Vesugen
Also known as: KED · Lys-Glu-Asp · Vezugen (alternate transliteration) · peptide KED · vascular Cytogen
Research focus
Vascular endothelium and the aging arterial wall
US regulatory status
Not FDA-approved · Not compoundable
Evidence rating
Theoretical
Origin
Vesugen is a synthetic tripeptide (Lys-Glu-Asp, often abbreviated KED) developed by the research group of Vladimir Khavinson at the St. Petersburg Institute of Bioregulation and Gerontology in Russia. It belongs to the group's family of "short peptide bioregulators" — very short, chemically synthesized sequences (typically 2-4 amino acids) that the group designed as putative analogues of larger tissue-extract "Cytomax" preparations. Unlike the original organ-extract bioregulators, KED is a fully synthetic, defined sequence. Within the Khavinson catalogue it is marketed as the "vascular" Cytogen, intended as a counterpart to the heart, thymus, pineal, and other tissue-targeted peptides in the same line. Essentially all primary literature on it originates from this single St. Petersburg group and its close collaborators (Linkova/Lin'kova, Kozlov, Tarnovskaia, Ryzhak, and colleagues); it has no independent development history outside that network.
Plain-language summary
Vesugen (also called KED) is a lab-made three-amino-acid peptide from the same Russian gerontology group behind Epitalon and the other "bioregulator" peptides. It is sold as a "vascular" peptide, with the idea that it supports the lining of blood vessels as people age. The published evidence, though, is very thin, and comes almost entirely from a single group in St. Petersburg. Most of it is test-tube experiments on cultured cells and computer-docking models, plus a handful of review articles. There is essentially one small, uncontrolled human report, and no rigorous, independently-replicated human trials. It is not an FDA-approved drug and is sold online only as a "research chemical." Treat strong vascular or anti-aging claims about it with heavy skepticism.
Claimed mechanism (as reported)
Published work from the Khavinson group proposes that KED acts as an epigenetic "peptidergic regulator" of the vascular endothelium — reportedly binding short promoter regions of specific genes and shifting their expression. In cell-culture and molecular-docking papers the group claims KED normalizes endothelin-1 expression, restores connexin-mediated cell contacts, raises sirtuin-1 (SIRT1), and increases the proliferation marker Ki-67 (via the MKI67 promoter) in aged endothelial cells. This DNA-/promoter-binding model is supported almost entirely by in-silico docking and in-vitro work from one research group; the mechanism remains unproven and has not been independently confirmed. All mechanistic claims here are reported findings, not established facts.
Evidence summary
The evidence base for Vesugen/KED is minimal and almost entirely preclinical and single-group. According to PubMed, the published record consists mainly of in-vitro endothelial cell-culture studies and molecular-docking papers from the St. Petersburg Institute of Bioregulation and Gerontology (Khavinson, Linkova/Lin'kova, Kozlov and colleagues), plus narrative reviews. There are no large, blinded, independently-replicated randomized controlled trials in peer-reviewed English-language literature as of 2026. The only human-subject report we could identify is a single small, open-label, uncontrolled case series (n=41) using the alternate-spelling "Vezugen" in vasculogenic erectile dysfunction, published in a Russian-language gerontology journal by the same affiliated group — far too weak and too conflicted to establish human efficacy. We therefore grade this "No Human Data": there is no credible, independent human evidence of clinical benefit. Mechanistic claims (endothelin-1, SIRT1, Ki-67, connexins) are reported in cell models only and have not been confirmed independently.
What the research reports
Molecular aspects of vasoprotective peptide KED activity during atherosclerosis and restenosis (in vitro)
Grade DKozlov KL, Bolotov II, Linkova NS, Drobintseva AO, Khavinson VKh et al. · Advances in Gerontology (Uspekhi Gerontologii) · 2016
Reported finding: The group reported that KED normalized endothelin-1 expression (elevated in atherosclerosis/restenosis models), restored connexin-mediated cell contacts, and increased SIRT1 expression in cultured endothelium. Presented as a proposed epigenetic mechanism, without independent replication.
Sample: Cell-culture experiments (normal, atherosclerotic, restenotic endothelium in vitro); no human subjects
Methodology: D — in-vitro endothelial cell cultures only, single research group, no human or animal outcomes
Limitations: Test-tube only; no human or in-vivo efficacy data; single group; Russian-language journal; mechanism inferred, not proven.
Epigenetic aspects of peptidergic regulation of vascular endothelial cell proliferation during aging
Grade DKhavinson VKh, Tarnovskaia SI, Lin'kova NS, Guton EO, Elashkina EV · Advances in Gerontology (Uspekhi Gerontologii) · 2014
Reported finding: Reported that vesugen (KED) increased the proliferation marker Ki-67 in aged endothelial cell cultures, and used molecular docking to propose KED binds a short core-promoter region of the MKI67 gene. Framed as a possible epigenetic basis for a previously claimed vasoprotective effect.
