Vesugen
Also known as: Vezugen, KED, Lys-Glu-Asp, T-38, lysyl-glutamyl-aspartic acid
4 notable studies · 6 references
TLDR
Vesugen is the synthetic tripeptide Lys-Glu-Asp (KED), studied primarily for vascular/endothelial aging and gene regulation, with substantial cell and animal research and a few small human studies reporting vascular and biological-aging signals, but no robust independently replicated clinical evidence establishing it as a treatment for vascular disease or aging.
Research Supports
- Studied for vascular endothelial-cell aging and proliferation
- Investigated for cell-differentiation and gene-expression changes during cellular aging
- Examined for effects on vascular blood flow in atherosclerosis-related conditions
- Studied for neuroplasticity effects in an Alzheimer's disease mouse model
- Investigated for biological-aging and CNS-related markers in small human studies
Observations Reported in Research
- Increased Ki-67 expression in aged vascular endothelial cultures, with molecular docking suggesting MKI67-promoter interaction (Khavinson et al., 2014)
- Reported improved arterial blood flow in 41 patients with vasculogenic erectile dysfunction (Kitachev et al., 2014)
- Reported the larger geroprophylactic effect compared with Pinealon among 32 adults with chronic conditions (Meshchaninov et al., 2015)
- Prevented dendritic-spine loss and showed a trend toward increased neuroplasticity in 5xFAD mice (2021)
These are brief summaries of what the referenced research examined or reported — not conclusions about safety or effectiveness, and not medical advice. See Notable Studies and Sources & References below for the full context and citations.
At a Glance
Classification: Synthetic tripeptide; short peptide bioregulator; experimental vascular/endothelial regulatory peptide
Vesugen is another three-amino-acid Khavinson peptide: Lys-Glu-Asp or KED. PubChem identifies KED as the tripeptide lysyl-glutamyl-aspartic acid with molecular weight approximately 390.39 g/mol. Vesugen is generally associated with vascular tissue / vascular endothelium. Research has examined: • Endothelial-cell aging • Cell proliferation • Vascular function • Atherosclerosis-related biology • Gene expression • Cellular senescence • Neuroplasticity • Biological-aging markers. Unlike Cartalax, Vesugen also has published human observations. But they are nowhere near the quality of a modern large randomized clinical program.
What Is Vesugen?
Vesugen is the synthetic tripeptide Lys-Glu-Asp (KED). It belongs to the same short-peptide bioregulator research family as Cartalax, Cortagen, Epitalon and Pinealon. The proposed tissue association is the vascular wall/endothelium. A 2012 study using aged cell cultures reported tissue-associated changes in differentiation markers after short peptide exposure, with Vesugen/KED influencing cultured fibroblasts. The underlying hypothesis is that KED can influence gene-regulatory processes involved in cellular differentiation and aging. There is no established classical Vesugen receptor.
What Are Researchers Studying?
Vascular endothelial aging
This is the core Vesugen research area. A 2014 experiment examined vascular endothelial cultures and tissue-specific cultures from young and old animals. Vesugen increased expression of Ki-67, a marker associated with cell proliferation that had declined with aging. Researchers also performed molecular docking suggesting interaction between Vesugen and the promoter region of MKI67. Important distinction: The Ki-67 result was experimental. The proposed DNA-promoter interaction was computational molecular docking. Those are different levels of evidence.
Cell differentiation and aging
A 2012 study examined aged human-derived cell cultures. Expression of differentiation-associated factors declined as cultures aged. Short peptides produced different effects depending on the cell type, with Vesugen/KED influencing differentiation-marker expression in fibroblast cultures. Researchers interpreted this as possible evidence of tissue-associated peptide effects during cellular aging. But: aged cells in culture ≠ aged humans.
Vascular blood flow
One of the more interesting Vesugen publications involved 41 patients with vasculogenic erectile dysfunction associated with atherosclerosis. Researchers compared penile arterial blood-flow measures before and after Vesugen treatment and reported significant improvement in both clinical and instrumental blood-flow measurements. This is genuine human evidence. But the publication as indexed does not describe the kind of rigorous randomized, blinded, placebo-controlled methodology we'd want before considering efficacy established. So: human signal = yes established vascular therapy = no.
Biological-aging markers
A 2015 study involved 32 people aged 41–83 with multiple chronic diseases and organic brain syndrome in remission. Researchers evaluated Pinealon and Vesugen and reported changes interpreted as improvements in several biological-aging and CNS-related measures, with Vesugen producing the larger reported geroprophylactic effect. The same paper also reported findings including prooxidant activity and changes in circulating CD34+ cells. This is another reason not to reduce the study to: “Vesugen reversed biological age.” It did not establish that.
Neuroplasticity
This one is surprising for a nominally “vascular” peptide. A 2021 study examined KED and EDR in 5xFAD mice, a transgenic model used in Alzheimer's disease research. KED treatment prevented dendritic-spine loss and showed a tendency toward increased neuroplasticity measures. Researchers also used molecular modeling to propose possible interactions between short peptides and DNA sequences associated with genes relevant to Alzheimer's biology. Again: mouse neuroplasticity + computational docking ≠ Alzheimer's treatment.
Mesenchymal stem-cell aging
The same 2020 human-cell study used for Cartalax also examined KED. KED modified expression of several genes associated with cellular aging, including: • IGF1 • FOXO1 • TNKS2 • NFκB. Its effects differed depending on the experimental model of cellular aging. That's important because it argues against a simplistic: KED switches aging genes in one universally beneficial direction story. The biology was context-dependent.
How Does It Work?
