What is Vesugen?
Vesugen, also transliterated Vezugen, is a short peptide associated with vascular-cell research. The clinical record identifies lysyl-glutamyl-aspartic acid, commonly abbreviated KED.
Mechanism & research focus
Laboratory work has examined changes in endothelial proliferation markers. A proposed interaction with the MKI67 promoter was based partly on molecular docking; docking predicts possible binding and does not by itself establish target engagement in people.
What the research covers
A 2014 cell-culture report examined Ki-67 responses and computational promoter interactions. A separate 2014 publication described before-and-after vascular measurements in 41 patients with vasculogenic erectile dysfunction, reporting improvement after Vezugen exposure.
What is vesugen?
Vesugen is the name used in the St Petersburg short-peptide literature for the synthetic tripeptide Lys-Glu-Asp, abbreviated KED (Khavinson et al., 2012). Some papers from the same group call it T-38 (Voicekhovskaya et al., 2012).
It belongs to the series developed at the St Petersburg Institute of Bioregulation and Gerontology alongside epitalon, pinealon and cardiogen, and the group links it to cardiovascular regulation (Khavinson et al., 2021). The literature is small and comes almost entirely from that institute and its collaborators.
Vesugen reference data
| Property | Value |
|---|---|
| Name | Vesugen |
| Aliases | Lys-Glu-Asp and T-38 (both filed with vesugen in NLM MeSH record C533570), KED peptide; spelled vezugen in some Russian-language abstracts |
| Sequence in the literature | Lys-Glu-Asp (L-lysyl-L-glutamyl-L-aspartic acid, PubChem CID 87571363) |
| Peptide class | Tripeptide |
| Molecular formula | C₁₅H₂₆N₄O₈ for the free peptide (PubChem) |
| Molecular weight | 390.39 g/mol for the free peptide (PubChem); a salt form weighs more |
| CAS number | 204271-66-9 (among the synonyms in PubChem) |
| Name search | PubChem returns no record for "vesugen"; the compound is filed under Lys-Glu-Asp |
| Size carried | 20MG |
Note that vesugen and epitalon (C₁₄H₂₂N₄O₉) share a nominal mass of 390, with monoisotopic masses only about 0.036 Da apart, so a low-resolution mass reading alone does not tell them apart.
What the research covers
Published work falls into five areas, and each summary below states the model used. A PubMed search for the name, its spellings, the T-38 code and the sequence returns about 40 relevant records once unrelated hits and longer Lys-Glu-Asp tetrapeptides are removed. More than 30 list V. Kh. Khavinson as an author or an affiliation with his institute or the Pavlov Institute of Physiology, nearly every primary study has a co-author from that network, about half are in Russian, and many test the tripeptide alongside other peptides.
Explant cultures from young and old rats
In splenic explants, the peptide at 0.05 ng/mL enlarged the growth zone, and with cyclophosphamide in the medium the cytostatic's inhibition did not appear (Chalisova et al., 2008). In skin explants, four of five related tripeptides stimulated proliferation in tissue from young rats, and this one had a marked effect in tissue from old rats, linked by the authors to less p53-associated apoptosis (Voicekhovskaya et al., 2012). In pineal cultures it raised Ki-67 without changing the apoptosis marker AIF (Khavinson et al., 2011).
Vascular cell cultures
The vascular label rests on a few cell studies. In organotypic and dissociated vascular cell cultures, T-38 and a dipeptide tested with it raised Ki-67, lowered p53 and reduced synthesis of the adhesion molecule E-selectin (Khavinson et al., 2014). A Russian-language study reported normalized endothelin-1 and higher connexin and sirtuin-1 expression in endothelial cultures modeling atherosclerosis and restenosis (Kozlov et al., 2016). Neither has been repeated elsewhere.
Immune, fibroblast and stem cell cultures
In human cortical thymocytes, it and a related tripeptide shifted differentiation towards regulatory T cells and lowered apoptosis (Khavinson et al., 2011), and in human prostatic fibroblasts it stimulated two differentiation factors, more strongly in aged cultures (Khavinson et al., 2012).
In fetal mesenchymal stem cells it was one of three peptides that raised IGF1 expression 3.5 to 5.6 times, and it lowered FOXO1 1.6 to 2.3 times, while its effect on TNKS2 ran in opposite directions in two aging models (Ashapkin et al., 2020). In human oral stem cells at passage 25, it lowered p16 and p21 messenger RNA 1.82 to 3.23 times (Sinjari et al., 2020).
Neuronal models
In mouse hippocampal neurons exposed to amyloid beta, 200 ng/mL raised mushroom spine numbers by 20 percent, against 71 percent for pinealon (Kraskovskaya et al., 2017). In cortical neurons transdifferentiated from elderly donors' skin fibroblasts, it was one of three peptides that increased dendrite number and length, with no change in mitochondrial or lysosomal activity or p16 (Kraskovskaya et al., 2024).
In 5xFAD mice given the peptide systemically each day from two to four months of age, neuroplasticity measures tended to rise and dendritic spine loss was prevented (Khavinson et al., 2021). A 2025 correction replaced two confocal figures in that paper that had been published as the same image; the authors state the conclusions are unaffected (PMID 39861198).
Other reports, including reports in people
Russian-language papers list the tripeptide among four short peptides with antihypoxic activity in a hypobaric hypoxia model, where pinealon had the strongest effect (Kozina, 2008). About seven Russian-language reports describe it given to adults, such as 41 patients assessed before and after receiving it following vascular surgery (Kitachov et al., 2013) and 32 people followed on markers of biological age (Meshchaninov et al., 2015).
None of the abstracts reports randomization, blinding or a placebo group, and the second also recorded pro-oxidant activity and a fall in circulating CD34-positive cells.
What remains uncertain
The accessible clinical abstract does not describe a randomized placebo-controlled comparison. A small before-and-after report is vulnerable to bias and cannot establish causality or broad cardiovascular benefit. The evidence does not validate every product sold under the name, and long-term safety and independent replication remain important gaps.
The evidence label describes the linked research, not the suitability of a catalog product for use in people. Formulation, identity, purity, and measured content must be assessed separately.
Sources & studies
Epigenetic aspects of peptidergic regulation of vascular endothelial cell proliferation during aging ↗
Vesugen-associated proliferation markers and a proposed promoter interaction derived from molecular docking.
Peptide bioregulators of vessels in chronic arterial insufficiency ↗
Abstract describes 41 patients and before-and-after blood-flow measurements; randomization and placebo control are not described.
Read the full paper for its design, controls and limitations. A source link is not a claim that its tested material matches a DA formulation.
Catalog formats & documentation
Formats grouped by compound identity. Availability and batch documentation remain on Disguised Alpha.
Original DA reference: Vesugen research guide ↗