Sample: Tissue-specific and dissociated endothelial cell cultures from young/old animals; computational docking; no human subjects
Methodology: D — in-vitro cell culture plus in-silico molecular docking, single group, no clinical data
Limitations: Docking + cell culture only; binding is computationally predicted, not experimentally confirmed; no in-vivo or human outcomes; single group.
Efficacy of peptide bioregulators of vessels in chronic lower-limb arterial insufficiency in older patients (Vezugen, vasculogenic erectile dysfunction)
Grade DKitachev KV, Sazonov AB, Kozlov KL, Petrov KIu, Sliusarev AS, Khavinson VKh · Advances in Gerontology (Uspekhi Gerontologii) · 2014
Reported finding: Authors reported that penile arterial blood flow (Doppler) improved after Vezugen monotherapy versus baseline. Indexed by PubMed as a 'Clinical Trial' but uncontrolled and not blinded; reported by the same group that developed the peptide, with no independent replication.
Sample: n=41 men with vasculogenic erectile dysfunction (before/after comparison, no control arm)
Methodology: D — small open-label, uncontrolled, unblinded case series; single affiliated group; foreign-language journal
Limitations: No control group, no blinding, no randomization, small sample, single conflicted group; cannot establish efficacy. This is the only human-subject report identified and does not constitute credible human evidence.
Peptide KED in neurogenesis and cellular aging (mechanistic reviews and in-vitro work, non-vascular)
Grade DKhavinson VKh, Lin'kova NS, Umnov RS; Kraskovskaya N, Linkova N, Ryzhak G et al. · Bulletin of Experimental Biology and Medicine; International Journal of Molecular Sciences · 2021–2024
Reported finding: These papers discuss KED alongside other short peptides (EDR, AEDG) in cell-aging and Alzheimer's-model contexts and restate an oral-KED memory/attention claim, but provide no controlled human vascular efficacy data. Included to show the corpus is dominated by mechanistic and review work from the same network, not clinical trials.
Sample: Review articles and induced-neuron / cell-culture experiments; no human efficacy cohorts
Methodology: D — narrative reviews and in-vitro cell models; no controlled human trials
Limitations: Reviews and in-vitro only; non-vascular endpoints; circular citation within one group; no independent human RCTs.
Administration reported in studies
There is no established or validated human dosing for Vesugen. The mechanistic studies are cell-culture and computational and involve no whole-organism dosing at all. In the single small open-label human report, KED was given as the commercial "Vezugen" capsule preparation (an oral short-peptide product) as monotherapy over a treatment course; the paper does not establish a standardized, validated regimen. Online "research chemical" vendors variously sell KED as oral capsules or as lyophilized powder for reconstitution, but those channels are unregulated and not standardized. This is a summary of research conditions — not a dosing recommendation and not a protocol endorsed by TPC.
This section reports what published studies describe. It is not a dosing recommendation from TPS.
Safety record
There is essentially no formal human safety dataset for Vesugen. No controlled safety trials, no published pharmacokinetics, and no long-term human follow-up could be identified. The single small open-label human report did not constitute a safety study and would not detect uncommon or delayed harms. Khavinson-group publications generally describe their short peptides as low-toxicity in their own models, but absence of reported harm in a tiny, conflicted, uncontrolled literature is not evidence of safety. Material sold online as a "research chemical" carries the usual unregulated-supply risks: unverified identity, purity, sterility, and dosing. Anyone considering it should involve a qualified clinician. TPC does not endorse use.
US legal status
Not FDA-approved for any use. Not on the FDA 503A compoundable bulk drug substances list, and not legally compoundable for human clinical use in the United States. Vesugen/KED is sold online only as a "research chemical" — vendors in that channel are unregulated and are not verified by TPC. It is not a dietary supplement and is not an approved drug; marketing it for the diagnosis, treatment, or prevention of any disease would be unlawful.
Open research questions
- ? Does Vesugen/KED produce any measurable vascular or endothelial benefit in humans under blinded, placebo-controlled conditions — and can any result be reproduced by a group with no ties to the original St. Petersburg developers?
- ? Is the proposed epigenetic mechanism (promoter binding, endothelin-1/SIRT1/Ki-67 modulation) real and specific in vivo, or an artifact of in-silico docking and isolated cell-culture systems?
- ? What are the basic pharmacokinetics of an orally administered Lys-Glu-Asp tripeptide — is it even absorbed intact and delivered to vascular tissue, or simply digested as dietary amino acids?
- ? What is the actual human safety profile, including long-term and uncommon adverse effects, given that no controlled safety study or formal toxicology in humans has been published?
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