The mechanism remains incompletely established. The proposed model is roughly: KED ↓ cellular uptake ↓ interaction with gene-regulatory systems ↓ changes in expression of proliferation/differentiation-associated genes ↓ changes in endothelial/cellular behavior. Specific proposed mechanisms include regulation involving: • MKI67 / Ki-67 • SIRT-related pathways in some literature • differentiation genes • cellular-aging pathways. But we need to distinguish demonstrated expression changes from computational predictions of direct DNA interaction. A direct, independently validated molecular receptor or DNA-binding mechanism has not been established.
What Does the Research Show?
Human research
Limited but not zero. That's the important correction. Vascular study 41 patients with vasculogenic erectile dysfunction were evaluated before and after Vesugen monotherapy, with reported improvements in arterial blood flow. Aging-marker study 32 adults with polymorbidity and organic brain syndrome received Vesugen or Pinealon in a study reporting changes in biological-aging/CNS measures. These studies are interesting. They are also: • small • from a concentrated research ecosystem • not sufficient to establish broad efficacy • lacking the large independently replicated randomized evidence expected for modern therapeutics. So Aminodex should classify human evidence as LIMITED / LOW-CERTAINTY rather than either “none” or “clinically proven.”
Animal research
KED has been investigated in: • aging models • vascular/endothelial research • 5xFAD Alzheimer's-model mice. The 2021 5xFAD work reported preservation of dendritic spines and neuroplasticity-related effects.
In-vitro research
This is the strongest mechanistic category. Research includes: • vascular endothelial cells • aged cell cultures • human mesenchymal stem cells • differentiation-marker expression • Ki-67 expression. KED clearly produces measurable biological effects in these experimental systems. Whether those effects translate into meaningful human vascular outcomes remains uncertain.
Notable Studies
Epigenetic Aspects of Peptidergic Regulation of Vascular Endothelial Cell Proliferation During Aging
in-vitroResearchers examined Vesugen and another peptide in young and aged tissue cultures and dissociated vascular endothelial cells. Vesugen increased Ki-67 expression that had declined during aging. Molecular docking predicted interaction between Vesugen and a region of the MKI67 promoter.
Limitations: Cell-culture and computational research. Molecular docking predicts possible interactions; it does not demonstrate direct DNA binding in humans or clinical vascular rejuvenation.
View publication →The Efficacy of Peptide Bioregulators of Vessels in Lower Limbs Chronic Arterial Insufficiency Treatment in Old and Elderly People
humanThe publication evaluated Vesugen in 41 patients with vasculogenic erectile dysfunction associated with atherosclerosis. Clinical and instrumental measurements of penile arterial blood flow were compared before and after treatment, with significant improvement reported following Vesugen.
Limitations: Small study, and the indexed report does not establish a robust randomized, blinded, placebo-controlled design. The title and detailed study population also illustrate the difficulty of interpreting portions of the regional literature.
View publication →Effect of Synthetic Peptides on Aging of Patients With Chronic Polymorbidity and Organic Brain Syndrome of the Central Nervous System in Remission
humanThirty-two adults aged 41–83 with multiple chronic conditions and organic brain syndrome were studied using Vesugen and Pinealon. Researchers reported anabolic and CNS-related effects and changes interpreted as slowing several biological-age indicators, with Vesugen showing the larger reported effect. The paper also reported prooxidant activity and changes involving circulating CD34+ cells.
Limitations: Small, heterogeneous population; limited methodological detail in the indexed English abstract; no large randomized independent replication; “biological age” measures are surrogate outcomes rather than lifespan or hard clinical outcomes.
View publication →Neuroprotective Effects of Tripeptides-Epigenetic Regulators in Mouse Model of Alzheimer's Disease
animalResearchers studied KED and EDR in 5xFAD mice. KED prevented dendritic-spine loss and showed a trend toward increased neuroplasticity. Computational modeling was used to investigate potential peptide-DNA interactions involving genes relevant to Alzheimer's disease.
Limitations: Transgenic mouse model plus computational predictions. It does not establish prevention or treatment of Alzheimer's disease in humans.
View publication →What We Still Don't Know
• Human pharmacokinetics • Human bioavailability • Long-term safety • Whether it improves clinically important cardiovascular outcomes • Whether it slows vascular aging • Whether it reduces cardiovascular events • Whether it meaningfully changes human endothelial function • Whether the erectile-function findings replicate in controlled trials • Whether proposed DNA interactions occur in living humans • Whether neuroplasticity findings translate to people • Whether it affects Alzheimer's disease • Whether “tissue specificity” is real in vivo • Whether biological-age-marker changes predict meaningful health outcomes • Whether findings replicate outside the originating research network • Whether research-market Vesugen matches the KED used experimentally.
Related Compounds
Recent publications
Latest titles from PubMed, not reviewed by Aminodex. Not an endorsement. See all on PubMed ↗
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Sources & References
- Khavinson VKh, et al. Epigenetic Aspects of Peptidergic Regulation of Vascular Endothelial Cell Proliferation During Aging. 2014.
- Khavinson VKh, et al. Peptides Tissue-Specifically Stimulate Cell Differentiation During Their Aging. Bulletin of Experimental Biology and Medicine. 2012.
- Kitachev KV, et al. Clinical Study of Vesugen in Vasculogenic Erectile Dysfunction/Atherosclerotic Vascular Disease. 2014.
- Meshchaninov VN, et al. Effect of Synthetic Peptides on Aging of Patients With Chronic Polymorbidity and Organic Brain Syndrome. 2015.
- Khavinson V, et al. Neuroprotective Effects of Tripeptides-Epigenetic Regulators in Mouse Model of Alzheimer's Disease. Pharmaceuticals. 2021.
- Ashapkin V, et al. Gene Expression in Human Mesenchymal Stem Cell Aging Cultures: Modulation by Short Peptides. 2020.
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