Vilon
Lys-Glu (immune bioregulator)
Vilon is two amino acids: lysine and glutamate. That is the whole molecule. It is also the single best test case for the claim the entire bioregulator field rests on, because Khavinson's own group ran the calculation on every possible dipeptide and Lys-Glu came out on top.
Vilon quick facts
| Reported research dose | 2mg-5mg (per course) |
| Route | Subq |
| Frequency | 1x Daily · Daily (course) |
| Half-life | ~20 min |
| Forms | Injectable |
| Evidence level | Russian studies; limited |
One of the most-studied, simplest bioregulators — immune/longevity, short courses. One of the simplest peptides in the group — a dipeptide — and one of the most studied within this literature. Course pattern: roughly 10 days on, then off, once or twice a year. To know whether it did anything, CBC with differential, and hs-CRP if inflammation is the reason you are running it. Run it as an experiment you measure, not a protocol you trust.
How Vilon works — what 2 residues can and cannot do
Vilon is Lys-Glu — a dipeptide, molecular weight 275.3 g/mol, isoelectric point 6.41, net charge about -0.1 at blood pH. Those four numbers are computed from the sequence, not quoted from a vendor.
Lys-Glu. Two residues, one positive and one negative, and of every compound in this catalog it is the one with the best-documented DNA interaction — which is not the same as a good one, and the difference is worth twelve paragraphs anywhere else and gets four here.
The result, precisely. Kolchina et al. docked all 400 possible dipeptides against 136 tetranucleotide contexts — 108,800 complexes — then ran molecular dynamics on the survivors. Their finding, in their own words, is that “the vast majority of the dipeptides were found to be unable to bind dsDNA”: about 30.8% bound any sequence at all, and only 57 complexes were both low-energy and selective. They set the threshold for counting as a binder at an ICM score of −32. KE scored −35.8 against the sequence TCGA, and the paper states it has the highest affinity to dsDNA among the selective charged dipeptides. Of everything in this family, this is the molecule the screen actually picked out.
Why that is less than it sounds. An ICM score is a computed docking energy, not a measured dissociation constant, and the screen compared dipeptides against each other rather than against anything real. TCGA is a four-base site, which occurs about once every 44 = 256 base pairs — roughly twelve million times in a 3.1-billion-base genome. A molecule that prefers TCGA over other four-base sequences is still a molecule with twelve million candidate targets and no mechanism for choosing between them. That is why the honest description of the mechanism is a chemical interaction with chromatin, not gene targeting.
The charge point, which is specific to this molecule. Lysine's ammonium and glutamate's carboxylate cancel: at blood pH Lys-Glu sits at a net charge near zero. Every other defined peptide on these pages carries net negative charge and is therefore electrostatically pushed away from a polyanionic DNA backbone. Vilon is the one that is not. It is also the one the group's own docking screen ranked highest, and the paper notes that the selective binders containing lysine never also contain arginine. Those two facts fitting together is the strongest internal consistency anywhere in this literature — and it is still computation agreeing with computation.
Lys-Glu. It is a designed sequence, not a fragment cut out of a larger human protein — so there is no parent entry in UniProt to check it against, and nothing here has ever claimed there was.
What the primary literature on Vilon actually says
Systematic search for structural motifs of peptide binding to double-stranded DNA
Kolchina N, Khavinson V, Linkova N, Yakimov A, Baitin D, Afanasyeva A, Petukhov M · Nucleic Acids Research 2019;47(20):10553–10563 · PMID 31598715
The paper that should be on every bioregulator page and is on none. Khavinson's group docked all 400 dipeptides against 136 tetranucleotide contexts — 108,800 complexes — then ran molecular dynamics on the survivors. