Vesugen (KED): blood-vessel health peptide
A tiny synthetic peptide studied for supporting blood-vessel lining health; sold as a supplement in Russia but not approved as a drug anywhere.
- Class
- Bioregulator peptide (Khavinson system) — synthetic vascular tripeptide
- Status
- Not approved by FDA, EMA, MHRA, Health Canada, or TGA. Sold in Russia as an oral peptide bioregulator in a dietary-supplement / functional-food category. Human-adjacent evidence (small uncontrolled Russian studies) exists but does not meet the threshold for human evidence tier.
- Best-supported effect
- Normalization of endothelin-1 and E-selectin in human vascular endothelial cell models (in vitro); antihypoxic effects in animal models (preclinical).
- Main caveat
- Virtually all evidence — mechanistic, in vitro, and clinical — originates from Khavinson-affiliated investigators; independent Western replication of the core KED-DNA epigenetic mechanism and any clinical claims is essentially absent.
A researcher, an agent, or an algorithm wrote down the sequence and picked a target to hit.
An AI model like OpenFold3 or AlphaFold built a 3D structure and scored how well it fits the binding site.
A second contributor repeated the computation on their own hardware and the scores matched.
A chemistry service or a researcher ordered the sequence, it was manufactured, and mass spectrometry confirmed the right molecule was produced.
A binding or activity measurement confirmed that it actually does what the computer predicted — or didn't.
Snapshot
Class: Bioregulator peptide (Khavinson system) — synthetic vascular tripeptide
Evidence tier: Animal-only evidence
Status: Not approved by FDA, EMA, MHRA, Health Canada, or TGA. Sold in Russia as an oral peptide bioregulator in a dietary-supplement / functional-food category. Human-adjacent evidence exists (small uncontrolled Russian studies) but does not meet the threshold for human evidence tier.
Best-supported effect: Normalization of endothelin-1 and E-selectin in human vascular endothelial cell models (in vitro); antihypoxic effects in animal models (preclinical)
Main caveat: Virtually all evidence — mechanistic, in vitro, and clinical — originates from Khavinson-affiliated investigators; independent Western replication of the core KED–DNA epigenetic mechanism and any clinical claims is essentially absent
What this is
Vesugen is a synthetic tripeptide — Lys-Glu-Asp (KED) — developed by Vladimir Khavinson as part of the Russian bioregulator peptide system. It belongs to the Cytogen class: short, lab-synthesized peptides intended to replicate regulatory activity attributed to peptides originally fractionated from animal vascular tissue (calf and porcine aorta). Vesugen is the synthetic counterpart to Ventfort, a cruder vascular-tissue Cytomax preparation, with the active sequence reduced to three amino acids.
The peptide shares nearly identical chemistry with Livagen (KEDA), differing only by a C-terminal alanine residue. The Khavinson group claims the two sequences exhibit distinct tissue tropism — KED targeting vascular endothelium and KEDA targeting liver and immune tissue — but this tissue-specificity claim has not been independently validated.
Vesugen has been investigated for vascular protection, endothelial function in aging, atherosclerosis, vasculogenic erectile dysfunction, and anti-aging effects within the Khavinson bioregulator framework. With approximately 27 indexed PubMed publications, it is among the more extensively published peptides from this program, though the evidence base is concentrated almost entirely within Khavinson-affiliated Russian research settings.
