Vesugen Research, Specifications & Scientific Information

Introduction

Vesugen is three residues long — lysine, glutamic acid, aspartic acid — and its literature is unusually hard to find, for a reason that has nothing to do with how much of it there is.

The compound is published under three labels. Papers from the originating group in St Petersburg call it Vesugen (transliterated Vezugen in some Russian-language titles), or KED after its sequence, or T-38 after its laboratory code. A search for any one of the three returns perhaps a third of the record. The identification is not in doubt — a 2012 paper names trade name and sequence in the same sentence ^[1], and the group's 2021 systematic review lists them as a single entry ^[12] — but a reader who searches once and concludes the compound is barely studied has been misled by the indexing rather than by the evidence.

What the evidence amounts to, stated once here rather than repeated under every heading: nearly all primary work originates with one institute and its collaborators; much of it is published in Russian in gerontology journals with limited circulation elsewhere; the human reports number two, with 32 and 41 participants and no control arm in either; the emphasis falls heavily on cell and organotypic culture; and no independent group has replicated the central endothelial findings.

What Is Vesugen?

A synthetic tripeptide with free termini, KED in single-letter code: L-lysyl-L-alpha-glutamyl-L-aspartic acid.

It occupies the vascular position in the bioregulator series. Each member of that series was designed from the amino acid composition of a polypeptide complex extracted from a particular tissue, on the premise that a short sequence reproduces the activity of the complex it came from; this one corresponds to blood-vessel tissue, and the research programme built around it is correspondingly endothelial.

The clearest single demonstration of what "tissue-specific" is supposed to mean for this series is a 2012 experiment in which three peptides were tested against three cell types. Reduced expression of differentiation markers was found in late-passage cultures of human embryonic pancreatic cells, human bronchial cells and human prostatic fibroblasts. Pancragen raised the markers in pancreatic cells, Bronchogen in bronchial epithelial cells, and this tripeptide in the fibroblasts ^[1]. Whether that pattern is specificity or is three assays each responding to its own peptide is a question the design does not settle — but it is a real cross-comparison, and those are rare in this literature.

Vesugen has not been approved by the U.S. Food and Drug Administration for any indication. No marketing application is on record in the United States and no study of it appears on ClinicalTrials.gov. It is sold in the Russian Federation as a non-pharmaceutical peptide preparation.

Vesugen Specifications

PubChem carries the free tripeptide as compound identifier 87571363 with CAS registry number 204271-66-9, formula C15H26N4O8 and an average mass of 390.39 g/mol. No unique ingredient identifier resolves for the substance in the FDA/NCATS Global Substance Registration System, so that field is published as unknown rather than estimated. The tripeptide appears in the primary literature under three labels that have to be recognised as one substance: the trade name Vesugen (also transliterated Vezugen), the single-letter sequence KED, and the laboratory code T-38. The identification of the trade name with the sequence is stated directly in a 2012 paper from the originating group and repeated in its 2021 systematic review. Reagent material is commonly supplied as an acetate salt, whose mass will not equal the free-peptide figure above.

Values that a public register does not carry are shown as not publicly characterised rather than estimated. Identifiers are reference values; the certificate of analysis supplied with a laboratory order is the record for a given lot.

How Does Vesugen Work?

Not established. The account the originating group offers is a promoter-binding hypothesis, and it is worth setting out precisely because it is more specific than most claims in this family — which makes it more testable, and makes the gap between what was computed and what was measured easier to see.

The proposal. Molecular docking placed the tripeptide at the core promoter of MKI67, the gene encoding the proliferation marker Ki-67, at a named 27-base-pair sequence spanning positions −14 to +12 relative to the transcription start site, contacting through the CATC motif. In the same papers, Ki-67 protein was reported to rise in exposed endothelial cultures, and the authors present the docking as the epigenetic mechanism for that rise ^[2].

