# Vesugen — Research Peptide Profile

> Vesugen (Lys-Glu-Asp, KED) is a Khavinson vascular tripeptide with in vitro endothelial data, a corrected mouse Alzheimer study, and no human trials.

Source: https://peptpedia.org/peptide/vesugen | Published: 2026-09-18 | Last updated: 2026-09-18

Vesugen (Lys-Glu-Asp, KED) is a Khavinson-network tripeptide positioned as a vascular bioregulator. Evidence is in vitro endothelial work (endothelin-1, connexin, sirtuin-1), one 5xFAD mouse Alzheimer study carrying a 2025 correction, and two small uncontrolled Russian human reports. No randomized trial or pharmacokinetic study exists.

## Overview

Vesugen (also spelled Vezugen) is a synthetic tripeptide with the sequence Lys-Glu-Asp (KED), developed at the Saint Petersburg Institute of Bioregulation and Gerontology as a vascular bioregulator and sold in Russia as a dietary supplement. The indexed evidence base is small: in vitro studies in vascular endothelial cells, a 5xFAD mouse Alzheimer model, a molecular-genetic review, and two small uncontrolled Russian-language human studies in elderly patients. Reported endothelial effects include normalization of elevated endothelin-1 expression, restoration of connexin-mediated intercellular contacts, and increased sirtuin-1 expression in atherosclerotic and restenotic cell models. The 2021 mouse Alzheimer paper received a formal correction in January 2025 whose public notice does not specify what changed. Vesugen sits in the same Khavinson short-peptide class as [Epithalon](/peptide/epithalon), and nearly all of its data originates from that single research network; no randomized trial, pharmacokinetic study, or independent replication has been published.

## Molecular Profile

- **Category:** bioregulators
- **Molecular formula:** C15H26N4O8
- **Molecular weight:** 390.39 g/mol
- **CAS number:** 204271-66-9
- **Amino acid sequence:** Lys-Glu-Asp
- **Also known as:** KED, Lys-Glu-Asp, Vezugen, Lysyl-glutamyl-aspartic acid
- **Half-life:** Not established; no pharmacokinetic study has been published
- **Solubility:** Soluble in water
- **Storage:** Store lyophilized at -20°C.

## Mechanism of Action

KED is proposed to act through epigenetic regulation rather than a membrane receptor: molecular modeling from the developing group reports peptide interaction with promoter regions of genes involved in neuronal differentiation and Alzheimer pathogenesis, including GAP43 and APOE. In the same modeling work the related peptide EDR, not KED, is the one credited with binding sites in the CASP3 promoter. In cultured vascular endothelium under atherosclerosis and restenosis conditions, KED normalized elevated endothelin-1 expression, restored connexin expression (re-establishing gap-junction-mediated cell contacts), and increased expression of sirtuin-1, a deacetylase involved in DNA repair. A separate molecular-genetic review attributes to KED regulation of p16 and p21 (cell aging), NES and GAP43 (neuronal differentiation), and SUMO, APOE, and IGF1 (Alzheimer-relevant) genes. No receptor target has been identified at molecular resolution, and no mechanism has been demonstrated outside the originating network.

## Key Research Findings

- Vesugen is the tripeptide Lys-Glu-Asp (KED); its vascular claims rest on in vitro work showing normalized endothelin-1, restored connexin contacts, and increased sirtuin-1 in atherosclerotic endothelial models.
- The 5xFAD mouse Alzheimer study (400 mcg/kg daily intraperitoneal) reported prevented dendritic spine loss but carries a January 2025 correction whose content is not specified in the public notice.
- The two human studies (n=41 and n=32) are uncontrolled Russian-language reports; the n=32 study also detected prooxidant activity and reduced CD34+ progenitor cells.
- No randomized trial, pharmacokinetic study, or independent replication outside the Khavinson network exists for Vesugen.

## Vesugen Pharmacokinetics: An Unmeasured Tripeptide

No pharmacokinetic parameter - half-life, Cmax, bioavailability, clearance - has been published for Vesugen (Lys-Glu-Asp) in any species. The only administered-dose information in the indexed literature is the 5xFAD mouse protocol, and a Russian-language review mentions oral use in elderly patients without exposure data.

