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A specimen of the Other drawer Drawer G · Other

Vesugen

Research Only

A synthetic tripeptide (Lys-Glu-Asp) developed by Russian scientist Vladimir Khavinson, claimed to support vascular health by modulating endothelial gene expression. The only published primary research is Russian in-vitro work on cultured endothelium. No animal vascular studies, no human clinical validation, and no regulatory approval anywhere.

KED-vascular · Lys-Glu-Asp (vascular) · Vascular tripeptide

Research evidence
Low

Preclinical evidence only

Preclinical
100%
Human research
0%

Based on 2 cited sources

Numeric assessment unreviewed

A historical numeric score is recorded but has not passed a current, compound-specific assessment review. No numeric score is displayed.

This is a limitation of the numeric assessment, not a measured absence of benefit. It does not re-review the separately recorded catalogue classification or establish efficacy or safety.

Scoring context and limitations
!
Evidence Level
low
Not FDA-approved.
Research Only
Identity
SCALE · 1:1 N-TERMINUS C-TERMINUS 3 AA · ~390 Da
Also Known As
KED-vascular • Lys-Glu-Asp (vascular) • Vascular tripeptide
Class
Tripeptide
Length
3 amino acids
Mol. weight
~390 Da
Sequence
KED
Molecular Structure
K
E
D
Hydrophobic
Polar
Positive
Negative

The proposed mechanisms of Vesugen are based entirely on Russian research from the St. Petersburg Institute of Bioregulation and Gerontology. No independent Western validation exists.

How It Works (Simplified)

Vesugen targets vascular health through endothelial gene modulation and related pathways:

Endothelial Gene Expression

Binds to DNA sequences in endothelial cells, modulating expression of genes related to vascular tone, permeability, and cell function.

Nitric Oxide Pathway

May influence nitric oxide signaling and endothelial-dependent vasodilation, supporting healthy blood flow and vascular reactivity.

Antioxidant Protection

Proposed to reduce oxidative stress in vascular tissue, protecting endothelial cells from age-related damage and dysfunction.

Vascular Aging Modulation

Claimed to counteract age-related changes in vascular gene expression patterns, potentially supporting healthier vascular aging.

Key Context: All research originates from the St. Petersburg Institute of Bioregulation and Gerontology (Khavinson’s institute). No independent Western validation exists for any claimed mechanisms.

Important Limitations

  • 100% of research from Russian institutes associated with Khavinson
  • No independent Western replication of any findings
  • Only in-vitro (cultured-cell) studies exist; no animal vascular studies
  • No human studies of any kind have been published
  • Human pharmacokinetics, bioavailability, and optimal dosing unknown
  • Translation from cell culture to meaningful cardiovascular benefits is unconfirmed
  • Regulatory status: Not approved anywhere; unregulated research peptide
i. Endothelial Gene Modulation Pathway · Vascular Function
VesugenDNA Binding in Endothelial CellsGene Transcription ModulationVascular Tone Genes ↑Endothelial Function SupportVasodilation FactorsBlood Flow Regulation
ii. Vascular Protection Pathway · Oxidative Defense
VesugenEndothelial Cell UptakeAntioxidant Gene Expression ↑Reduced Oxidative StressEndothelial Protection
Mechanism Modulation of endothelial cell gene expression affecting vascular function
Emerging 1 direct study
Benefit suggested to support healthy vascular endothelium
Evidence Level
Very Low
2 In Vitro
Mechanism Regulation of vascular tone factors (endothelin-1)
Emerging 1 direct study
Benefit may promote healthy blood flow
Evidence Level
Very Low
1 In Vitro
Mechanism Geroprotective regulation of endothelial cell maintenance (sirtuin1)
Emerging 1 direct study
Benefit may support endothelial cell maintenance during aging
Evidence Level
Very Low
1 In Vitro
Mechanism Modulation of age-related vascular cell renewal
Emerging 1 direct study
Benefit suggested to support healthy vascular aging
Evidence Level
Very Low
1 In Vitro
Mechanism Confidence
Established
Supported
Emerging
Evidence Level
High
Moderate
Low
Very Low
Phase 01 1
Week 1-2

Based on in-vitro data only: changes in endothelial gene expression (e.g. endothelin-1, connexin) have been observed in cultured cells. No human time-course data exist.

PMID:28539025
Phase 02 2
Week 2-4

No animal or human dosing-response data exist for KED in vascular tissue. Russian protocols are described anecdotally as 10-20 day cycles, but these are not supported by published pharmacological studies.

Phase 03 3
Week 4-8

In-vitro studies report effects on vascular-cell renewal markers (Ki-67, p53) and adhesion molecules (E-selectin). No measured effects in animals or humans are documented.

PMID:25408528
Phase 04 4
Week 8+

No long-term human data exist. Optimal treatment duration and cycling protocols are not established, and human pharmacokinetics are unknown.

Research-based observations

This timeline reflects observations from published clinical and preclinical studies. Individual responses may vary significantly. This is not a guarantee of effects or a dosing schedule. Consult qualified healthcare providers for personalized guidance.

Synergistic
Compatible
Caution
Avoid

Both Khavinson cardiovascular peptides - Cardiogen targets heart muscle, Vesugen targets blood vessel endothelium. May have complementary vascular system effects.

Both Russian bioregulator peptides with different targets - epithalon for telomerase/longevity, Vesugen for vascular health. No known direct interactions.

Both developed within Russian peptide bioregulation research - Thymalin for thymus/immunity, Vesugen for vascular endothelium. No known contraindications.

Different vascular mechanisms - BPC-157 promotes angiogenesis and tissue healing, Vesugen targets endothelial gene expression. Potentially complementary for vascular health.

Research Note: Interaction data is based on published literature, mechanistic understanding, and theoretical considerations. Most peptide combinations lack direct clinical study. This information is for educational purposes only and does not constitute medical advice. Always consult qualified healthcare providers.

2 Sources 0 Human 2 Preclinical

Use the source links in the research discussion above to inspect the referenced records.

This dossier synthesizes available evidence from peer-reviewed literature, regulatory documents, and clinical trial registries. Evidence strength labels summarize the cited material for this entry and should be read alongside its population, model, and study limitations.

For complete methodology details, see our Methodology page.

Important Disclaimer

This dossier is for educational purposes only and does not constitute medical advice. Always consult a qualified healthcare provider before making health decisions.

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Conditions Studied

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