Vilon
Also known as: Vilon · KE · Lys-Glu · L-Lysyl-L-Glutamic acid · lysylglutamic acid
Research focus
Immune / thymic regulation and geroprotection; studied in rodent carcinogenesis, lifespan, gastrointestinal-aging, and radiosensitive-tissue (thymus, spleen, gut) models.
US regulatory status
Not FDA-approved · Not compoundable
Evidence rating
Theoretical
Origin
Synthesized by Vladimir Khavinson's group at the St. Petersburg Institute of Bioregulation and Gerontology in the 1990s as part of a program to reduce thymic peptide extracts (the Thymalin/thymus-extract lineage) to short, fully synthetic "Cytogen" sequences with defined structure. Vilon is the dipeptide Lys-Glu (KE), positioned in the Khavinson literature as a synthetic immune-modulating bioregulator analogous to the thymic preparations. Co-authors recurring across the foundational papers include V. N. Anisimov (oncogerontology, N. N. Petrov Institute of Oncology), V. V. Malinin, and V. G. Morozov.
Plain-language summary
Vilon is a two-amino-acid synthetic peptide (lysine + glutamic acid, abbreviated KE) created in Russian gerontology research as a simplified, fully defined stand-in for thymus-gland extracts. Most of what is published comes from cell-culture and rodent experiments by the original research group: reports of longer lifespan and fewer spontaneous tumors in mice, changes in gene activity, and effects on the gut and immune tissue of aged rats. Notably, the animal record is not all positive — at least one mouse study found Vilon increased mammary tumors rather than decreasing them. Human data is very limited — small Russian reports and laboratory experiments on lymphocytes from elderly donors — with no rigorous, independently replicated clinical trials. It is not FDA-approved and is not legally compoundable in the United States.
Claimed mechanism (as reported)
Khavinson-group publications propose that Vilon acts as a peptide bioregulator that modulates gene expression in immune and epithelial tissue, reportedly stimulating proliferative activity of thymocytes and intestinal stem cells, shifting the expression of a subset of cardiac genes in microarray studies, and supporting recovery of radiosensitive organs after irradiation in rats. The proposed mechanism is the group's general "short peptide binds regulatory DNA regions and influences transcription" model and remains at the preclinical-hypothesis stage; it has not been independently validated outside the originating research group, and the proposed immune-restoring action has not been demonstrated in controlled human studies.
Evidence summary
Preclinical only. The literature is a real but narrow body of work, dominated by the Khavinson/Anisimov/Malinin group in St. Petersburg, spanning rodent carcinogenesis and lifespan studies, gastrointestinal-aging models, and gene-expression experiments. The animal findings are internally inconsistent: some studies report tumor inhibition and lifespan extension in mice, while a peer-reviewed study in a Western journal reported that Vilon increased spontaneous mammary tumor incidence in HER-2/neu transgenic mice. The only human-tissue data are ex-vivo chromatin and stem-cell experiments on cultured cells from elderly donors (a Georgian group and an Italian-Russian collaboration), not in-vivo clinical trials. No randomized controlled trials, no pharmacokinetic data, and no in-vivo human efficacy or safety studies of Vilon exist in the peer-reviewed English-language literature as of 2026.
What the research reports
A synthetic dipeptide Vilon (L-Lys-L-Glu) inhibits growth of spontaneous tumors and increases life span of mice; Effect of Vilon on biological age and lifespan in mice
Grade BKhavinson VKh, Anisimov VN, Zavarzina NY, Zabezhinskii MA, Morozov VG et al. · Doklady Biological Sciences; Bulletin of Experimental Biology and Medicine · 2000
Reported finding: Subcutaneous Vilon started in mid-life was reported to increase physical activity and endurance, prolong mean lifespan, and reduce the incidence of spontaneous tumors, with the authors reporting no unfavorable effects on development. Reported by the originating group without independent replication.
Sample: Female CBA mice, cohort studies (tens of animals per arm)
Methodology: B (preclinical) — long-duration rodent lifespan/carcinogenesis studies, single originating research group
Limitations: Rodent-only; single research group; abstracts sparse; outcomes not independently reproduced; translation to human endpoints unproven.
Inhibitory effect of the peptide Epitalon on the development of spontaneous mammary tumors in HER-2/neu transgenic mice (Vilon comparator arm)
Grade BAnisimov VN, Khavinson VKh, Provinciali M, Franceschi C et al. · International Journal of Cancer · 2002
Reported finding: In the same experiment where Epitalon reduced mammary tumors, the Vilon arm showed significant NEGATIVE effects versus control — increased mammary cancer incidence, a shorter latent period, and a higher cumulative tumor count. Included here deliberately because it contradicts the favorable Vilon tumor data and undercuts any simple 'tumor-modifying' claim.
