Vesugen (KED) Peptide Research Overview: Every Study Found

Vesugen is the three-amino-acid peptide lysine-glutamic acid-aspartic acid (Lys-Glu-Asp, “KED”). It was developed in the St. Petersburg group of Vladimir Khavinson and is described by its authors as vasoprotective. Everything we found on it was written by that group or by co-authors of it. We found no placebo-controlled human trial, no registered trial and no replication by an unconnected lab [1][30].

Key points

• We opened about 25 papers: cell and rodent work from 2008 to 2024, and five small human reports from 2013 to 2016. Human reports on blood flow have no control group described in their abstracts [1][2][3].
• The vascular claim rests on cultured endothelial cells (endothelin-1 normalised, sirtuin-1 raised) and on two reports of 41 patients each [2][3][7].
• Several human reports combine vesugen with pinealon or another supplement, so its own contribution cannot be separated [4][5][6].
• Every paper with a named group has a Khavinson-institute author or a Khavinson co-author. We found no independent replication [1].
• No regulator we checked approves vesugen as a medicine. Russia lists it as a dietary supplement. Human safety data are close to absent [26][27][28][29].

What vesugen is

Vesugen is Lys-Glu-Asp. In older papers it appears as “T-38” or “Vezugen” [11][3]. The group’s 2026 review describes KED as a component of a vascular polypeptide preparation (VPP) with, in the authors’ words, the same biological effects, and gives “Везуген®” and “Славинорм®” as the product names [10]. That is the authors’ statement; we could not open the primary VPP studies.

It belongs to the family covered in our Khavinson peptide bioregulators evidence review, alongside epitalon, vilon and pinealon. The proposed mechanism is the same as for the others: a short peptide enters the nucleus, binds DNA or histones and changes gene expression. For KED the support is molecular docking, which predicts contacts with promoter sequences of genes such as MKI67 (the Ki-67 gene) and TPH1, and cell-culture expression data [9][18][22]. A docking prediction is not a demonstration that binding happens in a living cell. The group’s own 2021 paper on KED calls testing in animal models of Alzheimer’s disease “very important” and not yet done at that point [23]. Prices for the compound are compared on our vesugen page.

Every study we could open

“Group” is the authors’ network. “Not stated” means the abstract gave no number and we did not see the full text. All were read as PubMed abstracts.

Year	System	Size	Finding	Group
2008	Rat spleen explants, cyclophosphamide	Not stated	More explant growth; no suppression by the cytostatic [11]	Khavinson institute (Chalisova)
2008	Irradiated old rats, pancreas	Not stated	Tripeptide T-38 “activated” post-irradiation repair (abstract cut off) [25]	Ryzhak, Kvetnoy
2011	Human thymocyte culture	Not stated	Shift of immature to regulatory T cells; more proliferation, less apoptosis [12]	Khavinson co-author
2011	Rat pineal culture	Not stated	Ki-67 up; apoptosis marker AIF unchanged [14]; immune-cell proliferation up, differentiation unchanged [13]	Khavinson
2012	Rat pineal culture; honey bee	Not stated	Less p53, more Ki-67; “modulation” of bee learning [15]	Khavinson co-author
2012	Young and old rat skin explants	Not stated	T-38 raised proliferation in old tissue [16]	Khavinson institute
2012	Human fibroblasts	Not stated	More CXCL12/WEGC1 expression, stronger in aged cultures [17]	Khavinson
2014	Cultured vascular cells	Not stated	More Ki-67, less p53 and E-selectin [8]	Khavinson
2014	Endothelial cells, docking	Not stated	More Ki-67; predicted binding to MKI67 promoter [9]	Khavinson
2014	Rat brain-cortex cells, docking	Not stated	More serotonin expression; TPH1 site predicted [18]	Khavinson
2016	Normal, atherosclerotic, restenotic endothelium in vitro	Not stated	Endothelin-1 returned to normal; connexin and sirtuin-1 up [7]	Khavinson institute (Kozlov)
2016	Skin fibroblasts	Not stated	MMP-9 down; Ki-67 and CD98hc up (KE, KED, AED, AEDG tested) [32]	Khavinson
2019	Human periodontal stem cells	Not stated	More GAP43 and nestin [21]	Chieti-Pescara with Khavinson
2020	Human embryonic mesenchymal stem cells	Not stated	IGF1 up 3.5-5.6-fold; FOXO1 down; mixed TNKS2 effect [19]	Moscow State with Khavinson
2020	Oral stem cells at passage 25	Not stated	p16/p21 mRNA down 1.82-3.23-fold [20]	Chieti-Pescara with Khavinson
2021	5xFAD Alzheimer’s mice, intraperitoneal	Not stated here	A “tendency” toward more neuroplasticity; less spine loss [22]	Khavinson
2024	Fibroblast-derived human neurons	Not stated	More dendrites; no effect on mitochondria, lysosomes or p16 [24]	St. Petersburg (Linkova, Ryzhak)

Most results are fold-changes in markers (Ki-67, p53, endothelin-1), not function. The 2016 endothelial work is the closest cell-level match to the vascular claim [7]. The 2026 review adds that endothelial cells from patients with atherosclerosis and restenosis showed raised endothelin-1 that KED returned to normal, and it summarises animal blood-pressure and flow effects of the VPP, not of KED alone [10]. The 2024 neuron paper is the only one that reports a null finding on aging markers [24].

