| Sequence | Lys-Glu (KE) |
| Length | Dipeptide |
| Category | Experimental synthetic peptide bioregulator |
| Human clinical evidence | No controlled outcome trials identified |
Vilon, also called the KE peptide or Lys-Glu, is an experimental synthetic dipeptide studied mainly in cells and animals. Laboratory findings are biologically interesting, but they do not establish that Vilon improves health, slows aging, or treats disease in people.
Aliases
Key points
What people use it for
⚠️ CRITICAL INFORMATION
The accepted biomedical sources in this review do not establish an approved human indication, an authorized consumer product, or a standardized pharmaceutical formulation for Vilon. Availability from a seller is not evidence of regulatory approval, identity, purity, sterility, effectiveness, or safety.
Before considering any experimental peptide, verify its current status with the relevant national regulator and a qualified clinician. Products sold online as research chemicals may not contain what their labels claim. This page does not provide instructions for obtaining, preparing, or self-administering Vilon.
Vilon is the dipeptide L-lysyl-L-glutamic acid. Published research also calls it the KE peptide. Unlike an approved peptide medicine with a defined indication and clinical-development program, the evidence located for Vilon consists primarily of cell experiments, ex vivo work with human cells, and animal models.
The most recent accepted mechanistic study exposed cultured human mesenchymal stem cells to KE peptide and measured gene expression, protein production, and modeled peptide–DNA interactions.[1:1] Other studies examined cultured lymphocytes from older adults or animal tissues.[6][2:1][3:1][7] These designs can generate hypotheses, but they cannot show that using Vilon makes a person live longer, feel better, or avoid disease.
No accepted study measured a patient-centered outcome after giving Vilon to people. Claims about longevity, immune restoration, kidney protection, cancer prevention, or “rejuvenation” therefore remain unproven.
In cultured human mesenchymal stem cells, KE peptide altered expression and synthesis of SIRT1, PARP1, and PARP2.[1:2] In cultured lymphocytes from older donors, studies reported changes in heterochromatin organization and ribosomal-gene activity.[2:2][3:2] These are mechanistic observations, not evidence that Vilon reverses human aging.
Animal studies reported anti-apoptotic effects in irradiated rat lymphocytes, altered IL-2 gene expression in mouse lymphocytes, and changes in an experimental rat kidney-failure model.[6:1][8][7:1] Separate animal studies reported conflicting tumor and lifespan outcomes.[4:1][5:1][9] None of these results can be assumed to apply to humans.
| Outcome / Goal | Effect* | Consistency** | Evidence quality | Trials*** | Notes |
|---|---|---|---|---|---|
| Longevity or healthspan in humans | Not established | Very low | 0 clinical trials | Cell and animal findings do not establish a human longevity effect.[1:3][9:1] | |
| Immune-related clinical outcomes | Not established | Very low | 0 clinical trials | Evidence is limited to cultured cells and animal work.[6:2][7:2] | |
| Treatment or prevention of cancer | Conflicting animal results | Very low | 0 clinical trials | Mammary-tumor outcomes worsened in one mouse model, while induced bladder tumors decreased in one rat model.[4:2][5:2] | |
| Age-related chromatin changes | Mechanistic only | Very low | 0 clinical trials | Ex vivo lymphocyte findings are not clinical outcomes.[2:3][3:3] |
? means the effect on human health is unknown.The 2023 mesenchymal-stem-cell study reported increased SIRT1 expression and protein synthesis in one experimental context, along with lower PARP1 and PARP2 measures during cellular aging.[1:4] Molecular modeling in the same report proposed interactions between KE peptide and DNA sequences found in the promoters of those genes.[1:5]
These results require careful interpretation:
Ex vivo studies using lymphocytes from older donors reported decondensation of selected chromatin regions and activation of ribosomal-gene processes after exposure to peptide bioregulators including Vilon.[2:4][3:4] The studies did not test whether these cellular changes improve symptoms, function, disease risk, or survival.
In mouse spleen lymphocytes, Lys-Glu exposure was associated with IL-2 gene-expression changes.[7:3] A rat study reported inhibition of irradiation-induced lymphocyte apoptosis.[6:3] Both findings are preclinical and leave the direction of any human health effect uncertain.
The accepted evidence set does not provide reliable human pharmacokinetic data for Vilon. Human half-life, absorption by different routes, bioavailability, metabolism, and dose–exposure relationships remain undetermined.
The cellular studies support further investigation of Vilon as a research probe for gene regulation and chromatin biology.[1:6][2:5][3:5] They do not support calling it an anti-aging treatment.
Cell and animal studies suggest that Vilon can affect lymphocyte signaling and apoptosis.[6:4][7:4] Whether this would help, harm, or have no meaningful effect in humans is unknown. Immune stimulation and apoptosis inhibition are not inherently beneficial and may carry context-specific risks.
The strongest safety signal comes from HER-2/neu transgenic mice predisposed to mammary cancer. Vilon exposure increased mammary-cancer incidence, shortened tumor latency, and increased cumulative tumors compared with controls.[4:3] In a different model, Vilon reduced carcinogen-induced bladder tumors in rats.[5:3] Another mouse report described fewer spontaneous tumors and longer lifespan, but the available PubMed record provides little methodological detail.[9:2]
The disagreement across models means Vilon should not be described as either an anti-cancer agent or a proven carcinogen in humans. It does justify caution and makes unsupervised human experimentation especially difficult to defend.