What is missing. A docking result is a computed pose. It is not a binding constant, not a footprinting experiment, not a structure, and not a demonstration that the peptide reaches a nucleus in the cells where Ki-67 was measured. A tripeptide carrying two carboxylate side chains and a lysine amine is a strongly charged, highly water-soluble species with no obvious route across a membrane, and no transport measurement for it has been published — only further docking, at amino acid and peptide transporters, in a separate paper about the series as a whole.

No receptor is proposed, and the specification table above therefore shows primary target, receptor family and agonist status as not publicly characterised. That is the accurate entry rather than a missing one.

No pharmacokinetic data exist for this tripeptide in any species.

Vesugen Mechanism of Action

In vitro research

Endothelium under disease conditions. In cultured endothelium representing normal, atherosclerotic and restenotic states, the tripeptide was reported to normalise endothelin-1 expression, which was raised in the two disease conditions; to restore intercellular coupling through connexin expression; and to increase sirtuin-1, a protein involved in DNA repair ^[3]. The framing is normalisation rather than stimulation, which is a consistent feature of this programme's reporting and is also harder to falsify than a directional claim.

Proliferation and adhesion markers in vascular cells. In organotypic and dissociated cultures of vascular cells during ageing, the tripeptide — under its T-38 code — raised Ki-67, reduced p53 synthesis, and reduced synthesis of E-selectin, an adhesion molecule involved in plaque formation ^[4]. The dipeptide tested alongside it behaved similarly, which again places the finding at the level of the series rather than the molecule.

Thymocytes. In cultured human cortical thymocytes, this tripeptide and one sibling enhanced differentiation of immature CD4+CD8+ cells towards regulatory T cells, with increased proliferation and reduced apoptosis, and stimulated mature CD4+CD25+ cells as well ^[9].

Neuroimmunoendocrine tissue. In organotypic culture the tripeptide stimulated proliferation and inhibited apoptosis, with a larger effect in cultures from old animals than young ones, and induced CD5 and CD68 marker expression — less pronounced in the old cultures, the opposite direction from the proliferation result ^[5]. The same paper also reports an effect on associative learning in honey bees, which is an unusual endpoint to find beside a tissue-culture experiment and is noted here rather than interpreted.

Skin and lymphoid explants. In organotypic skin explants from old rats the tripeptide produced a marked stimulatory effect on proliferation where several sibling tripeptides did not, with reduced p53 expression offered as the explanation ^[7]. In splenic lymphoid explants the presence of cyclophosphamide suppressed proliferation and raised p53; adding the tripeptide removed the observed inhibition ^[8].

Everything in this section was observed in cultured cells or excised tissue. None of it establishes anything about an intact animal or about a person.

What Is Vesugen Being Researched For?

• Endothelial biology in ageing and vascular disease models — Ki-67, endothelin-1, E-selectin, connexins and sirtuin-1 ^{[2, 3, 4]}.
• Proposed promoter-level gene regulation — the MKI67 docking work ^[2].
• Thymic and lymphoid cell differentiation — regulatory T-cell development and protection of explant growth against a cytostatic ^{[9, 8]}.
• Tissue-specific differentiation across cell types — the three-peptide, three-tissue comparison ^[1].
• Neurogenesis-related gene expression — a review of reported effects on p16, p21, NES, GAP43, SUMO, APOE and IGF1 in the context of Alzheimer's disease ^[6].

None of that is research into, or evidence about, research-grade material supplied for laboratory use.

Human Research on Vesugen

Human clinical research

Results from pharmaceutical clinical trials describe the investigational material and populations used in those studies and should not be interpreted as establishing the effects of research-grade materials offered for laboratory use.

Two reports have been identified, both Russian-language, both in Advances in Gerontology, neither randomised or controlled.

Biological-age indices, 32 participants, 2015

Thirty-two people (18 men, 12 women, aged 41 to 83) with chronic polymorbidity and organic brain syndrome in remission received this tripeptide or Pinealon. The authors report a significant anabolic effect on biological-age indicators and describe this compound's effect as more visible than the comparator's ^[10].

