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What it is
A 3-amino-acid peptide (Lys-Glu-Asp) from the Khavinson short peptide series, in which each sequence is proposed to act on a specific tissue — here vascular. Epitalon is the best-known member of the same family.
How it is proposed to work
The programme's central hypothesis is that very short peptides can enter cells, reach the nucleus and interact with DNA in a sequence-specific way, modulating gene expression in the tissue each peptide is matched to. This is a strong and specific claim. It is also testable, and independent testing is what the literature most lacks.
Approved medical uses
None. Vesugen has no approved human medical indication in the jurisdictions we track. Any use is outside an approved label.
Human research
Each entry states what the study found and, separately, what it cannot show.
- Human open-label2013n = 41
Uncontrolled before-and-after report of Vezugen monotherapy after surgery for lower-limb arterial insufficiency
Finding. The authors studied 41 patients who had had surgery for chronic arterial insufficiency of the lower limbs. They compared clinical and ultrasound measures of blood flow in the legs before and after a course of Vezugen given on its own. The Russian abstract calls Vezugen a vasoactive tripeptide ('вазоактивного трипептида препарата «Везуген»'). The authors report that blood flow in the lower limbs improved significantly after Vezugen monotherapy, on both clinical and ultrasound measures ('significantly improves both on clinical and on the ultrasonic parameters'). The abstract gives no effect sizes, p-values or treatment duration.
Limitation. Not independent work. Five of the six authors are listed at the S. M. Kirov Military Medical Academy in St Petersburg; the sixth, Sedova EV, is listed at a St Petersburg cardiology clinic. Co-author Kozlov KL is affiliated with the St Petersburg Institute of Bioregulation and Gerontology on that institute's 2016 KED paper (PMID 28539025). The same surgical team's 2014 report (PMID 25051774) also lists Khavinson as an author. We therefore treat this as work from inside the originating programme. The abstract describes a before-and-after comparison. It does not describe a control group, how patients were allocated or whether anyone was blinded. The 'open-label' kind reflects that single-group design; the report itself does not use the term. The abstract names the product Vezugen, but it does not print the sequence, the formulation or the route. Only the Russian abstract calls it a tripeptide; the English abstract says 'peptid'. The 2014 report by largely the same authors also gives 41 patients. Despite its lower-limb title, it describes penile artery blood flow in men with vasculogenic erectile dysfunction. The abstracts do not let us tell whether the two reports share a cohort. We read the abstract only; the article is in Russian and we have not read it.
Preclinical research
Animal and laboratory work. Useful for generating hypotheses; it cannot establish that something works in people.
- Animal2021
KED in the 5xFAD mouse model of Alzheimer's disease
Finding. The mice were the 5xFAD-M line, a 5xFAD Alzheimer's model crossed with a fluorescently labelled neuron line. They were given synthetic KED, obtained from a commercial supplier (GARMONIA, Russia), daily by intraperitoneal injection from two to four months of age. There were ten mice per group, five male and five female. The abstract reports that KED and the related tripeptide EDR prevented dendritic spine loss. The full text shows that the KED result differed by sex. In males, KED restored total spine density and mushroom-spine numbers in hippocampal CA1 neurons. In females, it did not change total spine density; it only brought a raised thin-spine count back to the control level. The authors describe a positive trend for KED to restore long-term potentiation, a measure of neuroplasticity, but say it did not reach statistical significance. They then ran molecular docking of the peptides into DNA. Promoter binding sites in genes linked to Alzheimer's disease are listed for EDR only. For KED, the abstract says only that similar DNA sequences appeared in the lowest-energy peptide-DNA complexes.
Limitation. From the originating group. Khavinson is first author, and the first listed affiliation is the Saint Petersburg Institute of Bioregulation and Gerontology. Other listed affiliations include the Pavlov Institute of Physiology, Peter the Great St Petersburg Polytechnic University, the Kurchatov Institute's Petersburg Nuclear Physics Institute and the A. M. Granov Russian Scientific Center of Radiology and Surgical Technologies. We found no independent group reporting the result. The groups are small, the spine effect of KED appears in males but not in females, and the neuroplasticity effect is not statistically significant. The proposed DNA mechanism comes from computational docking, not a measured interaction. This is a brain-disease model, not a vascular one, so it does not test the vascular association in this dossier. The same group also reports KED activity in endothelial, skin-fibroblast, pineal and brain-cortex cultures (PMIDs 28539025, 27259496, 22803060, 24909721). A 2025 correction (PMID 39861198) reports that Figures 5 and 8, the male and female dendritic-spine images, had been published as the same image. The authors replaced them and state that the conclusions are unaffected. We read the abstract and checked the spine results, the neuroplasticity result and the peptide source in the full text (PMC8227791).