In rats with experimentally induced chronic renal failure, Vilon changed TGF-beta1 concentrations and mesenteric microvessel permeability at an early time point.[8:1] This does not establish a treatment for human kidney disease.
No validated human formulation, preparation method, route, sterility standard, stability period, or storage protocol was identified in the accepted evidence. Accordingly, this page does not provide reconstitution calculations or handling instructions.
Do not infer human preparation guidance from animal experiments, seller instructions, peptide-community posts, or protocols for other compounds.
There is no evidence-based human dose or protocol for Vilon.
This encyclopedia intentionally does not reproduce seller or community dosing instructions when no credible human clinical evidence supports them.
Human adverse-event rates are unknown because adequate human trials were not identified.
Important uncertainties include:
No reliable human interaction studies were identified. Mechanistic speculation about SIRT1, PARP enzymes, apoptosis, or immune signaling is insufficient to predict safe combinations. In particular, there is no evidence supporting combination with cancer treatment, immunosuppressants, anticoagulants, or other experimental peptides.
No Vilon stack has established human efficacy or safety. Combining multiple experimental compounds makes it harder to identify the cause of adverse effects and can create interactions that have never been studied. The evidence does not support a recommended Vilon stack.
Unknown. Cell experiments and mouse studies cannot establish that Vilon slows aging in humans.[1:7][2:6][3:6][9:4]
No such conclusion is justified. Animal tumor studies conflict, and one model found worse mammary-tumor outcomes.[4:5][5:5]
Human safety is not established. The lack of controlled human trials, uncertain product quality, and conflicting animal cancer findings create substantial uncertainty.
No evidence-based human dose exists. This page does not provide a dosing recommendation.
No. They are laboratory measurements in cultured cells. A useful clinical intervention must demonstrate meaningful benefits and acceptable harms in people.[1:8]
We prioritized studies specifically evaluating Vilon or Lys-Glu. Evidence was separated by level:
Papers about different peptides, generic peptide chemistry, unrelated longevity compounds, and commercial claims were excluded from the assessment.
Khavinson VK, Linkova NS, Ashapkin VV. KE peptide regulates SIRT1, PARP1, PARP2 gene expression and protein synthesis in human mesenchymal stem cells aging. Advances in Gerontology. 2023. https://pubmed.ncbi.nlm.nih.gov/37782636/ ↩︎ ↩︎ ↩︎ ↩︎ ↩︎ ↩︎ ↩︎ ↩︎ ↩︎ ↩︎
Lezhava T, Jokhadze T, Monaselidze J. Epigenetic modification under the influence of peptide bioregulators on the “old” chromatin. Georgian Medical News. 2023. https://pubmed.ncbi.nlm.nih.gov/37042594/ ↩︎ ↩︎ ↩︎ ↩︎ ↩︎ ↩︎ ↩︎ ↩︎
Lezhava T, Monaselidze J, Kadotani T. Anti-aging peptide bioregulators induce reactivation of chromatin. Georgian Medical News. 2006. https://pubmed.ncbi.nlm.nih.gov/16705247/ ↩︎ ↩︎ ↩︎ ↩︎ ↩︎ ↩︎ ↩︎ ↩︎
Anisimov VN, Khavinson VK, Provinciali M. Inhibitory effect of the peptide epitalon on the development of spontaneous mammary tumors in HER-2/neu transgenic mice. International Journal of Cancer. 2002. https://pubmed.ncbi.nlm.nih.gov/12209581/ ↩︎ ↩︎ ↩︎ ↩︎ ↩︎ ↩︎ ↩︎
Pliss GB, Mel'nikov AS, Malinin VV. Inhibitory effect of peptide vilon on the development of induced rat urinary bladder tumors in rats. Bulletin of Experimental Biology and Medicine. 2001. https://pubmed.ncbi.nlm.nih.gov/11586406/ ↩︎ ↩︎ ↩︎ ↩︎ ↩︎ ↩︎ ↩︎
Khavinson VK, Kvetnoii IM. Peptide bioregulators inhibit apoptosis. Bulletin of Experimental Biology and Medicine. 2000. https://pubmed.ncbi.nlm.nih.gov/11276315/ ↩︎ ↩︎ ↩︎ ↩︎ ↩︎ ↩︎ ↩︎
Khavinson VK, Morozov VG, Malinin VV. Effect of peptide Lys-Glu on interleukin-2 gene expression in lymphocytes. Bulletin of Experimental Biology and Medicine. 2000. https://pubmed.ncbi.nlm.nih.gov/11177276/ ↩︎ ↩︎ ↩︎ ↩︎ ↩︎ ↩︎ ↩︎
Gavrisheva NA, Malinin VV, Ses TP. Effect of peptide Vilon on the content of transforming growth factor-beta and permeability of microvessels during experimental chronic renal failure. Bulletin of Experimental Biology and Medicine. 2005. https://pubmed.ncbi.nlm.nih.gov/16142267/ ↩︎ ↩︎ ↩︎
Khavinson VKh, Anisimov VN. A synthetic dipeptide vilon (L-Lys-L-Glu) inhibits growth of spontaneous tumors and increases life span of mice. Doklady Biological Sciences. 2000. https://pubmed.ncbi.nlm.nih.gov/10944717/ ↩︎ ↩︎ ↩︎ ↩︎ ↩︎ ↩︎