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!FDA Disclaimer — Research Use Only

Statements regarding these products have not been evaluated by the U.S. Food and Drug Administration. These products are intended for laboratory and in-vitro research use only and are not for human or veterinary consumption of any kind. They are not drugs, foods, or supplements, are not FDA approved, and are not intended to diagnose, treat, cure, or prevent any disease. All products are sold exclusively to qualified researchers and must be handled by trained professionals. Read the full disclaimer →

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Research/Vesugen

Signaling

Vesugen

A synthetic ultrashort tripeptide investigated in vascular-endothelial, gene-expression, and cellular-aging research models.

What It’s Studied For

Vesugen is the synthetic tripeptide Lys-Glu-Asp (KED), one of the short peptide bioregulators associated with the St. Petersburg Institute of Bioregulation and Gerontology. It is studied primarily as a molecular tool in vascular-endothelial cell biology and in investigations of how ultrashort peptides may interact with DNA and modulate gene expression. It is a research-use-only compound; the literature base is concentrated in a small number of collaborating research groups, with limited independent replication to date.

  • Vascular endothelial cell models (young vs. aged cultures; in vitro atherosclerosis and restenosis endothelium models)
  • Gene-expression and epigenetic-mechanism studies (ultrashort peptide–DNA promoter interaction modeling)
  • Cellular-aging and gerontology research models
  • Molecular-docking and structure–activity studies of ultrashort peptides
  • Neuro-vascular model systems (5xFAD transgenic mouse model)
  • Peptide membrane-transport modeling (LAT1/LAT2 and PEPT1 carrier docking)

Molecular Profile

Type

Synthetic linear tripeptide

Molecular formula

C15H26N4O8

Molecular weight

390.39 g/mol

Amino acids

3

Sequence

Lys-Glu-Asp (KED); H-Lys-Glu-Asp-OH

Modification

Free N- and C-termini (no modifications).

Mechanism & Target Class

Vesugen belongs to the class of ultrashort peptide bioregulators (2–4 residues) studied by the Khavinson group. The proposed mechanism centers on direct interaction of the small peptide with DNA: molecular-docking work places KED in the minor groove of double-stranded DNA, where it is hypothesized to associate with gene-promoter regions and influence transcription in a tissue-associated manner. Docking studies have examined KED binding to promoter regions including the MKI67 gene (encoding the proliferation marker Ki-67). Because of its small size and charged lysine residue, transport modeling has explored candidate uptake via LAT-family amino-acid transporters and the PEPT1 peptide transporter. This DNA-interaction model is the originating group's hypothesis and is not independently established consensus pharmacology.

Research Focus

Investigated in vascular-endothelial cell biology, gene-expression and epigenetic-mechanism research, ultrashort-peptide structure and transport modeling, and cellular-aging and neuro-vascular model systems.

Identity, origin, and classification

Vesugen is the synthetic tripeptide Lys-Glu-Asp (abbreviated KED), one of a family of short peptide bioregulators developed at the St. Petersburg Institute of Bioregulation and Gerontology and associated with the work of V. Kh. Khavinson. In the originating literature it is described as derived from a vascular-tissue polypeptide complex and reproduced by chemical synthesis (Khavinson et al., 2021). It is grouped with related ultrashort peptides such as the dipeptide KE (Vilon), the tripeptide EDR (Pinealon), and the tetrapeptide AEDG (Epithalon), and frequently appears as a comparator in structure–activity work. The compound's chemical identity (formula C15H26N4O8; PubChem CID 87571363; ChEBI:159909) is consistent across chemistry databases, and a synthesis route for H-Lys-Glu-Asp-OH is documented in a granted US patent covering peptides investigated in microcirculation research.

Vascular endothelial cell models

The most directly relevant slice of the literature examines KED in vascular endothelial cell cultures. Khavinson and colleagues (2014) studied dissociated vascular endothelial cell cultures from young and aged animals, measuring the proliferation-associated protein Ki-67 and using molecular docking to model peptide interaction with the MKI67 gene promoter; the work characterizes docking contacts within the core promoter region. Kozlov, Khavinson and colleagues (2016) used an in vitro model of normal, atherosclerotic, and restenotic endothelium to examine the relationship between KED and signaling-molecule expression, measuring endothelin-1, connexin-37 (Cx-37), and sirtuin-1 (SIRT1) across culture conditions. These are cell-culture, marker-level measurements characterizing molecular signaling at the cellular level.

Gene-expression and epigenetic-mechanism studies

A recurring theme across the literature is the hypothesis that ultrashort peptides regulate gene expression through direct DNA binding. A systematic review by Khavinson, Popovich, Linkova and colleagues (2021) compiles evidence from studies examining whether peptides of 2–7 residues can penetrate cell nuclei and interact with histones and with single- and double-stranded DNA. Earlier docking work (Khavinson, Lin'kova, Tarnovskaya, 2016) generated spatial models of DNA–peptide complexes for a set of short peptides and identified candidate binding sites for certain sequences. This body of work frames the proposed mechanism but originates primarily within a small number of collaborating groups; independent replication by unaffiliated laboratories is limited.

Neuro-vascular and neurodegeneration model systems

KED appears in neurodegeneration-model research, typically alongside the EDR (Pinealon) peptide. In a study using the 5xFAD transgenic mouse model (Khavinson et al., 2021, Pharmaceuticals), investigators measured hippocampal dendritic-spine density and morphology (mushroom, thin, and stubby spine populations) and long-term potentiation, alongside molecular-docking analysis of peptide binding to gene promoters. The docking analysis examined an eight-gene set — including CASP3, NES, GAP43, APOE, SOD2, PPARA, PPARG, and GDX1 — with KED analyzed in parallel to EDR. That article received a 2025 published correction (DOI 10.3390/ph18010111) addressing duplicated figures; the authors stated the scientific conclusions were unaffected. An in vitro amyloid-synaptotoxicity model (Kraskovskaya et al., 2017) used primary hippocampal neuron cultures to measure dendritic-spine counts under KED and EDR treatment.