Potential safety concerns
- CautionInsufficient
No systematic human safety dataset we could inspect. Very short peptides are often assumed benign on the basis of size alone, which is an assumption rather than a finding.
- CautionInsufficient
If the nuclear gene-expression mechanism is real, its long-term consequences would need study. If it is not real, the compound does nothing. Both possibilities argue for evidence before use, and neither has been resolved.
Known interactions and contraindication considerations
- Uncharacterised in accessible literature.
This list is not exhaustive and is not a substitute for a clinician reviewing your full medication history.
Regulatory status
Status is shown per jurisdiction and is accurate only as of the date stated. Where a compound is approved, the approval is bound to a specific formulation, manufacturer and indication — shown in the detail column.
| Jurisdiction | Standing | Detail |
|---|---|---|
Russian Federation Ministry of Health / Roszdravnadzor | Listed as of 11 Aug 2026 | Marketed in Russia, generally in a supplement or parapharmaceutical category rather than as a registered medicine. Certificate details in circulation could not be verified: the same number appears against different products on the manufacturer's own materials, and they follow a format from a registration regime since superseded. |
United States FDA | Unapproved / investigational as of 11 Aug 2026 | No marketing authorisation. The FDA has not evaluated this compound — that is an absence of any opinion, not a negative finding. |
European Union EMA | Unapproved / investigational as of 11 Aug 2026 | No marketing authorisation. |
India CDSCO | Unapproved / investigational as of 11 Aug 2026 | Not approved for human use. A first-time synthetically manufactured peptide falls under the new-drug pathway. |
How it is being used
What the grey community actually runs, the reasoning they give, and our read on whether it follows from known biology. This is observation, not evidence, and not a recommendation.
No community use documented for this compound yet. Absence here means our editorial team has not reviewed and verified a pattern — not that none exists.
Active clinical trials
No registered trials currently tracked for Vesugen.
What remains unknown
The questions that would change our assessment if they were answered.
- Can any of the central findings be replicated by a group with no connection to the originating institute?
- Does a peptide this short reach the nucleus intact in a human?
- Is tissue specificity demonstrated, or inferred from the tissue each peptide was derived from?
References
- 1.Kitachov KV, Sazonov AD, Kozlov KL, et al. The role of vasoactive peptid in lower limbs chronic arterial insufficiency treatment. Adv Gerontol. 2013.PMID 28976154
- 2.Khavinson V, Ilina A, Kraskovskaya N, et al. Neuroprotective Effects of Tripeptides-Epigenetic Regulators in Mouse Model of Alzheimer's Disease. Pharmaceuticals (Basel). 2021.PMID 34071923doi
Editorial change history
When we change a grade or a regulatory note, we log it here rather than editing quietly.
Dossier created. All registration certificate numbers and all trial figures excluded as unverifiable. Graded on absence of independent replication, not on country of origin.
We replaced the generic template human entry (vesugen-h1) and its placeholder reference with a sourced entry, and added the dossier's first preclinical entry. The human entry is Kitachov et al. 2013 (PMID 28976154), a 41-patient before-and-after report of Vezugen monotherapy after lower-limb arterial surgery. We mark it as from inside the originating programme because of the co-author and team overlap with the Institute of Bioregulation and Gerontology. It is uncontrolled and was read from the abstract only. The preclinical entry is Khavinson et al. 2021 (PMID 34071923), synthetic KED in 5xFAD-M mice. We checked it against the full text. The spine effect differed by sex, restoring spine density in males only. The neuroplasticity effect was a non-significant trend. A 2025 correction (PMID 39861198) replaced duplicated male and female spine figures, and the authors say the conclusions are unaffected. We confirmed the sequence Lys-Glu-Asp (KED; alias T-38) from primary literature. The evidence grade stays 'insufficient'. We refined the evidence summary to note the limited independent work that exists: one null in-vitro test of the commercial product (PMID 28124601) and uncontrolled Ekaterinburg human reports that combine vesugen with Pinealon. None of it replicates an originating-group finding.
Spotted something wrong? Tell us — we publish corrections.