### What Is Known About Exposure

- In the 5xFAD mouse Alzheimer model, KED was administered intraperitoneally at 400 mcg/kg once daily from 2 to 4 months of age; plasma or brain concentrations were not reported (PMID 34071923).
- A 2021 review states oral KED improved memory and attention in elderly individuals with functional CNS disorders, implying oral activity, but provides no dose, concentration, or trial data to support exposure claims (PMID 34173097).

### Class-Level Expectations

- As an unmodified tripeptide with two acidic residues, KED is expected to be water-soluble and rapidly degraded by peptidases; no KED-specific measurement confirms this.
- A 2023 docking analysis of 26 ultrashort peptides from this research network proposed LAT1, LAT2, and PEPT1 transporters as a general cellular uptake route for the class; KED was not among the top-ranked ligands named (PMID 36979488).

## Safety & Tolerability

Vesugen's human safety is uncharacterized: two small uncontrolled Russian studies reported no adverse events but had no formal adverse-event protocols, and one of them detected prooxidant activity and a significant decrease in circulating CD34+ hematopoietic progenitor cells. The flagship mouse Alzheimer paper carries a formal 2025 correction. No pharmacokinetic or toxicology study has been published.

**Human data status:** Human evidence is two small, uncontrolled, single-center Russian-language observational reports (n=41 vasculogenic erectile dysfunction; n=32 polymorbidity with organic brain syndrome). No randomized, controlled, or pharmacokinetic human study exists.

**Regulatory status:** Not approved as a drug by the FDA, EMA, or any major regulator; sold in Russia as a biologically active food supplement (BAFS).

- In 41 patients with vasculogenic erectile dysfunction, KED monotherapy was reported to improve penile artery blood flow with no adverse events mentioned, but the study was uncontrolled and used no formal safety reporting. (evidence tier: human-observational; [PMID 25051774](https://pubmed.ncbi.nlm.nih.gov/25051774/))
- In 32 elderly patients with polymorbidity, Vesugen shifted biological-age markers favorably but also showed prooxidant activity by chemiluminescence and a significant decrease in circulating CD34+ hematopoietic progenitor cells, interpreted by the authors as inhibition of hemopoiesis. (evidence tier: human-observational; [PMID 26390612](https://pubmed.ncbi.nlm.nih.gov/26390612/))
- In 5xFAD Alzheimer mice, KED at 400 mcg/kg intraperitoneally daily prevented dendritic spine loss; the paper carries a formal January 2025 correction whose public notice does not specify the change. (evidence tier: animal; [PMID 34071923](https://pubmed.ncbi.nlm.nih.gov/34071923/))
- The January 2025 correction to the 2021 Pharmaceuticals mouse study does not disclose, in its public abstract, what was corrected; the mouse neuroprotection findings should be read as corrected-record data. (evidence tier: theoretical; [PMID 39861198](https://pubmed.ncbi.nlm.nih.gov/39861198/))

## Dosing Information (Research Context)

No human dosing or pharmacokinetic study exists. The 5xFAD mouse study used 400 mcg/kg intraperitoneally once daily from 2 to 4 months of age. A Russian-language review describes oral KED use in elderly patients with functional CNS disorders without controlled dosing data. Microgram-range daily courses circulating in vendor materials are extrapolations, not published protocols.

| Route | Dose | Frequency | Notes |
| --- | --- | --- | --- |
| Intraperitoneal (mouse) | 400 mcg/kg | Once daily, months 2-4 of age | 5xFAD Alzheimer model (PMID 34071923); no human dosing established |

## Researched Effects

- **Endothelial Function Markers (In Vitro)** (evidence: moderate): In cultured vascular endothelial and smooth muscle cells under atherosclerosis and restenosis conditions, KED normalized elevated endothelin-1 expression, restored connexin-mediated intercellular contacts, and increased sirtuin-1 expression. Endothelin-1 elevation is a core feature of endothelial dysfunction, and connexins maintain the gap-junction communication lost in atherosclerotic vessels, so the reported direction of effect is biologically coherent; the evidence remains single-network cell culture without independent replication.
- **Neuroprotection in Alzheimer Models** (evidence: preliminary): In 5xFAD transgenic mice, daily intraperitoneal KED (400 mcg/kg, months 2-4 of age) prevented dendritic spine loss and showed a trend toward improved neuroplasticity, with molecular docking suggesting promoter-level interaction with Alzheimer-relevant genes. This paper received a formal correction in January 2025 whose public notice does not specify the change, so the findings should be read with that caveat; no independent group has replicated them.
- **Peripheral Blood Flow (Uncontrolled Human Data)** (evidence: preliminary): A Russian-language study of 41 patients with vasculogenic erectile dysfunction as a manifestation of atherosclerosis reported improved blood flow in the main penile arteries after KED monotherapy, assessed by clinical and instrumental parameters. The study had no control arm, randomization, or blinding, so placebo effects and natural course cannot be excluded.
- **Biological Aging Markers (Uncontrolled Human Data)** (evidence: preliminary): In 32 patients aged 41-83 with chronic polymorbidity and organic brain syndrome in remission, Vesugen and the related tripeptide pinealon were reported to shift biological-age indicators in a favorable direction, with Vesugen showing the stronger effect. The same study observed prooxidant activity by chemiluminescence and a significant decrease in circulating CD34+ hematopoietic progenitor cells, which the authors read as inhibited hemopoiesis - a safety-relevant signal, not just a benefit.

## Research Applications

- Vascular Biology
- Endothelial Research
- Atherosclerosis Models
- Neurodegeneration Research
- Gerontology

## Key Studies

### Molecular aspects of vasoprotective peptide KED activity during atherosclerosis and restenosis

Kozlov KL, Bolotov II, Linkova NS, et al. — *Advances in Gerontology* (2016) — [PMID 28539025](https://pubmed.ncbi.nlm.nih.gov/28539025/)

This Russian-language in vitro study examined KED effects on signal molecule expression in normal, atherosclerotic, and restenotic vascular endothelium. KED normalized endothelin-1 expression (elevated in atherosclerosis and restenosis), restored connexin-mediated intercellular contacts, and increased expression of sirtuin-1, a protein involved in DNA repair. It is the core mechanistic paper behind Vesugen's vasoprotective framing and has not been independently replicated.

### Neuroprotective Effects of Tripeptides-Epigenetic Regulators in Mouse Model of Alzheimer's Disease

Khavinson V, Ilina A, Kraskovskaya N, et al. — *Pharmaceuticals (Basel)* (2021) — [PMID 34071923](https://pubmed.ncbi.nlm.nih.gov/34071923/) | [doi:10.3390/ph14060515](https://doi.org/10.3390/ph14060515)

In 5xFAD transgenic Alzheimer mice, daily intraperitoneal KED at 400 mcg/kg from 2 to 4 months of age tended to increase neuroplasticity and, together with the EDR peptide, prevented dendritic spine loss; molecular docking proposed DNA-level interaction with Alzheimer-relevant gene promoters. This paper received a formal correction in January 2025 (PMID 39861198) whose public notice does not specify what was corrected, so its findings should be cited with that caveat.

### Correction: Khavinson et al. Neuroprotective Effects of Tripeptides-Epigenetic Regulators in Mouse Model of Alzheimer's Disease. Pharmaceuticals 2021, 14, 515

Khavinson V, Ilina A, Kraskovskaya N, et al. — *Pharmaceuticals (Basel)* (2025) — [PMID 39861198](https://pubmed.ncbi.nlm.nih.gov/39861198/) | [doi:10.3390/ph18010111](https://doi.org/10.3390/ph18010111)

Formal correction notice for the 2021 Pharmaceuticals 5xFAD mouse study of KED and EDR peptides. The public abstract of the correction does not state what content was changed. Readers and citers of the original mouse Alzheimer findings should treat this notice as part of the record.

### The efficacy of peptide bioregulators of vessels in lower limbs chronic arterial insufficiency treatment in old and elderly people

Kitachev KV, Sazonov AB, Kozlov KL, et al. — *Advances in Gerontology* (2014) — [PMID 25051774](https://pubmed.ncbi.nlm.nih.gov/25051774/)

This uncontrolled Russian-language study assessed the vasoactive tripeptide Vezugen in 41 patients with vasculogenic erectile dysfunction as a manifestation of atherosclerosis. Comparative analysis of clinical and instrumental parameters before and after monotherapy found significantly improved blood flow through the main penile arteries. With no control arm, randomization, or blinding, the result is hypothesis-generating only.

### Effect of synthetic peptides on aging of patients with chronic polymorbidity and organic brain syndrome of the central nervous system in remission

Meshchaninov VN, Tkachenko EL, Zharkov SV, et al. — *Advances in Gerontology* (2015) — [PMID 26390612](https://pubmed.ncbi.nlm.nih.gov/26390612/)

In 32 patients aged 41-83 with chronic polymorbidity and organic brain syndrome in remission, the tripeptides Vesugen and Pinealon were reported to produce anabolic effects and shift biological-age indicators favorably, with Vesugen the stronger. The same study found prooxidant activity by chemiluminescence and a significant decrease in circulating CD34+ hematopoietic progenitor cells, interpreted as inhibition of hemopoiesis, making this uncontrolled study as relevant to safety assessment as to efficacy.

### Peptide KED: Molecular-Genetic Aspects of Neurogenesis Regulation in Alzheimer's Disease

Khavinson VK, Lin'kova NS, Umnov RS — *Bulletin of Experimental Biology and Medicine* (2021) — [PMID 34173097](https://pubmed.ncbi.nlm.nih.gov/34173097/) | [doi:10.1007/s10517-021-05192-6](https://doi.org/10.1007/s10517-021-05192-6)

This molecular-genetic review of KED in the Alzheimer context states that oral KED improved memory and attention in elderly individuals with functional CNS disorders (no controlled data presented) and that KED restores synaptic plasticity in an in vitro Alzheimer model. It catalogs KED regulation of cell-aging genes (p16, p21), neuronal differentiation genes and proteins (NES, GAP43, nestin), and Alzheimer-relevant genes (SUMO, APOE, IGF1), arguing for formal animal-model efficacy studies.

## Frequently Asked Questions

### What is Vesugen?

Vesugen (also spelled Vezugen) is the synthetic tripeptide Lys-Glu-Asp (KED), developed at the Saint Petersburg Institute of Bioregulation and Gerontology as a vascular endothelial bioregulator. It is sold in Russia as a dietary supplement. Its indexed literature is small, mostly in vitro and animal work from one research network, with two small uncontrolled human studies.

### What human evidence exists for Vesugen?

Two small Russian-language studies, both uncontrolled: 41 patients with vasculogenic erectile dysfunction showed improved penile artery blood flow after KED monotherapy, and 32 elderly patients with polymorbidity showed favorable shifts in biological-age markers but also prooxidant activity and reduced CD34+ progenitor cells. Neither study had a control group, so neither establishes efficacy or safety. No randomized trial has been published.

### What is the correction on the Vesugen Alzheimer mouse study?

The 2021 Pharmaceuticals paper reporting that KED prevented dendritic spine loss in 5xFAD Alzheimer mice received a formal correction published in January 2025 (PMID 39861198). The public correction notice does not specify what was changed. The findings remain on the record but should be cited with the correction attached, and no independent group has replicated them.

### Is Vesugen safe?

Uncharacterized in humans. The two small human studies reported no adverse events but used no formal adverse-event protocols, and the 32-patient study detected prooxidant activity and a significant drop in circulating CD34+ hematopoietic progenitor cells, which the authors themselves flagged as inhibited hemopoiesis. No pharmacokinetic study, no drug-interaction data, and no pregnancy or organ-impairment data exist.

## Related Peptides

- [Vilon](https://peptpedia.org/peptide/vilon)
- [Pinealon](https://peptpedia.org/peptide/pinealon)
- [Epithalon](https://peptpedia.org/peptide/epithalon)
- [Cortagen](https://peptpedia.org/peptide/cortagen)

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This content is for educational and research purposes only. It is not medical advice, and the compounds covered are research chemicals not approved for human use unless explicitly stated otherwise.

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