The human reports

Year	Population	Size	Design in abstract	Reported	Attributable to vesugen?
2013	Patients operated for chronic leg arterial insufficiency	41	Before and after “monotherapy”; no control described	Better clinical and ultrasound blood flow [2]	Possibly, but no control
2013	Elderly with chemical stomatitis after cancer treatment	22	Added to usual care plus a supplement (Algiklam)	“Enhances effectiveness” [4]	No; two additions
2014	Men with vascular erectile dysfunction	41	Before and after; no control described	Better penile artery flow [3]	Possibly, but no control
2015	Ages 41-83, polymorbidity, brain syndrome	32	Vesugen and pinealon; no control described	Better “biological age” scores; vesugen “more visible” effect than pinealon; pro-oxidant activity; fewer CD34+ cells [5]	Partly; compared two peptides, no placebo
2016	Mixed ages	110	Peptides vs baths, oxygen, massage	Best result when both peptides were combined [6]	No; combination

Two clarifications. The two 41-patient reports are separate papers, from the Kirov Military Medical Academy with Khavinson as last author on the 2014 paper. The leg-ischemia paper’s authors do not include him [2][3]. We could not tell whether the patient groups overlap. Second, “biological age” in the 2015 and 2016 studies is a composite index, not a vascular outcome. The 2016 record lists Ekaterinburg affiliations, not Khavinson’s institute [6].

The 2021 review says oral KED “improved memory and attention in elderly individuals with functional CNS disorders” [23]. We could not open the study behind that sentence, so we do not count it.

None of the abstracts reports blinding, randomisation, placebo or clinical events such as amputation, heart attack or death. Only the 2015 and 2016 records discuss safety, and only in general terms [5][6].

Has anyone outside the network replicated it?

Not that we can confirm. We searched PubMed for “vesugen” (27 records), a title-and-abstract search for “Lys-Glu-Asp”, “KED peptide” and vesugen (61 records), and “Vezugen” (5 records), all on 2026-11-09 [1]. Of the papers that name vesugen or KED, the only ones from outside St. Petersburg are the Chieti-Pescara (Italy) and Moscow State University papers, and each lists Khavinson as an author [19][20][21]. Georgian cytogenetics papers concern related peptides (livagen, prostamax, vilon), not vesugen. A 2026 review of the cardiovascular work was written at Khavinson’s own institute [10]. We did not search Russian-language databases such as eLibrary, so independent Russian work could exist.

Regulatory status

• United States (checked 2026-11-09). No match for vesugen in the openFDA Drugs@FDA endpoint [29]. FDA’s page on bulk substances that may present safety risks (current 2026-04-22) and its 503A bulks page (current 2026-05-14) do not mention vesugen or KED [27][28]. No approved product, and it is not a listed bulk substance for compounding. Whether it is lawful as a supplement ingredient we did not examine.
• Russia. The RLS drug reference lists “Везуген” as a dietary supplement (БАД) in capsule and tablet forms, “additional source of peptides (lysine, glutamic acid, aspartic acid)”. The page, updated 2022-08-08, shows no registration number or manufacturer [26]. RLS is a commercial reference, not the state register, which we did not search.
• EU, UK, Germany: not checked against EMA, MHRA or BfArM registers.
• ClinicalTrials.gov: no registered study for vesugen or Vezugen (searched 2026-11-09) [30].
• “Research use only” means a product is sold as a laboratory reagent, outside medicine and food rules. It is a seller’s label, not an approval, and implies no regulator has checked purity, identity or safety.

Risks and unknowns

Documented adverse effects: none systematically recorded. In the 32-adult study the authors saw pro-oxidant activity on chemiluminescence and a fall in CD34+ blood cells, which they read as “significant inhibition of hemopoiesis”, while stating the peptides did not change chromatin condensation [5]. The clinical meaning is unknown, and a before-and-after design cannot show cause. The group’s 2016 comparison called oligopeptide preparations among the safest of the methods compared, with no event counts in the abstract [6].

