vilon

Q: What is Vilon?

Vilon is a synthetic dipeptide, L-lysyl-L-glutamic acid, developed in Vladimir Khavinson's short-peptide program at the St Petersburg Institute of Bioregulation and Gerontology. Two amino acids, 275.30 Da, CAS 45234-02-4. It has no FDA or EMA approval and is sold as a research chemical.

Q: What does Vilon do?

In cell culture the published effects are quantified: SIRT1 gene expression up 6-fold and SIRT1 protein up 8.2-fold in young human mesenchymal stem cells, collagen type I up 83 percent in aged skin fibroblasts, and a 1.4 to 6.0-fold reduction in IL-1 beta, IL-6 and TNF-alpha across Thymalin and its two constituent dipeptides in blood cells from four donors. In animals the record is split: three tumour models favour the compound and one transgenic mammary model from the same group reports significantly worse outcomes on three endpoints. On lifespan, the one head-to-head experiment reports the survival gain for the sibling pineal peptide and no survival figure for this one. In people, three Russian-language papers carry PubMed clinical publication tags and not one of them states a sample size or an effect size.

Q: How is Vilon studied in the published literature?

Almost entirely in cells and rodents. There is no registered trial and therefore no protocol to report. The only human dose figures in the whole literature appear inside patent examples written by the applicants: 1 microgram intramuscular daily for 5 or 10 days in the repair-processes patent, and 10 micrograms parabulbar daily for 10 days in the ophthalmology patent. Animal work runs at 0.1 to 1 microgram per animal on monthly five-day courses. The two patents claim different active ranges, 0.01 to 100 micrograms per kilogram in one and 0.1 to 100 in the other.

Q: What are the side effects of Vilon?

Very little has been characterised, because no registered trial has ever been run and the three human papers report no adverse-event data of any kind. The one quantified harm signal in the literature is an animal result: in HER-2/neu transgenic mice the originating group reported increased mammary cancer incidence, a shorter mean latent period and a larger cumulative tumour count, each at p below 0.05. Three other rodent tumour models report the opposite direction, so the tumour picture is genuinely conflicting rather than settled either way. One interaction finding is documented and belongs here: in mice bearing transplanted Lewis lung carcinoma, giving Vilon at the same time as cyclophosphamide decreased survival, and the authors of that paper conclude the two should not be administered together. Rodent toxicology in the patent examples was run at milligram-per-kilogram doses, roughly a thousand to a hundred thousand times the microgram-per-kilogram range the same documents claim as active, so it does not characterise long-term exposure at the claimed dose.

Q: Is Vilon FDA approved?

No. Vilon has no FDA approval and no EMA marketing authorisation for any indication. A harmonised drug registry of more than 22,000 molecules that does index thymalfasin, alanyl-glutamine and thymic humoral factor gamma-2 returns nothing at all for Vilon. It is sold as a research chemical. No Russian registration certificate was located either, which is notable because the two preparations it is most often conflated with, Thymalin and Thymogen, both carry Soviet-era registration numbers.

Q: How much does Vilon cost?

There is no clinical retail price, because there is no approved product anywhere. On the research-chemical market it is inexpensive, which is what two amino acids cost to make.

russian two-amino-acid geroprotector. no trial registration in any registry checked, human papers that state no sample size, and the strongest animal study in its own file runs the wrong way.

tier D · focus · 0 registered trials · ClinicalTrials.gov + WHO ICTRP

verdict

does it work: mixed, and neither selling claim survives intact. the one head-to-head lifespan experiment reports the survival gain for the sibling pineal peptide and no survival figure for this one. the oncostatic claim splits three models to one, with the best-refereed study reporting more mammary tumours. the human immune claim has never been tested at all.

on whether vilon has been tested in people — not in a registered trial. a direct ClinicalTrials.gov intervention query returns totalCount 0, and a sweep of ClinicalTrials.gov plus the WHO ICTRP mirror returns nothing under the name either. the whole human literature is three russian-language papers carrying pubmed clinical publication tags, and none of the three abstracts states a patient count, a dose or a p value. the colorectal authors call their own work preliminary. roughly 194 human subjects do appear with counts, and every one of them sits inside a patent example the inventors wrote themselves.

on the oncostatic claim — the animal file points two ways and the best paper points the wrong one. three models favour the compound: induced bladder tumours in rats at 56 percent against 75.5 percent in controls, dimethylhydrazine tumours in mice at 14.3 percent against 60 percent, and transplanted lewis lung carcinoma where 1 mg/kg significantly increased survival. the most rigorous paper in the file, published in int j cancer by the originating group with italian co-authors, reports the opposite in her-2/neu transgenic mice: higher mammary cancer incidence, shorter latency and a larger cumulative tumour count, each at p below 0.05. one interaction warning sits inside the lung paper: given at the same time as cyclophosphamide it decreased survival, and its authors say the two should not be combined. thin and conflicting is what the D tier is for.