The same report contains findings that cut the other way, and they are the reason it is worth reading rather than summarising. Prooxidant activity was detected by chemiluminescence. Circulating CD34-positive haematopoietic cells fell, which the authors describe as significant inhibition of haemopoiesis. And the paper's own recommendation is qualified accordingly: the peptides are proposed as geroprotectors of an anabolic, non-antioxidant type. A report that publishes its unfavourable measurements alongside its favourable ones is more credible than one that does not — and none of it is controlled evidence.

Arterial blood flow, 41 participants, 2014

Forty-one older people with a vascular condition arising from atherosclerosis received the tripeptide as monotherapy. Clinical and instrumental measurements of blood flow in the main penile arteries before and after the course were compared, and the authors report significant improvement on both ^[11].

Limitations. A before-and-after comparison in a single arm, with no control group, no blinding and no randomisation. Instrumental blood-flow measurement is operator-dependent and is not blinded here. The indexed abstract gives no effect size.

A claim without a locatable source

A 2021 review by the originating group states that oral administration of the tripeptide improved memory and attention in elderly people with functional central nervous system disorders ^[6]. No primary report supporting that statement has been located in the indexed literature. It is recorded here as a review assertion, which is what it is.

Current Research Status

Status as of September 22, 2026. This block is rendered from maintained fields, not from prose, so it cannot go stale in one place and stay current in another.

Vesugen vs Related Compounds

Pinealon :: Glu-Asp-Arg, the neural member of the same series, and the compound this one was compared against directly in the 32-participant human report ^[10]. Different sequence, different proposed tissue, shared methodology and shared limitations. Pancragen and Bronchogen :: The two peptides tested beside this one in the tissue-specificity experiment, acting on pancreatic and bronchial cells respectively where this one acted on fibroblasts ^[1]. Vilon and Cartalax :: Lys-Glu and Ala-Glu-Asp. The three are frequently tested as a set in ageing fibroblast and stem-cell cultures, where their reported effects overlap substantially — which is an argument for treating results obtained on the set as results about the set. Cardiogen :: The other cardiovascular-positioned peptide of the series, Ala-Glu-Asp-Arg. A 2022 review from the originating group discusses the two together as regulators of molecules involved in cardiovascular cell senescence.

Evidentiary position

Not approved by the U.S. Food and Drug Administration, no registered trial, two uncontrolled human reports, and a proposed mechanism resting on molecular docking.

No comparison of effect between these compounds is made on this page.

Chemical & Molecular Characteristics

Charge is the dominant property. Three residues supply one basic group — the lysine side-chain amine — against three acidic ones: the glutamate side chain, the aspartate side chain and the C-terminal carboxyl. At physiological pH the molecule is net negatively charged and extremely hydrophilic. That is a poor profile for passive membrane crossing, and it sits awkwardly beside a proposed mechanism that operates on a gene promoter inside a nucleus.

No aromatic residue, so no absorbance at 280 nm. Quantification by ultraviolet absorbance has to rely on peptide-bond absorbance near 214 nm, where buffers and solvents also absorb. This applies to every lot of this material and is a real constraint on how much a bare "purity by HPLC" figure can mean.

Weak reversed-phase retention. A 390-dalton peptide of this polarity is poorly retained on conventional C18 columns and can elute close to the void volume, where it is difficult to resolve from salts and from synthesis-related impurities. The separation method matters more for this compound than it would for a larger, more hydrophobic peptide.

Aspartate and glutamate bring isomerisation. Both residues are subject to the alpha/beta and alpha/gamma rearrangement chemistry that affects Asp- and Glu-containing peptides, particularly under acidic or thermal stress. The rearranged products have identical molecular formulas and identical masses. Mass spectrometry confirms composition; it does not confirm that the three residues are joined in the intended way through the intended bonds. For a compound whose reported activity is attributed to a specific sequence contacting a specific promoter motif, that distinction is not academic.