We found no pharmacokinetic data, no data on interactions, on pregnancy or children, on people with cancer, on long-term use, on immunogenicity, or on product purity. The 2021 mouse paper was short (two months of treatment) and used a transgenic model [22]. People with vascular disease are the population the human reports target, and they are also those most likely to take other drugs. Several cell studies report raised proliferation markers such as Ki-67; whether that matters for people with a cancer history is unstudied in anything we opened.

Evidence gaps

• No blinded or placebo-controlled human trial of vesugen alone.
• No hard vascular endpoint (events, walking distance, blood pressure over time) in any human report we opened.
• No in-vivo animal study of KED on atherosclerosis that we could open; the animal vascular data in the 2026 review concern the VPP [10].
• No receptor, transporter or DNA-binding experiment in living cells; docking only.
• No independent lab.

What the @Hoostethics post claims

On 2026-10-15, @Hoostethics posted a tier list titled “ranking the most cope supplements”. Vesugen sits in “somewhat cope”, the mildest of five tiers, next to turmeric, collagen peptides, noopept, creatine monohydrate and GHK-Cu [31]. The post gives no reasons, so there is no specific claim to test. We read the text through the fxtwitter mirror because X blocks automated access.

Verdict: could not be verified. “Cope” is an opinion. The record does support a cautious reading: the vascular findings are cell-culture changes in marker expression and two uncontrolled reports of 41 patients each, all from one network. No benefit is established, and the placement is not contradicted. We did not review the evidence for the other items in the tier, so we make no comparison with them. See our cope-supplements tier-list check.

Frequently asked questions

Has vesugen been tested in people? In five small reports from 2013 to 2016, with 22 to 110 participants. None describes a placebo group, and three involve other treatments given alongside it [2][3][4][5][6].

Does the evidence show vesugen protects blood vessels? It shows changes in marker expression in cultured vascular cells and improved blood-flow measures in two uncontrolled patient series. Neither is a clinical outcome such as fewer cardiovascular events [2][3][7].

Is vesugen approved anywhere? Not as a medicine in the sources we checked. Russia lists it as a dietary supplement, and we found no US listing. We did not check EMA, MHRA or BfArM registers [26][27][29].

Has anyone outside Khavinson’s group confirmed the results? We found no such replication. The Italian and Moscow papers on KED list Khavinson as an author [19][20][21].

Sources

1. NCBI PubMed, searches “vesugen” (27 records), “vesugen OR Lys-Glu-Asp OR KED peptide” in title/abstract (61 records), “Vezugen” (5 records); run 2026-11-09, relevance judged by us. https://pubmed.ncbi.nlm.nih.gov/?term=vesugen
2. Kitachov KV, et al., “The role of vasoactive peptid in lower limbs chronic arterial insufficiency treatment,” Adv Gerontol (2013). https://pubmed.ncbi.nlm.nih.gov/28976154/
3. Kitachev KV, et al., “The efficacy of peptide bioregulators of vessels in lower limbs chronic arterial insufficiency treatment in old and elderly people,” Adv Gerontol (2014). https://pubmed.ncbi.nlm.nih.gov/25051774/
4. Filippova, “Treatment of chemical stomatitis in people of advanced and senile age,” Adv Gerontol (2013). https://pubmed.ncbi.nlm.nih.gov/28976153/
5. Meshchaninov VN, et al., “Effect of synthetic peptides on aging of patients with chronic polymorbidity and organic brain syndrome in remission,” Adv Gerontol (2015). https://pubmed.ncbi.nlm.nih.gov/26390612/
6. Myakotnykh VS, et al., “Comparative analysis of different methods of geroprotective,” Adv Gerontol (2016). https://pubmed.ncbi.nlm.nih.gov/28539017/
7. Kozlov KL, et al., “Molecular aspects of vasoprotective peptide KED activity during atherosclerosis and restenosis,” Adv Gerontol (2016). https://pubmed.ncbi.nlm.nih.gov/28539025/
8. Khavinson VKh, et al., “Molecular aspects of anti-atherosclerotic effects of short peptides,” Bull Exp Biol Med (2014). https://pubmed.ncbi.nlm.nih.gov/25408528/
9. Khavinson VKh, et al., “Epigenetic aspects of peptidergic regulation of vascular endothelial cell proliferation during aging,” Adv Gerontol (2014). https://pubmed.ncbi.nlm.nih.gov/25051766/
10. Ryzhak GA, et al., “Peptidergic regulation of age-related alterations in the cardiovascular system,” Adv Gerontol (2026). https://pubmed.ncbi.nlm.nih.gov/42935327/
11. Chalisova NI, et al., “Protective effect of tripeptide in the presence of cyclophosphamide on the growth of cultured lymphoid tissue from rats of different age,” Bull Exp Biol Med (2008). https://pubmed.ncbi.nlm.nih.gov/19110568/
12. Iarilin AA, Khavinson VKh, et al., “Changes of thymocyte differentiation, proliferation and apoptosis induced by syntetic peptides,” Morfologiia (2011). https://pubmed.ncbi.nlm.nih.gov/22171428/
13. Linkova NS, et al., “Peptidegic stimulation of differentiation of pineal immune cells,” Bull Exp Biol Med (2011). https://pubmed.ncbi.nlm.nih.gov/22803057/
14. Khavinson VKh, et al., “Effect of short peptides on expression of signaling molecules in organotypic pineal cell culture,” Bull Exp Biol Med (2011). https://pubmed.ncbi.nlm.nih.gov/22803060/
15. Chalisova NI, et al., “Effect of tripeptide Lys-Glu-Asp on physiological activity of neuroimmunoendocrine system cells,” Bull Exp Biol Med (2012). https://pubmed.ncbi.nlm.nih.gov/22977872/
16. Voicekhovskaya MA, et al., “Effect of bioregulatory tripeptides on the culture of skin cells from young and old rats,” Bull Exp Biol Med (2012). https://pubmed.ncbi.nlm.nih.gov/22803085/
17. Khavinson VKh, et al., “Peptides tissue-specifically stimulate cell differentiation during their aging,” Bull Exp Biol Med (2012). https://pubmed.ncbi.nlm.nih.gov/22808515/
18. Khavinson VKh, et al., “Short peptides stimulate serotonin expression in cells of brain cortex,” Bull Exp Biol Med (2014). https://pubmed.ncbi.nlm.nih.gov/24909721/
19. Ashapkin V, et al., “Gene expression in human mesenchymal stem cell aging cultures: modulation by short peptides,” Mol Biol Rep (2020). https://pubmed.ncbi.nlm.nih.gov/32399807/
20. Sinjari B, et al., “Short Peptides Protect Oral Stem Cells from Ageing,” Stem Cell Rev Rep (2020). https://pubmed.ncbi.nlm.nih.gov/31677028/
21. Caputi S, et al., “Effect of short peptides on neuronal differentiation of stem cells,” Int J Immunopathol Pharmacol (2019). https://pubmed.ncbi.nlm.nih.gov/30791821/
22. Khavinson V, et al., “Neuroprotective Effects of Tripeptides-Epigenetic Regulators in Mouse Model of Alzheimer’s Disease,” Pharmaceuticals (2021). https://pmc.ncbi.nlm.nih.gov/articles/PMC8227791/
23. Khavinson VKh, et al., “Peptide KED: Molecular-Genetic Aspects of Neurogenesis Regulation in Alzheimer’s Disease,” Bull Exp Biol Med (2021). https://pubmed.ncbi.nlm.nih.gov/34173097/
24. Kraskovskaya N, et al., “Short Peptides Protect Fibroblast-Derived Induced Neurons from Age-Related Changes,” Int J Mol Sci (2024). https://pubmed.ncbi.nlm.nih.gov/39518916/
25. Ryzhak GA, et al., “Peptidergic regulation of the pancreas function in the experimental model of rats with accelerated aging,” Adv Gerontol (2008). https://pubmed.ncbi.nlm.nih.gov/18942368/
26. RLS (rlsnet.ru), “Везуген” dietary supplement entry (updated 2022-08-08), read 2026-11-09. https://www.rlsnet.ru/baa/vezugen-30388
27. FDA, “Certain Bulk Drug Substances for Use in Compounding that May Present Significant Safety Risks” (content current 2026-04-22). https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks
28. FDA, “Bulk Drug Substances Used in Compounding Under Section 503A of the FDCA” (content current 2026-05-14). https://www.fda.gov/drugs/human-drug-compounding/bulk-drug-substances-used-compounding-under-section-503a-fdc-act
29. openFDA, Drugs@FDA endpoint, search “vesugen”, no matches (run 2026-11-09). https://api.fda.gov/drug/drugsfda.json
30. ClinicalTrials.gov API v2, queries “vesugen” and “Vezugen”, empty results (run 2026-11-09). https://clinicaltrials.gov/api/v2/studies?query.term=vesugen
31. @Hoostethics, “ranking the most cope supplements” (2026-10-15), text read through the fxtwitter mirror; tier placement taken from the project’s transcription of the image. https://x.com/Hoostethics/status/2110728908735979632
32. Lin’kova NS, et al., “Peptide Regulation of Skin Fibroblast Functions during Their Aging In Vitro,” Bull Exp Biol Med (2016). https://pubmed.ncbi.nlm.nih.gov/27259496/

This article is information, not medical advice.