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Professor Peptides
Research compound

Vesugen

Also known as Vesugen · Lys-Glu-Asp · KED peptide · lysyl glutamyl aspartic acid

Lys-Glu-Asp tripeptide studied for vascular endothelial gene expression

Last reviewed · Educational reference — not medical advice.

NCKED3 residuesN → C
  • Small / Pro
  • Hydrophobic
  • Polar
  • Acidic
  • Basic
Primary sequence, N → C, by residue class.
Formula
C15H26N4O8
Molecular weight
390.4 g/mol
Half-life
Not characterised in published pharmacokinetic studies
Route
Subcutaneous or intramuscular in the source literature
PubChem
87571363 (opens in new tab)
Status
Research compound — vascular short peptide bioregulator
Sequence
KED
Mechanism
Reported to act on endothelial gene expression: normalisation of endothelin-1, restoration of connexin-mediated intercellular coupling, and upregulation of sirtuin-1. Framed as epigenetic regulation rather than receptor agonism; no receptor has been identified.
01

Overview

Vesugen is a synthetic tripeptide, Lys-Glu-Asp (KED). The US National Library of Medicine indexes "Vesugen" as a synonym of the supplementary concept lysyl glutamyl aspartic acid, which independently confirms the sequence — unlike several other members of this peptide family, whose marketed sequences are not supported by any indexed source.

The published research positions KED as a vasoprotective peptide. In endothelial cell models of atherosclerosis and restenosis, KED was reported to normalise endothelin-1 expression (which is elevated in both conditions), to restore cell–cell communication via connexin expression, and to increase sirtuin-1 expression, a protein involved in DNA repair. The authors frame this as epigenetic regulation of endothelial function markers rather than a direct vasoactive drug effect.

Separately, KED has been studied in neuronal differentiation. In human periodontal ligament stem cells, KED alone — and a compound of KED with AED, KE and AEDG — increased expression of GAP-43 (a neurotransmission and neuroplasticity protein) and nestin (a neurofilament protein expressed in early neuronal precursors).

All of this is cell-culture work. No clinical trial has tested whether any of it translates to a cardiovascular or neurological outcome in humans.

Research areasVascular endothelial biologyAtherosclerosis and restenosis modelsNeuronal differentiation of stem cellsPeptide regulation of gene expression
02

What the evidence shows

Separated by study type
HumanClinical trials and human studies
No controlled clinical trials. Cell models used human endothelial and human periodontal ligament stem cells, but no human subject has been studied in a controlled setting.
AnimalRodent and other animal models
No independently replicated animal outcome data in the indexed literature.
In vitroCell and tissue studies
In endothelial models of atherosclerosis and restenosis, KED normalised elevated endothelin-1 expression, restored connexin expression, and increased sirtuin-1 expression. In human periodontal ligament stem cells, KED increased GAP-43 and nestin expression, markers of neuronal differentiation.
03

Key studies & findings

2 studies
  1. 1

    KED normalised endothelin-1 expression elevated in atherosclerotic and restenotic endothelium, restored connexin expression, and increased sirtuin-1 expression in vitro.

    In vitro2016Advances in Gerontology, 2016

  2. 2

    KED alone, and in compound with AED/KE/AEDG, increased GAP-43 and nestin expression in human periodontal ligament stem cells, indicating a push toward neuronal differentiation.

    In vitro2019International Journal of Immunopathology and Pharmacology, 2019 (opens in new tab)

04

Benefits & effects

4 documented

  • Normalisation of endothelin-1 expression in damaged endothelium

    Verified

  • Restoration of connexin-mediated endothelial cell coupling

    Verified

  • Increased sirtuin-1 expression

    Verified

  • Increased GAP-43 and nestin expression in stem cells

    Verified
05

Side effects & safety

1 reported

Safety noteResearch compound for laboratory use only. No regulatory safety review, no established human safety database, and no controlled toxicology data in the public literature.

Recorded in the cited literature No controlled human safety data exist for this compound.

  • Purity and identity of research-grade material are unverified

    unknown
06

Limitations & open questions

Nearly all published work on this compound originates from a single research programme (the St Petersburg Institute of Bioregulation and Gerontology, Khavinson group) and its collaborators. Independent replication outside that network is sparse to non-existent, sample sizes are small, and much of the source literature is published in Russian-language journals with limited peer-review transparency. Effects reported in cell culture and in aged-donor lymphocytes have not been shown to produce clinical outcomes in controlled human trials.

07

Pharmacology

Vesugen is the tripeptide Lys-Glu-Asp (C15H26N4O8, MW 390.39, PubChem CID 87571363). No published human pharmacokinetic data exist. Like other unmodified short peptides it would be expected to undergo rapid peptidase hydrolysis in plasma; the source literature does not address this.

08

Frequently asked questions

Is Vesugen's sequence actually confirmed?

Yes. The National Library of Medicine maps the name "Vesugen" to the supplementary concept *lysyl glutamyl aspartic acid* (Lys-Glu-Asp), and PubChem CID 87571363 gives the matching formula C15H26N4O8. This is stronger sourcing than most peptides in this family have.

Does Vesugen improve cardiovascular health?

Unknown. The vascular findings are cell-culture measurements of gene and protein expression in endothelial models. No trial has measured blood pressure, arterial stiffness, events, or any clinical cardiovascular endpoint.

Is Vesugen the same peptide as Vilon?

No. Vilon is the dipeptide Lys-Glu (KE). Vesugen is the tripeptide Lys-Glu-Asp (KED) — one additional aspartate residue.

09

Citations

4 sources
  1. 1
    Molecular aspects of vasoprotective peptide KED activity during atherosclerosis and restenosisKozlov KL, Bolotov II, Linkova NS, Drobintseva AO, Khavinson VKh, Dyakonov MM, Kozina LS (2016)
  2. 2
    Effect of short peptides on neuronal differentiation of stem cells (opens in new tab)Caputi S, Trubiani O, Sinjari B, Trofimova S, Diomede F, Linkova N, Diatlova A, Khavinson V (2019) · doi:10.1177/2058738419828613
  3. 3
    Peptide Regulation of Gene Expression: A Systematic Review (opens in new tab)Khavinson VKh, Popovich IG, Linkova NS, Mironova ES, Ilina AR (2021) · doi:10.3390/molecules26227053
  4. 4
    Neuroepigenetic Mechanisms of Action of Ultrashort Peptides in Alzheimer's Disease (opens in new tab)Ilina A, Khavinson V, Linkova N, Petukhov M (2022) · doi:10.3390/ijms23084259