Cellular aging and stem-cell differentiation models

KED appears in cellular-aging research within the gerontology literature. Sinjari, Diomede, Khavinson and colleagues (2020) studied human periodontal-ligament stem cells and examined whether a set of short peptides including KED was associated with neuronal differentiation markers in that culture system, positioning KED as a tool for studying peptide modulation of cell differentiation. Review articles from the group situate KED among peptides examined for expression of senescence- and proliferation-associated genes during in vitro cell aging.

Structure, transport, and SAR modeling

Because KED is an ultrashort, charged peptide, several modeling studies address candidate cellular uptake mechanisms. Khavinson, Linkova and colleagues (2022; 2023) performed molecular docking of large peptide libraries against the amino-acid transporters LAT1/LAT2 and the peptide transporter PEPT1, examining candidate binding interactions for KED and related peptides. A review by Ilina, Khavinson, Linkova, and Petukhov (2022) situates these transport studies in the context of neuroepigenetic-mechanism research. These are in silico/computational characterizations of candidate transport feasibility, not measured pharmacokinetic data.

Storage & Handling

Lyophilized

Store desiccated at -20°C

protect from light and moisture.

Reconstituted

2–8°C for short-term use

aliquot and freeze for longer storage to limit freeze–thaw cycles.

Small linear peptide susceptible to degradation in aqueous solution; handle under standard sterile peptide-laboratory practice.

References

Reviews

  1. 1

    Khavinson VK, Linkova NS, Rudskoy AI, Petukhov MG (2023). Biomolecules — Molecular-modeling and docking review of ultrashort-peptide transport via LAT and PEPT carriers

    DOI: 10.3390/biom13030552
  2. 2

    Ilina A, Khavinson V, Linkova N, Petukhov M (2022). International Journal of Molecular Sciences — Review of neuroepigenetic mechanisms of ultrashort peptides in an Alzheimer's-disease context

    DOI: 10.3390/ijms23084259PubMed 35457077
  3. 3

    Khavinson V, Linkova N, Kozhevnikova E, Dyatlova A, Petukhov M (2022). International Journal of Molecular Sciences — Review and modeling of ultrashort-peptide transport via POT and LAT carrier systems

    DOI: 10.3390/ijms23147733

Reviews

  1. 4

    Khavinson VK, Lin'kova NS, Umnov RS (2021). Bulletin of Experimental Biology and Medicine — Review of molecular-genetic aspects of the KED peptide in a neurogenesis and Alzheimer's-disease context

    DOI: 10.1007/s10517-021-05192-6PubMed 34173097
  2. 5

    Khavinson VK, Popovich IG, Linkova NS, Mironova ES, Ilina AR (2021). Molecules — Systematic review of peptide regulation of gene expression via DNA interaction

    DOI: 10.3390/molecules26227053PubMed 34834147

Primary research

  1. 6

    Khavinson V, Ilina A, Kraskovskaya N, Linkova N, Kolchina N, Mironova E, Erofeev A, Petukhov M (2025). Pharmaceuticals (Basel) — Published correction (duplicated figures) to the 2021 Pharmaceuticals study; authors state scientific conclusions unaffected

    DOI: 10.3390/ph18010111
  2. 7

    Khavinson V, Ilina A, Kraskovskaya N, Linkova N, Kolchina N, Mironova E, Erofeev A, Petukhov M (2021). Pharmaceuticals (Basel) — In vivo 5xFAD mouse model and molecular-docking study of KED and EDR tripeptides examining hippocampal dendritic-spine morphology and gene-promoter interactions

    DOI: 10.3390/ph14060515PubMed 34071923
  3. 8

    Sinjari B, Diomede F, Khavinson V, Mironova E, Linkova N, Trofimova S, Trubiani O, Caputi S (2020). Stem Cell Reviews and Reports — In vitro study of short peptides including KED in human oral stem cells examining differentiation markers under aging conditions

    DOI: 10.1007/s12015-019-09921-3PubMed 31677028
  4. 9

    Kraskovskaya NA, Kukanova EO, Lin'kova NS, Popugaeva EA, Khavinson VKh (2017). Bulletin of Experimental Biology and Medicine — In vitro hippocampal-neuron amyloid-synaptotoxicity model measuring dendritic spines under KED and EDR tripeptide treatment

    DOI: 10.1007/s10517-017-3847-2
  5. 10

    Kozlov KL, Bolotov II, Linkova NS, Drobintseva AO, Khavinson VK, Dyakonov MM, Kozina LS (2016). Advances in Gerontology — In vitro endothelial-cell study examining KED in atherosclerosis and restenosis models measuring signaling-molecule expression

    PubMed 28539025
  6. 11

    Khavinson VKh, Lin'kova NS, Tarnovskaya SI (2016). Bulletin of Experimental Biology and Medicine — Molecular-docking study of DNA–short-peptide complexes examining candidate gene-expression regulation mechanisms

    DOI: 10.1007/s10517-016-3596-7
  7. 12

    Khavinson VKh, Tarnovskaia SI, Lin'kova NS, Guton EO, Elashkina EV (2014). Advances in Gerontology — In vitro vascular-endothelial cell-proliferation study examining Ki-67 expression and MKI67-promoter docking during aging

    PubMed 25051766

Primary Database

PubChem CID 87571363↗

Also known as: KED, Lys-Glu-Asp

Research Use Only

These products are intended for research purposes only and are not for human consumption. Not FDA approved. Not intended to diagnose, treat, cure, or prevent any disease.