on the cell-culture numbers in the marketing — they are real numbers from real journals, and they are bench numbers. sirt1 gene expression up 6-fold and sirt1 protein up 8.2-fold in young human mesenchymal stem cells, with no peptide concentration, donor age or passage number stated in the retrievable abstract. collagen type I up 83 percent in aged skin fibroblasts. the anti-inflammatory paper reports a 1.4 to 6.0-fold cytokine reduction across three preparations in blood cells from four donors. one thp-1 macrophage paper found this was the single peptide of five that did not raise phosphorylated erk1/2.

based on published evidence and the public registry record. not medical advice.

why D-tier

D-tier because the evidence is thin and it conflicts. The human data comes first: three Russian-language papers carry PubMed clinical publication tags, and not one of them states a sample size, an allocation method, a blinding procedure or a single effect size. Every reported outcome is a direction word. The largest human dataset with actual counts, roughly 194 subjects, sits inside patent specifications the inventors wrote themselves. A direct registry check returns nothing at all. That rules out C, which fits a compound whose preclinical work points one way and simply has not reached people yet. Vilon's preclinical work points two ways: it inhibited chemically induced bladder tumours in rats and dimethylhydrazine tumours in mice and raised survival in transplanted Lewis lung carcinoma, while the most rigorous study in the file, run by the originating group with Italian co-authors in Int J Cancer, found significantly increased mammary tumour incidence, a shorter mean latent period and a larger tumour burden in HER-2/neu transgenic mice. The efficacy answer on the other selling claim is sharper still and it is not favourable: the one head-to-head lifespan experiment, Mech Ageing Dev 2001, reports mean survival up 5.3 percent and maximum lifespan up 10 months for the sibling pineal tetrapeptide, and no survival figure at all for Lys-Glu. It does not reach F, because there is real quantified signal here and the harm result is one dose in one transgenic strain, contradicted in direction by two other rodent models. What holds it at D is the combination: thirty-two years since the founding patent was filed, no trial registration in any registry checked, human results with no numbers in them, and one author on 49 of the 80 PubMed records, including the modern Western-journal papers that read as independent replication.

the core tension

Vilon is marketed as an oncostatic geroprotector, and the single most rigorous animal study in its literature, run by the men who invented it and published in Int J Cancer, reports that it made cancer worse in HER-2/neu transgenic mice: higher incidence, shorter latency, more tumours, each at p below 0.05. Three other rodent tumour models say the opposite, which is why this is a conflict rather than a verdict. Meanwhile the lifespan claim was actually tested, in a head-to-head the marketing never cites: Mech Ageing Dev 2001 reports mean survival up 5.3 percent and maximum lifespan up 10 months for the sibling pineal tetrapeptide, and reports no survival figure at all for Lys-Glu. The numbers that do exist for Vilon appear later, in a review the developers wrote about their own work and in a patent specification they filed themselves, neither of which reports a p value.

what it is

Vilon is L-lysyl-L-glutamic acid, a synthetic dipeptide from Vladimir Khavinson's short-peptide program at the St Petersburg Institute of Bioregulation and Gerontology. Two residues, 275.30 Da, CAS 45234-02-4. Chemical identity is not in dispute: eight independent commercial and reference registries agree on the formula and mass. The founding patent was filed in July 1994, with a July 1993 priority, and published in February 1995. Its first claim covers an L-Lys-L-Glu or an L-Glu-L-Trp preparation, which puts Vilon and its sibling Thymogen inside a single founding document. The word Vilon appears in none of the patents. They call it only the L-Lys-L-Glu dipeptide.

what it does

In cell culture the reported effects are quantified and sometimes large. In animals they point in two directions. In people the published literature states no sample size anywhere. The cell numbers are where the marketing comes from: SIRT1 gene expression up 6-fold and SIRT1 protein up 8.2-fold in young human mesenchymal stem cells, collagen type I up 83 percent in aged skin fibroblasts, and a 1.4 to 6.0-fold reduction in IL-1 beta, IL-6 and TNF-alpha across Thymalin and its two constituent dipeptides in blood cells from four donors. Each figure is exact, and each was measured on a bench.

origin

The Khavinson group in St Petersburg produced the compound, the patents, the animal work and the human reports. The program grew out of calf-thymus peptide extracts that Morozov and Khavinson had been publishing on since the 1970s, and the developers describe the method in their own words: analyse the amino acid composition of a tissue extract, then synthesise the two-to-four-residue peptide it points to. Thymalin is the extract. Vilon is one of the dipeptides the extract was reduced to. Khavinson is an author on 49 of the 80 PubMed records that mention Vilon. He is also a co-author on the recent Western-journal papers that read at first glance like independent replication.

why researchers are interested

It is two amino acids, it is cheap to make, and the geroprotector framing has been running for three decades. The cell-culture figures quoted in vendor copy are genuine figures from genuine journals, which is more than several compounds in this category can say. The sibling preparations carry real institutional history, Thymalin registered in the USSR in 1982 and Thymogen in 1990, and Vilon gets carried along with them.

does it work

Mixed, and each of the two selling claims fails differently. On geroprotection the experiment was run and the answer landed on a different molecule. The one head-to-head lifespan study, Mech Ageing Dev 2001;122(1):41-68, reports mean survival up 5.3 percent (P<0.05) and maximum lifespan up 10 months for the pineal tetrapeptide, and no survival figure at all for Lys-Glu. Everything Vilon-specific comes from the developers' own 2013 review, claiming maximum lifespan up by nearly two months, with no p value. On the oncostatic claim the file splits three to one and the best study is on the wrong side. Three rodent tumour models favour it: induced bladder tumours in rats at 56 against 75.5 percent, dimethylhydrazine tumours in mice at 14.3 against 60 percent, and transplanted Lewis lung carcinoma where 1 mg/kg significantly increased survival. Against them, Int J Cancer reports significantly increased mammary cancer incidence, a shorter mean latent period and a larger cumulative tumour count in HER-2/neu transgenic mice, and that study came from the originating group rather than from a critic. The human immune claim has never been tested. No trial registration exists under this name in ClinicalTrials.gov or the WHO ICTRP registries. The three clinically tagged PubMed records report directions with no numbers attached. The roughly 194 human subjects that do appear with counts exist inside patent examples written by the applicants, and patent offices examine novelty and inventive step rather than efficacy.

claims vs the data

clinically proven in humans, backed by russian clinical trials — overreach — No trial registration was found under this name in ClinicalTrials.gov or the WHO ICTRP registries. The three PubMed records carrying clinical publication tags state no patient count, no dose, no route, no control-arm description, no percentage and no p value. A PubMed publication type is a cataloguing decision made by an indexer, and it is not a result.
oncostatic, inhibits tumour development — partially true — True in three rodent models: induced bladder tumours in 56 percent of treated rats against 75.5 percent of controls, dimethylhydrazine tumours in 14.3 percent of treated mice against 60 percent, and transplanted Lewis lung carcinoma where 1 mg/kg significantly increased survival. Caveats on each: the dimethylhydrazine denominator is animals surviving to first tumour detection at 46 weeks and the control figure is not stated to share it, the bladder experiment is one study published twice, and the lung paper also reports that giving the peptide synchronously with cyclophosphamide decreased survival. Contradicted in HER-2/neu transgenic mice by the same research group, with three separate endpoints worse at p below 0.05, in the highest-impact journal on the list. Conflicting and model-dependent.
extends lifespan — contradicted — The experiment exists and the survival gain in it belongs to a different peptide. Anisimov, Khavinson, Mikhalski and Yashin, Mech Ageing Dev 2001;122(1):41-68, is the head-to-head lifespan study: mean survival up 5.3 percent (P<0.05) and maximum lifespan up 10 months for the pineal tetrapeptide, and no survival figure at all reported for Lys-Glu. The two papers from 2000 that the claim usually cites report direction words with no sample size, no dose and no p value, and one carries no abstract on PubMed. What is left for Vilon comes from the developers' own 2013 review of their own work, claiming maximum lifespan up by nearly two months and 2.6 times as many CBA mice reaching 23 months, with no p value. No source anywhere reports a median survival for Vilon.
activates SIRT1 by 8.2 times — partially true — The figure is exact and it applies to young human mesenchymal stem cells in vitro, alongside a 6-fold rise in SIRT1 gene expression. The retrievable abstract states no peptide concentration, no donor age and no passage number, so the result cannot be placed on a dose-response curve at all. The PARP1 and PARP2 figures in the same paper describe what happens across stem-cell ageing rather than a clean peptide effect.
anti-inflammatory — partially true — The strongest version is a 1.4 to 6.0-fold reduction in IL-1 beta, IL-6 and TNF-alpha, reported across Thymalin and both of its constituent dipeptides together, in LPS-stimulated blood cells from four donors. Four donors is four donors, and the range is not attributed peptide by peptide. In a separate THP-1 macrophage paper at 100 ng/mL, this was the one peptide of five that did not raise phosphorylated ERK1/2 and the authors describe it as showing a small modulatory capacity.
binds specific gene promoters to switch genes on — unverified — The evidence located for this is molecular docking, in silico, and the same group's two 2023 papers do not agree on which sequence. Int J Mol Sci reports a preference for GCGC on curved nucleosomal DNA; Adv Gerontol reports GCGG in classical B-form DNA and GGGC on the curved nucleosome. No cell-level or structural confirmation appeared in the retrievable record, and docking is a prediction about binding rather than a demonstration of transcriptional control.
a registered medicine in russia — unverified — No Russian registration certificate was located for Vilon in this check, and the entry makes no claim either way. What is documented is the contrast: Thymalin carries USSR registration 82/1108/8 from 1982 and Thymogen carries 90/250/1 from 1990, both printed by the developers themselves. The two preparations Vilon is most often conflated with are registered in their home jurisdiction and Vilon is not.
independently replicated in western journals — contradicted — The modern Int J Mol Sci papers that look like outside replication carry Khavinson as a co-author, along with Mironova and Trofimova from the same St Petersburg institute. He is an author on 49 of the 80 PubMed records mentioning the compound. The genuinely separate strand, the Tbilisi State University genetics group, reports qualitative chromatin findings with no donor count and no concentrations.

