independent replications are missing. The groups are small, several papers are accessible only as abstracts, and data on uptake, distribution and brain exposure are missing.
As a research material, Pinealon is offered as a 10 mg product in vials. The study preparations are not automatically identical with this material; batch, purity and formulation are separate variables. Statements on storage or reconstitution cannot be derived from the studies evaluated here. The Pinealon calculator is available for the pure conversion of mass and volume; it is not linked to a dosing instruction. The product details and vial sizes describe the material on offer.
The next step would be an independent replication with prespecified endpoints, a dose-response curve in human neurons and a controlled human study with a functional endpoint. Until then Pinealon remains a preclinically studied peptide with a concrete morphological signal and an open clinical question.
Which Questions About Pinealon Are Asked Most Often?
What Benefits Do the EDR Studies Show?
The studies report less oxidative stress in cell models, more neurites in human induced neurons, higher spine density in the 5xFAD model and better learning scores in hypoxia models. A functional benefit in humans is not established.
Is Pinealon an Antioxidant?
Not in the classical sense. In one cell model EDR limited ROS and necrotic cell death; in another it raised the intracellular ROS level while lowering the share of dead neurons. The data argue for a modulation of stress and survival pathways, not for simple scavenging of free radicals.
Are There Human Studies of Pinealon?
Yes, four human reports from 2012 to 2016, including 150 professional drivers and 110 patients. Several examined combinations of Pinealon and Vesugen. A placebo-controlled study of isolated EDR cannot be found.
Is Dendrite Growth Proof of Neuroprotection?
No. The findings come from human cells in culture and from mouse models. They show a structural effect on neuronal processes, not protection from a human disease. Neuroprotection would require controlled studies with functional endpoints.
Where Can I Find the Research Material?
The Pinealon product page describes the 10 mg material on offer and the vial sizes. For scientific assessment the original papers linked below are authoritative; the product page is not a study.
Which Original Papers Underpin This Article?
- Kozina LS, Arutiunian AV, Stvolinskiĭ SL, Khavinson VKh (2008). Biological activity of regulatory peptides in model experiments in vitro. Advances in Gerontology 21(1):68-73. PubMed
- Kozina LS (2008). Investigation of antihypoxic properties of short peptides. Advances in Gerontology 21(1):61-67. PubMed
- Khavinson VK, Ribakova NO, Kulebiakin KA et al. (2011). Pinealon increases cell viability by suppression of free radical levels and activating proliferative processes. Rejuvenation Research 14(5):535-541. DOI
- Fedoreyeva LI, Kireev II, Khavinson VK, Vanyushin BF (2011). 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 (Moscow) 76(11):1210-1219. DOI
- Khavinson VKh, Linkova NS, Chalisova NI, Dudkov AV, Koncevaya EA (2011). Effect of short peptides on expression of signaling molecules in organotypic pineal cell culture. Bulletin of Experimental Biology and Medicine 152(1):138-141. DOI
- Mendzheritskiĭ AM, Karantysh GV, Ivonina KO (2011). Effects of introduction of short peptides before carotid artery occlusion on behaviour and caspase-3 activity in the brain of old rats. Advances in Gerontology 24(1):74-79. PubMed
- Voicekhovskaya MA, Chalisova NI, Kontsevaya EA, Ryzhak GA (2012). Effect of bioregulatory tripeptides on the culture of skin cells from young and old rats. Bulletin of Experimental Biology and Medicine 152(3):357-359. DOI
- Arutjunyan AV, Kozina LS, Stvolinskiy SL et al. (2012). Pinealon protects the rat offspring from prenatal hyperhomocysteinemia. International Journal of Clinical and Experimental Medicine 5(2):179-185. PMC
- Nazimko EV, Morgul EV, Petrova IV et al. (2012). Analysis of some parameters of biological age and adaptation possibilities of workers of locomotive brigades. Advances in Gerontology 25(1):57-62. PubMed
- Bashkireva AS, Artamonova VG (2012). The peptide correction of neurotic disorders among professional truck-drivers. Advances in Gerontology 25(4):718-728. PubMed
- Fedoreyeva LI, Smirnova TA, Kolomijtseva GY, Khavinson VKh (2013). Interaction of short peptides with FITC-labeled wheat histones and their complexes with deoxyribooligonucleotides. Biochemistry (Moscow) 78(2):166-175. DOI
