Vesugen is the trade name for a synthetic tripeptide with the sequence lysine-glutamic acid-aspartic acid, written Lys-Glu-Asp and abbreviated KED, another member of the short-peptide bioregulator program described generally in bioregulator peptides explained. Within that program, KED has most often been associated with vascular tissue, and the bulk of its published research looks at vascular endothelial cells under conditions modeling atherosclerosis and restenosis. More recent papers have extended KED into skin fibroblast aging and, in a 2024 study, into a human induced-neuron model, alongside some of the same peptides examined in the Pinealon literature. This article covers what those specific cell-culture and mechanistic studies reported.
| Attribute | Detail |
|---|---|
| Name | Vesugen, synthetic tripeptide |
| Sequence | Lys-Glu-Asp (KED), three amino acids |
| Class | Short peptide bioregulator, vascular-associated in the Khavinson peptide series |
| What studies examine | Endothelin-1 and connexin expression in vascular endothelium, sirtuin-1 expression, skin fibroblast proliferation and matrix remodeling markers, dendritic arborization in induced neurons |
| Model systems used | Cultured normal, atherosclerotic and restenotic vascular endothelium, aging skin fibroblast cultures, fibroblast-derived induced cortical neurons, cultured brain cortex cells |
| Form supplied | Lyophilized powder, research use only |
What is the Lys-Glu-Asp sequence, and how does it relate to other short peptides in this family?
KED is a three-amino-acid peptide from the same research program that produced Pinealon (Glu-Asp-Arg) and Epithalon (Ala-Glu-Asp-Gly); how that program organizes peptides by tissue association is described in bioregulator peptides explained. KED shares one early cell-culture paper with EDR, the sequence behind Pinealon, and the two are sometimes tested side by side, which makes it useful to read this article alongside what is Pinealon rather than treating either peptide's results as standing alone.
What has research examined in vascular endothelium models of atherosclerosis?
A 2016 study examined KED's effect on signaling molecule expression in cultured vascular endothelium under normal conditions and under two disease-relevant conditions, atherosclerosis and restenosis, reporting that KED normalized endothelin-1 expression, which the authors found elevated under both disease conditions, and restored cell-to-cell interactions mediated by connexin proteins. The same study reported that KED increased expression of sirtuin-1, a protein involved in DNA repair, and proposed epigenetic gene regulation as one likely mechanism behind the peptide's effects on these endothelial markers (Kozlov et al., 2016).
What has research examined in vascular endothelial cell proliferation during aging?
A related 2014 paper looked specifically at epigenetic aspects of how short peptides, including KED, regulate proliferation of vascular endothelial cells as these cells age in culture, extending the mechanistic picture from the atherosclerosis and restenosis study into a more general framework for peptide effects on aging vascular tissue at the gene-expression level (Khavinson et al., 2014).
What has research examined in skin fibroblast aging?
A 2016 study tested four short peptides, including KED, on aging skin fibroblasts in culture, measuring markers of proliferation, cell renewal, apoptosis and extracellular matrix remodeling by confocal microscopy. All four peptides tested, including KED, reduced synthesis of MMP-9, a matrix metalloproteinase whose production increases as skin fibroblasts age, and increased expression of the proliferation marker Ki-67 and the aging-related marker CD98hc, both of which are less actively produced in aged cultures (Linkova et al., 2016).
What has the most recent research examined in neuronal aging models?
A 2024 study introduced a human cell model built by converting aged skin fibroblasts from elderly donors into induced cortical neurons, then tested KED alongside EDR and the tetrapeptide AEDG for effects on age-related neuronal changes in this new model. All three peptides, including KED, promoted greater dendritic tree branching, increasing both the number of primary dendritic processes and total dendrite length, in these induced neurons; the study also reported that EDR specifically reduced oxidative DNA damage in neurons derived from elderly donor fibroblasts, a measure the other peptides tested did not significantly change in this experiment (Kraskovskaya et al., 2024). An earlier, related study had reported that KED, together with EDR, stimulated serotonin expression in aging cultures of brain cortex cells through an epigenetic mechanism involving the tryptophan hydroxylase gene, a finding that connects this newer neuronal work back to some of the earliest published characterization of the KED sequence (Khavinson et al., 2014).
Has Vesugen appeared in observational human reports?
One small observational report in the published record describes cellular and biological-age markers in an older adult cohort. It is not a controlled trial and is listed here only for completeness of the literature; this article draws no conclusions from it.