key facts

molecular formula: C11H21N3O5
molecular weight: 275.30 Da
amino acids: 2
half-life: not characterised; no published human pharmacokinetic study was located
type: synthetic dipeptide (L-Lys-L-Glu, written KE in the Russian literature)
CAS: 45234-02-4
0 trial registrations found, ClinicalTrials.gov and WHO ICTRP
3 human papers on PubMed, none stating a sample size
194 human subjects, all inside applicant-written patent examples
49/80 PubMed records with Khavinson as an author

frequently asked questions

What is Vilon?

Vilon is a synthetic dipeptide, L-lysyl-L-glutamic acid, developed in Vladimir Khavinson's short-peptide program at the St Petersburg Institute of Bioregulation and Gerontology. Two amino acids, 275.30 Da, CAS 45234-02-4. It has no FDA or EMA approval and is sold as a research chemical.

What does Vilon do?

In cell culture the published effects are quantified: SIRT1 gene expression up 6-fold and SIRT1 protein up 8.2-fold in young human mesenchymal stem cells, collagen type I up 83 percent in aged skin fibroblasts, and a 1.4 to 6.0-fold reduction in IL-1 beta, IL-6 and TNF-alpha across Thymalin and its two constituent dipeptides in blood cells from four donors. In animals the record is split: three tumour models favour the compound and one transgenic mammary model from the same group reports significantly worse outcomes on three endpoints. On lifespan, the one head-to-head experiment reports the survival gain for the sibling pineal peptide and no survival figure for this one. In people, three Russian-language papers carry PubMed clinical publication tags and not one of them states a sample size or an effect size.

How is Vilon studied in the published literature?

Almost entirely in cells and rodents. There is no registered trial and therefore no protocol to report. The only human dose figures in the whole literature appear inside patent examples written by the applicants: 1 microgram intramuscular daily for 5 or 10 days in the repair-processes patent, and 10 micrograms parabulbar daily for 10 days in the ophthalmology patent. Animal work runs at 0.1 to 1 microgram per animal on monthly five-day courses. The two patents claim different active ranges, 0.01 to 100 micrograms per kilogram in one and 0.1 to 100 in the other.

What are the side effects of Vilon?

Very little has been characterised, because no registered trial has ever been run and the three human papers report no adverse-event data of any kind. The one quantified harm signal in the literature is an animal result: in HER-2/neu transgenic mice the originating group reported increased mammary cancer incidence, a shorter mean latent period and a larger cumulative tumour count, each at p below 0.05. Three other rodent tumour models report the opposite direction, so the tumour picture is genuinely conflicting rather than settled either way. One interaction finding is documented and belongs here: in mice bearing transplanted Lewis lung carcinoma, giving Vilon at the same time as cyclophosphamide decreased survival, and the authors of that paper conclude the two should not be administered together. Rodent toxicology in the patent examples was run at milligram-per-kilogram doses, roughly a thousand to a hundred thousand times the microgram-per-kilogram range the same documents claim as active, so it does not characterise long-term exposure at the claimed dose.

Is Vilon FDA approved?

No. Vilon has no FDA approval and no EMA marketing authorisation for any indication. A harmonised drug registry of more than 22,000 molecules that does index thymalfasin, alanyl-glutamine and thymic humoral factor gamma-2 returns nothing at all for Vilon. It is sold as a research chemical. No Russian registration certificate was located either, which is notable because the two preparations it is most often conflated with, Thymalin and Thymogen, both carry Soviet-era registration numbers.

How much does Vilon cost?

There is no clinical retail price, because there is no approved product anywhere. On the research-chemical market it is inexpensive, which is what two amino acids cost to make.

related peptides

epithalon — sister Khavinson peptide, same single-lab problem, graded a tier higher
pinealon — another Khavinson short peptide with a small clinical base
thymosin α-1 — thymic peptide that does carry registered trials, the fair comparison

reptides grades the research record and cites the literature behind every call. research reference only; not medical advice.