- Mendzheritski AM, Karantysh GV, Abramchuk VA, Ryzhak GA (2013). Effect of peptide geroprotectors on the navigation system learning and caspase-3 in brain structures in rats of different age. Advances in Gerontology 26(2):252-257. PubMed
- Khavinson VKh, Linkova NS, Tarnovskaya SI et al. (2014). Short peptides stimulate serotonin expression in cells of brain cortex. Bulletin of Experimental Biology and Medicine 157(1):77-80. DOI
- Korenevskii AV, Arutyunyan AV, Milyutina NP, Zaloznyaya IV (2014). Pinealon corrects hyperhomocysteinemia-induced disturbances of the diurnal dynamics of hypothalamic norepinephrine content in female rats. Neurochemical Journal 8:205-207. DOI
- Mendzheritskiĭ AM, Karantysh GV, Ryzhak GA, Dem'ianenko SV (2014). 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 27(1):94-97. PubMed
- Mendzheritsky AM, Karantysh GV, Ryzhak AP, Prokofiev VN (2015). Pinealon and Cortexin influence on behavior and neurochemical processes in 18-month aged rats within hypoxia and hypothermia. Advances in Gerontology 28(3):532-539. PubMed
- Meshchaninov VN, Tkachenko EI, Zharkov SV et al. (2015). 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 28(1):62-67. PubMed
- Myakotnykh VS, Torgashov MN, Egorin KV et al. (2016). Comparative analysis of different methods of geroprotective. Advances in Gerontology 29(4):594-601. PubMed
- Kraskovskaya NA, Kukanova EO, Lin'kova NS, Popugaeva EA (2017). Tripeptides Restore the Number of Neuronal Spines under Conditions of In Vitro Modeled Alzheimer's Disease. Bulletin of Experimental Biology and Medicine 163(4):550-553. DOI
- Khavinson VK, Linkova NS, Kukanova EO et al. (2017). Neuroprotective Effect of EDR Peptide in Mouse Model of Huntington's Disease. Journal of Neurology and Neuroscience 8:1. DOI
- Silanteva IA, Komolkin AV, Morozova EA, Vorontsov-Velyaminov PN, Kasyanenko NA (2019). Role of Mono- and Divalent Ions in Peptide Glu-Asp-Arg-DNA Interaction. Journal of Physical Chemistry B 123(9):1896-1902. DOI
- Kuznetsova et al. (2019). The influence of the Pinealon tripeptide on the rehabilitation of cognitive functions in the aging process using the example of rhesus monkeys (Macaca mulatta). Moscow University Anthropology Bulletin 2019(1):62-73. DOI
- Karantysh GV, Fomenko EV, Menzheritskii AM, Prokof'ev VN (2020). Effect of Pinealon on Learning and Expression of NMDA Receptor Subunit Genes in the Hippocampus of Rats with Experimental Diabetes. Neurochemical Journal 14:314-320. DOI
- Fomenko EV, Menzheritsky AM, Karantysh GV et al. (2020). Influence of Pinealon on expression of genes of pro- and antioxidant enzymes and free radical processes in rats in the model of sugar diabetes. Interagro-Tagungsband 2:232-234. DOI
- Khavinson VK, Ilina AR, Kraskovskaya NA et al. (2021). Neuroprotective Effects of Tripeptides: Epigenetic Regulators in Mouse Model of Alzheimer’s Disease. Pharmaceuticals 14(6):515. DOI
- Khavinson VK, Linkova NS, Rudskoy AI, Petukhov MG (2023). Feasibility of Transport of 26 Biologically Active Ultrashort Peptides via LAT and PEPT Family Transporters. Biomolecules 13(3):552. DOI
- Kraskovskaya NA, Linkova NS, Sakhenberg EI et al. (2024). Short Peptides Protect Fibroblast-Derived Induced Neurons from Age-Related Changes. International Journal of Molecular Sciences 25(21):11363. DOI
- Khavinson VK, Ilina AR, Kraskovskaya NA et al. (2025). Correction: Neuroprotective Effects of Tripeptides: Epigenetic Regulators in Mouse Model of Alzheimer’s Disease. Pharmaceuticals 18(1):111. DOI
- Marín-Jerez et al. (2026). Short-Term Performance Assay Identifies Functional Benefits and Early Toxicity of Longevity Interventions in Mice. Research Square Preprint. DOI
For research use only. Not for human consumption. Scientific Editorial Team: Dr. Sieglinde Klaus
References
- https://pubmed.ncbi.nlm.nih.gov/18546826/
- Kozina LS. Investigation of antihypoxic properties of short peptides]. Advances in gerontology = Uspekhi gerontologii. 2008.PMID
- Khavinson V., et al. Pinealon Increases Cell Viability by Suppression of Free Radical Levels and Activating Proliferative Processes. Rejuvenation Research. 2011.DOI
- Fedoreyeva L., 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 (Moscow). 2011.DOI
- Khavinson V., et al. Effect of Short Peptides on Expression of Signaling Molecules in Organotypic Pineal Cell Culture. Bulletin of Experimental Biology and Medicine. 2011.DOI