What cell and tissue models have published studies used for Vesugen?
Published work on KED has used cultured vascular endothelium under normal, atherosclerotic and restenotic conditions, aging skin fibroblast cultures, cultured brain cortex tissue, and the induced-neuron model described above. Across these models the readouts are proliferation markers, gene and protein expression associated with cell aging, and, in the neuronal work, dendritic branching. None of these are outcome measures in a living subject; they are bench measurements taken from cells and tissue, which is the level at which this peptide is characterized in the research literature. Researchers comparing across the Khavinson short-peptide family will find the same model set reused for Pinealon and Vilon, which makes side-by-side comparison of published results more straightforward than it is for compounds studied in unrelated systems.
Frequently asked questions
What sequence does Vesugen contain?
Vesugen is a synthetic tripeptide with the sequence lysine-glutamic acid-aspartic acid, written Lys-Glu-Asp or abbreviated KED in the primary literature. It is supplied as a lyophilized powder; see the Vesugen 20 mg product page for lot documentation.
What cell and tissue models have published studies used for Vesugen?
Published work has used cultured vascular endothelium under normal, atherosclerotic and restenotic conditions, aging skin fibroblast cultures, cultured brain cortex cells, and, most recently, human induced cortical neurons derived from elderly donor fibroblasts.
Is Vesugen the same peptide as Pinealon?
No. Vesugen is the KED tripeptide and Pinealon is the EDR tripeptide. They come from the same research program and have appeared together in some of the same cell-culture experiments, but they are chemically distinct sequences; see what is Pinealon for that peptide's own literature.
What mechanism has research proposed for KED's effects on vascular endothelium?
Published work has proposed epigenetic gene regulation, including normalization of endothelin-1 expression, restoration of connexin-mediated cell-to-cell interactions, and increased sirtuin-1 expression, as candidate mechanisms observed in cultured endothelial cells.
Has Vesugen been studied in humans directly?
The literature identified for KED in this article consists of cell-culture studies, including cultures derived from human tissue donors. This article summarizes laboratory research models, not clinical evidence, and nothing here describes a protocol for use in any subject.
How is Vesugen supplied for laboratory use?
As a lyophilized powder intended for research use only, sold by lot with an accompanying certificate of analysis.
References
- Khavinson VK, Lin'kova NS, Umnov RS, et al. Peptide KED: Molecular-Genetic Aspects of Neurogenesis Regulation in Alzheimer's Disease. Bull Exp Biol Med. 2021;171(2):190-193. PubMed 34173097.
- Kozlov KL, Bolotov II, Linkova NS, Drobintseva AO, Khavinson VK, Dyakonov MM, Kozina LS. Molecular aspects of vasoprotective peptide KED activity during atherosclerosis and restenosis. Adv Gerontol. 2016;29(4):646-650. PubMed 28539025.
- Khavinson VKh, Tarnovskaia SI, Lin'kova NS, et al. Epigenetic aspects of peptidergic regulation of vascular endothelial cell proliferation during aging. Adv Gerontol. 2014;27(1):108-114. PubMed 25051766.
- Lin'kova NS, Drobintseva AO, Orlova OA, Kuznetsova EP, Polyakova VO, Kvetnoy IM, Khavinson VKh. Peptide Regulation of Skin Fibroblast Functions during Their Aging In Vitro. Bull Exp Biol Med. 2016;161(1):175-178. PubMed 27259496.
- Kraskovskaya N, Linkova N, Sakhenberg E, Krieger D, Polyakova V, Medvedev D, Krasichkov A, Khotin M, Ryzhak G. Short Peptides Protect Fibroblast-Derived Induced Neurons from Age-Related Changes. Int J Mol Sci. 2024;25(21):11363. PubMed 39518916.
- Khavinson VKh, Lin'kova NS, Tarnovskaya SI, Umnov RS, Elashkina EV, Durnova AO. Short peptides stimulate serotonin expression in cells of brain cortex. Bull Exp Biol Med. 2014;157(1):77-80. PubMed 24909721.
- Meshchaninov VN, Tkachenko EL, Zharkov SV, Gavrilov IV, Katyreva IuE. Effect of synthetic peptides on aging of patients with chronic polymorbidity and organic brain syndrome of the central nervous system in remission. Adv Gerontol. 2015;28(1):62-67. PubMed 26390612.
Research use only. Homegrown Peptides products are for laboratory research and are not for human or animal use. Nothing in this article is medical advice.