One register field is genuinely empty. No unique ingredient identifier resolves for this tripeptide in the FDA/NCATS Global Substance Registration System, although CAS registry number 204271-66-9 and PubChem compound identifier 87571363 both exist. The entry above shows that field as unknown rather than filling it with a neighbouring substance's code.

Frequently Asked Questions

Scientific References

1. Khavinson VKh, Linkova NS, Polyakova VO, et al.. Peptides tissue-specifically stimulate cell differentiation during their aging Bulletin of experimental biology and medicine; 2012. PMID 22808515 doi:10.1007/s10517-012-1664-1
2. Khavinson VKh, Tarnovskaia SI, Lin'kova NS, et al.. [Epigenetic aspects of peptidergic regulation of vascular endothelial cell proliferation during aging] Advances in gerontology = Uspekhi gerontologii; 2014. PMID 25051766
3. Kozlov KL, Bolotov II, Linkova NS, et al.. [Molecular aspects of vasoprotective peptide KED activity during atherosclerosis and restenosis] Advances in gerontology = Uspekhi gerontologii; 2016. PMID 28539025
4. Khavinson VKh, Lin'kova NS, Evlashkina EV, et al.. Molecular aspects of anti-atherosclerotic effects of short peptides Bulletin of experimental biology and medicine; 2014. PMID 25408528 doi:10.1007/s10517-014-2713-8
5. Chalisova NI, Lopatina NG, Kamishev NG, et al.. Effect of tripeptide Lys-Glu-Asp on physiological activity of neuroimmunoendocrine system cells Bulletin of experimental biology and medicine; 2012. PMID 22977872 doi:10.1007/s10517-012-1768-7
6. Khavinson VK, Lin'kova NS, Umnov RS. Peptide KED: Molecular-Genetic Aspects of Neurogenesis Regulation in Alzheimer's Disease Bulletin of experimental biology and medicine; 2021. PMID 34173097 doi:10.1007/s10517-021-05192-6
7. Voicekhovskaya MA, Chalisova NI, Kontsevaya EA, et al.. Effect of bioregulatory tripeptides on the culture of skin cells from young and old rats Bulletin of experimental biology and medicine; 2012. PMID 22803085 doi:10.1007/s10517-012-1527-9
8. Chalisova NI, Lesnyak VV, Oganezova EV, et al.. Protective effect of tripeptide in the presence of cyclophosphamide on the growth of cultured lymphoid tissue from rats of different age Bulletin of experimental biology and medicine; 2008. PMID 19110568 doi:10.1007/s10517-008-0189-0
9. Iarilin AA, Khavinson VKh, Poliakova VO, et al.. [Changes of thymocyte differentiation, proliferation and apoptosis induced by syntetic peptides] Morfologiia (Saint Petersburg, Russia); 2011. PMID 22171428
10. 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] Advances in gerontology = Uspekhi gerontologii; 2015. PMID 26390612
11. Kitachev KV, Sazonov AB, Kozlov KL, et al.. [The efficacy of peptide bioregulators of vessels in lower limbs chronic arterial insufficiency treatment in old and elderly people] Advances in gerontology = Uspekhi gerontologii; 2014. PMID 25051774
12. Khavinson VK, Popovich IG, Linkova NS, et al.. Peptide Regulation of Gene Expression: A Systematic Review Molecules (Basel, Switzerland); 2021. PMID 34834147 doi:10.3390/molecules26227053

Every identifier above is resolved against PubMed, Crossref or ClinicalTrials.gov at build time, and the title returned by the register is compared with the title stored here. A page does not publish if a reference fails to resolve.

Research-Use Information

For in vitro research use only. This material is a laboratory reagent. It is not a drug, food, dietary supplement, or cosmetic and is not for human or veterinary use, including ingestion, injection, or any other administration. No information on this page describes or implies any effect in humans or animals. Sold only to researchers under our Terms of Sale.