Sample: Female HER-2/neu transgenic mice, multiple arms
Methodology: B (preclinical) — transgenic mouse model, peer-reviewed Western journal, includes a Vilon treatment arm
Limitations: Rodent-only and strain/model-specific; illustrates that the animal record for Vilon is inconsistent rather than uniformly protective.
Effects of Vilon (and Epithalon) on gene expression, digestive-enzyme activity, intestinal transport, and functional morphology of radiosensitive organs in rats
Grade CKhavinson VKh, Malinin VV, Anisimov SV, Yuzhakov VV, Kvetnoi IM, Timofeeva NM et al. · Bulletin of Experimental Biology and Medicine; Voprosy Onkologii · 2001–2005
Reported finding: The group reported that Vilon altered expression of a subset of cardiac genes by DNA-microarray, increased digestive-enzyme activity and glucose transport in aged-rat gut, and stimulated proliferation of thymocytes and intestinal stem cells, aiding post-irradiation recovery of critical organs. These underpin the proposed 'peptide bioregulator' mechanism.
Sample: Rat and mouse models; cDNA-microarray and tissue-morphometry experiments
Methodology: C — mechanistic preclinical (in-vitro / rodent), single originating group, small samples
Limitations: All preclinical; author overlap with essentially the entire Vilon literature creates an independence-of-review concern; mechanism not validated by outside laboratories.
Bioregulator Vilon-induced reactivation of chromatin in cultured lymphocytes from old people; aging-related peptide bioregulators induce reactivation of chromatin
Grade CLezhava T, Monaselidze J, Jokhadze T, Khavinson V et al. (Tbilisi State University) · Biogerontology; Georgian Medical News · 2004–2006
Reported finding: Adding Vilon to cultured lymphocytes from old donors reportedly induced decondensation of facultative heterochromatin and reactivation of ribosomal genes; unlike Epitalon/Livagen, Vilon did NOT decondense pericentromeric structural heterochromatin. This is the closest thing to 'human' data — but it is cell-culture work, not evidence of any clinical effect in living people.
Sample: Lymphocytes cultured from a small number of elderly (≈75–88 yr) donors
Methodology: C (ex vivo) — laboratory study on cultured human cells, NOT an in-vivo clinical trial
Limitations: Ex-vivo cultured cells only; very small donor pools; no clinical endpoints; does not demonstrate in-vivo human efficacy or safety.
Administration reported in studies
Published studies are preclinical and describe parenteral or oral dosing in animals — typically microgram-level subcutaneous injection in mice (e.g., on the order of 1 microgram per animal for several consecutive days per month) or per-oral/microgram-per-kg administration in rats over courses of weeks. No validated human dosing exists anywhere in the peer-reviewed literature, and the ex-vivo human work simply added peptide to cultured cells. This is a summary of research conditions — not a dosing recommendation and not a protocol endorsed by TPC.
This section reports what published studies describe. It is not a dosing recommendation from TPS.
Safety record
No human in-vivo safety data exist. In rodent studies the originating group reported acceptable tolerability with no unfavorable developmental effects over the follow-up examined, but those studies were small, not designed to modern toxicology standards, and come almost entirely from one research group. The contradictory HER-2/neu mouse result — in which Vilon was associated with MORE mammary tumors — is itself a cautionary signal that the compound's biological effects are not uniformly benign. No pharmacokinetic, reproductive, or long-term oncologic safety data meeting current regulatory standards has been published.
US legal status
Not FDA-approved. Not on the 503A compoundable bulk substances list. Not legally compoundable for human clinical use in the United States. Sold online only as a "research chemical" — vendors in that channel are unregulated and not verified by TPC.
Open research questions
- ? Do any of the favorable rodent findings (lifespan extension, tumor inhibition) replicate in independent, non-Khavinson-affiliated laboratories — and how is that reconciled with the HER-2/neu study where Vilon increased tumors?
- ? Is there any in-vivo human evidence at all, beyond ex-vivo lymphocyte cell-culture experiments, for Vilon's proposed immune or geroprotective effects?
- ? What is Vilon's pharmacokinetic profile and bioavailability in humans by any route, given it is a tiny dipeptide likely subject to rapid peptidase degradation?
- ? What controlled, blinded toxicology and oncologic-safety data would be needed before any first-in-human study could be justified?
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