PeptideTrace
Research CompoundKhavinson Bioregulator Tripeptide (Unregulated)Metabolic

Vesugen (KED)

E

Evidence Grade E — Very limited evidence. 6 published studies. 0 registered clinical trials.

6 studiesUSEUCA

Medically reviewed by a licensed medical professional

Overview

Vesugen is a synthetic tripeptide from the Khavinson bioregulator programme, proposed to target blood vessel lining (vascular endothelium). Among Khavinson vascular peptides, it has the strongest mechanistic data, with quantitative cell proliferation measurements and specific DNA binding studies. No human clinical trials have been conducted and it has no regulatory approval.

Also Known As

Vesugen is also known by these brand and alternate names:

Research Activity

6studies
Human 3
Animal 3
In-vitro 1

6 published studies: 3 human, 3 animal, 1 in-vitro, 0 reviews

Regulatory Status

US
Not approved by FDA(FDA)
EU
Not authorised by EMA(EMA)
CA
Not approved by Health Canada(Health Canada)

Legal Status

USNot applicable (not approved)
EUNot applicable (not authorised)
CANot applicable (not approved)

Summary

Vesugen has no marketing authorisation from any major regulatory agency. No human clinical trials have been conducted. In vitro studies in vascular tissue cultures reported increased Ki-67 expression (a cell proliferation marker), with greater effects observed in senescent versus young tissue cultures.

As with other Khavinson bioregulator peptides, the proposed vascular-targeting mechanisms and gene-regulatory effects have not been independently validated or tested in clinical trials. Products available through unregulated channels lack pharmaceutical quality assurance.

Mechanism of Action

Research from the Khavinson group proposes that Vesugen binds to specific DNA sequences in gene promoter regions, with a validated gene target (Ki-67/MKI67) involved in cell proliferation. Molecular docking studies and vascular tissue culture experiments have been published. These mechanisms are based on in vitro and computational work from the originating research group.

Research Summary

Research suggests approximately 8-12 indexed studies exist, with quantitative data on cell proliferation markers and DNA binding that provide stronger mechanistic grounding than most Khavinson peptides. Effects were more pronounced in aged versus young tissue cultures — an observation consistent with the bioregulation theory. However, virtually all research originates from a single laboratory. No large controlled human trials, no pharmacokinetic data, and no independent Western replication exist. Products from unregulated channels lack pharmaceutical quality assurance.

Clinical Trials

PeptideTrace tracks 0 registered clinical trials for Vesugen sourced from ClinicalTrials.gov.

No trials registered on ClinicalTrials.gov for this compound.

Scientific Detail

Overview (Scientific)

Vesugen is a synthetic tripeptide bioregulator with the sequence Lys-Glu-Asp (KED). Its molecular weight is 390.39 Da with the molecular formula C15H26N4O8 (PubChem CID 87571363, ChEBI 159909). Developed by Vladimir Khavinson as part of the cytomedine program, Vesugen targets vascular endothelium. Also known as T-38. Vesugen contains the complete Vilon sequence (Lys-Glu) plus aspartic acid. It is the most mechanistically characterized of the Khavinson vascular peptides, with approximately 8-12 PubMed-indexed studies.

Mechanism of Action (Scientific)

Research suggests Vesugen binds to the minor groove of double-stranded DNA, forming donor-acceptor bonds and hydrogen bonds with specific nucleotide sequences (CATC, CACC, GGCG, TGGC in promoter regions). The primary validated gene target is MKI67 (Ki-67 proliferation marker), with molecular docking demonstrating binding to the MKI67 promoter at the CATC sequence (interaction energy -7.04 to -8.14 kcal/mol). Research suggests Vesugen upregulates Ki-67, normalizes endothelin-1, restores connexins (Cx37, Cx40, Cx43), upregulates SIRT1, and reduces p53, p16, p21 (senescence markers) and MMP-9 in aging fibroblasts.

Summary (Scientific)

Ki-67 and MKI67 promoter binding studies (Khavinson et al. 2014/2015) in vascular tissue explant cultures showed Ki-67 expression area increased 1.25-fold (25%) in young cultures and 1.97-fold (97%) in senescent cultures at 20 ng/mL. Neurogenesis studies (Khavinson et al. 2021) showed 20-27% increase in functional mushroom spines in hippocampal neurons under synaptotoxic conditions. Skin fibroblast studies (Linkova et al. 2016) showed MMP-9 inhibition and Ki-67 enhancement during replicative aging.

The information on this page is provided for educational and research reference purposes only. This is not medical advice. Always consult a qualified healthcare professional before making any health-related decisions.

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This content is for informational purposes only and does not constitute medical advice. Always consult a qualified healthcare professional before making decisions about your health.