Evidence map
| Evidence layer | Grade | What it supports |
|---|---|---|
| Human | Weak — small uncontrolled Russian studies; does not qualify for human evidence tier | Two small uncontrolled Russian clinical reports with efficacy endpoints are present in the available literature: a 41-patient vasculogenic ED study and a 32-patient chronic polymorbidity cohort. Both are uncontrolled, originate within the Khavinson research network, and do not meet modern RCT standards. A review of oral KED in elderly cognitive disorders is also present. No blinded controlled trials; no registered trial IDs; no Western replication. |
| Animal | Moderate (preclinical) | Antihypoxic properties in animal models. In vitro endothelial cell work (using human cell lines in preclinical research context) demonstrating endothelin-1 normalization, connexin restoration, sirtuin-1 enhancement, Ki-67 upregulation, and E-selectin reduction (, 22808515, 25051766). |
| In vitro | Moderate | Multiple in vitro studies in human vascular endothelial cell cultures: normalization of atherosclerosis-related endothelial markers; aging-specific induction of differentiation factors (CXCL12, Hoxa3, WEGC1) with stronger effects in late-passage cultures; modulation of senescence markers p16/p21 and neurogenesis-related genes in neural tissue models; molecular docking data showing KED contact with the MKI67 gene promoter (, 25051766, 22808515, 27259496, 25408528, 39518916). |
| Computational | Weak | Molecular docking demonstrates KED contact with the MKI67 gene promoter at positions −14 to +12 relative to the transcription start site. Interpreted by Khavinson-affiliated authors as supporting an epigenetic mechanism; no independent computational replication identified in source. |
| Mechanism | Plausible (within Khavinson framework; not independently replicated) | Proposed direct DNA–histone interaction in vascular endothelial cell nuclei with epigenetic reactivation of vascular maintenance genes. Supported by in vitro and docking data from Khavinson-affiliated investigators. Independent Western laboratory replication is essentially absent. |
Replication caveat: The large majority of published evidence — mechanistic, in vitro, and clinical — originates from a single research network (Khavinson-affiliated laboratories and Russian clinical settings). Independent replication depth is a defining limitation of the current evidence base across all layers, not only the clinical reports.
Claim check
| Claim | Verdict | Evidence layer | Confidence |
|---|---|---|---|
| Normalizes endothelin-1, E-selectin, and sirtuin-1 in vascular endothelial cell models | Supported (in vitro) | In vitro | Medium — Khavinson-affiliated labs only; no independent Western replication |
| Improves vasculogenic erectile dysfunction | Weak | Human | Low — single 41-patient uncontrolled Russian study; no RCT; no comparator arm; single research network |
| Cognitive or anti-aging benefit in elderly patients | Weak | Human | Low — single 32-patient uncontrolled Russian cohort; below modern RCT standards; single research network |
| Reverses or clinically reduces atherosclerosis in living patients | Not established | In vitro | High confidence in verdict — in vitro endothelial biomarker modulation is not equivalent to clinical plaque regression; no imaging or hard cardiovascular outcome data in source |
| Tissue-specific tropism for vascular endothelium (distinct from Livagen/KEDA) | Not established | Computational | Low — based on molecular docking and Khavinson-framework claims only; no independent mechanistic validation |
Experimental exposure
This section reports exposure described in the available literature material for the Russian clinical reports. It does not establish human dosing.
| Context | System / population | Exposure described | Duration | Endpoint | Limitation |
|---|---|---|---|---|---|
| Russian clinical study (uncontrolled) | 41 patients with vasculogenic erectile dysfunction | Vesugen; route and exact regimen not individually extracted in available literature | Not individually extracted | Penile arterial blood flow (Doppler) | Uncontrolled; no placebo arm; Khavinson-affiliated authorship; no Western replication |
| Russian clinical study (uncontrolled) | 32 patients with chronic polymorbidity and organic brain syndrome | Vesugen; route and exact regimen not individually extracted in available literature | Not individually extracted | Anti-aging markers; CNS function (comparison with Pinealon) | Uncontrolled; methodology below modern RCT standards; single research network |
| Russian clinical review | Elderly patients with CNS disorders | Oral KED formulation; regimen not individually extracted | Not individually extracted | Memory and attention assessments | Review-level evidence; individual study data not separately extracted in this card |
Preclinical safety signals
| Signal | System | Notes |
|---|---|---|
| No significant adverse effects reported | Khavinson-affiliated Russian clinical studies | Reported as generally well-tolerated in available studies; surveillance scale is limited and studies are not designed for comprehensive AE capture |
| Mild injection-site reactions | Injectable form — per available sources | Noted as possible; not systematically quantified in available sources |
| Ki-67 upregulation in vascular endothelial cells | In vitro (preclinical) | published literature explicitly identifies the claimed Ki-67/chromatin reactivation mechanism as mechanistically the wrong direction in oncology contexts; no clinical oncology safety data present |
| Long-term safety | Not established | No chronic controlled human safety data identified in source; 32-patient study found no chromatin condensation changes, but this single small short-term observation does not establish long-term safety |
Source-described contraindications (theoretical or source-framework based):
- Active or recent malignancy — claimed mechanism includes Ki-67 upregulation and chromatin reactivation, which source identifies as mechanistically inappropriate in oncology contexts
- Concurrent anti-angiogenic oncology therapy — source describes theoretical mechanistic opposition (same rationale as anti-angiogenic conflicts described for other vascular peptides)
- Pregnancy — no reproductive toxicology data in source
- Breastfeeding — no data on transfer or infant exposure in source
- Pediatric use — no pediatric data; vascular-development signaling effects unknown
Drug interaction note from source: No documented clinical drug interactions exist due to absence of human pharmacovigilance studies. a theoretical concern with anti-angiogenic and anti-proliferative oncology agents (bevacizumab, VEGF-pathway TKIs) based on proposed mechanism. A more speculative concern is noted for antihypertensives and nitrate-class vasodilators given claimed endothelin-1 modulation; magnitude in humans is unknown. Source states: absence of documented interaction is not absence of interaction. No CYP-mediated interactions are described.
Regulatory status
| Region / body | Status | Notes |
|---|---|---|
| US (FDA) | Not approved | Not FDA-approved for any indication; not on FDA's compounding-eligible peptide list; not recognized as a dietary supplement ingredient; available in the US only through research-chemical suppliers not authorized for human use |
| EU (EMA / MHRA) | Not authorized | Per available sources, not authorized as a medicine by EMA or MHRA |
| Canada (Health Canada) | Not authorized | per available sources; not independently verified in this card |
| Australia (TGA) | Not mentioned in source | not individually extracted |
| Russia | Sold as oral peptide bioregulator (dietary-supplement / functional-food category) | Registered and sold under the Peptides.ru / Khavinson Peptides brand; per available sources; not independently verified in this card. Not classified as a prescription medicine under the Russian system per source description. |
| WADA | Source-reports probable prohibition under S0 | Injectable Vesugen falls under the WADA S0 catch-all for substances not approved by any governmental health authority for human therapeutic use; source-bundle reported; current WADA Prohibited List status not independently verified in this card |
Mechanism
Vesugen (Lys-Glu-Asp, KED) is proposed to penetrate cell membranes and interact directly with DNA and histone proteins in vascular endothelial cell nuclei — an epigenetic mechanism of action. Molecular docking studies from Khavinson-affiliated investigators show the tripeptide contacts the MKI67 gene promoter at positions −14 to +12 relative to the transcription start site, consistent with a proposed transcriptional regulation of the Ki-67 proliferation marker.
In endothelial cell models, the peptide is reported to normalize endothelin-1 expression (elevated in atherosclerosis), restore connexin-mediated cell-cell communication, enhance sirtuin-1 expression (associated with DNA repair and senescence regulation), reduce E-selectin (associated with atherosclerotic plaque formation), and upregulate Ki-67 while suppressing p53. In aging cell cultures, effects are reportedly more pronounced in late-passage cells, with induction of differentiation factors CXCL12, Hoxa3, and WEGC1. Source also describes modulation of senescence markers p16/p21 and neurogenesis-related markers (nestin, GAP43) in neural tissue models.
Mechanism limitations: The primary target and proposed epigenetic mechanism derive almost entirely from Khavinson-affiliated publications. Independent Western laboratory replication of the KED–DNA docking interaction and the downstream endothelial effects is essentially absent from available literature. The proposed tissue specificity of KED for vascular endothelium — as distinct from the near-identical KEDA/Livagen — lacks an independent mechanistic explanation. Ki-67 upregulation as part of the proposed vascular benefit mechanism is identified in available literature as mechanistically the wrong direction in oncology contexts.
Chemistry
| Field | Value |
|---|---|
| Sequence | Lys-Glu-Asp (single-letter: K-E-D) |
| Full name | Lysine-Glutamic acid-Aspartic acid |
| Length | 3 amino acids |
| Topology | Linear |
| Modifications | None described in source |
| Molecular weight | Not provided in available literature |
| Formula | Not provided in available literature |
| CAS | Not provided in available literature |
| Salt form | Not specified in source |
| Related peptide | Livagen (KEDA) — shares the KED backbone; differs by a C-terminal alanine residue |
| Sequence confidence | Verified — consistently reported as Lys-Glu-Asp across all source sections |
Open questions
- Independent replication of the epigenetic mechanism: Western laboratory replication of the KED–DNA docking interaction and in vitro endothelial effects is essentially absent. This is the central unresolved question for the entire mechanistic framework.
- Tissue-specificity mechanism: The claim that KED targets vascular endothelium while the near-identical KEDA targets liver and immune tissue lacks an independently validated mechanistic explanation. Whether this distinction is real or an artifact of the Khavinson classification system requires investigation outside the originating laboratory.
- Randomized controlled trials for vascular endpoints: The existing Russian clinical reports on vasculogenic ED and elderly polymorbidity cohorts do not meet modern RCT standards. Blinded, randomized, placebo-controlled trials with pre-registered endpoints are absent.
- Human pharmacokinetics: Absorption (particularly oral and sublingual bioavailability of a tripeptide), distribution to vascular endothelium, and clearance have not been characterized in humans across routes.
- Long-term safety given Ki-67 upregulation: Chronic activation of the Ki-67 proliferation marker in vascular tissue has not been studied for off-target proliferative effects in any long-duration exposure setting.
- Oral and sublingual vs. injectable bioequivalence: No head-to-head bioavailability data exists. The Khavinson capsule product and the research-chemical injectable operate in different regulatory and supply contexts; systemic exposure of oral KED in humans has not been characterized.
- Comparative efficacy versus first-line pharmacotherapy: No head-to-head studies against statins, antiplatelets, ACE inhibitors, or PDE5 inhibitors exist in available literature.
Research directions for this peptide, selected from the current sources — hypotheses you can explore and model. None of it is proven yet; tap any one to see the full thinking.
Does one extra building block on KED completely change which organ it targets in the body?
If confirmed, this finding would reveal a simple rule for directing tiny peptides to specific tissues, which could be used to design targeted drugs for blood vessel disease and blood disorders using the same basic peptide scaffold, making drug development faster and cheaper.
Could KED protect normal blood vessels from the damage caused by anti-cancer drugs that block blood vessel growth?
Drugs that block tumour blood vessel growth are widely used in cancer but often cause high blood pressure and heart problems in patients. If KED can protect normal blood vessels without interfering with the anti-cancer effect, it could allow more patients to complete their cancer treatment safely.
▸full evidence table2 metrics
| metric | value | tool |
|---|---|---|
| ipTM | 0.8437104225158691 | openfold3-mlx |
| ranking score | 0.8984699249267578 | openfold3-mlx |
▸structural qualityopenfold3
| metric | value | note |
|---|---|---|
| gpde | 0.403 | global PDE — lower = better |
| disorder | 0.097 | fraction disordered |
| chain pair ipTM (A, B) | 0.844 | interface quality |
▸3-letter notation
▸recipeopenfold3-mlx 0.3.1
| parameter | value |
|---|---|
| model | openfold3-mlx 0.3.1 |
| weights | — |
| hardware | — |
| mlx version | — |
| python | — |
| random seed | — |
| msa strategy | — |
| diffusion samples | 1 |
| runtime | 77s |
| predicted by | mlx@peptide |
| predicted at | 2026-05-03 |
▸citationbibtex
@peptide{pep10934,
sequence = {KED},
target = {longevity},
author = {peptidemodel},
year = {2026},
status = {computed}
}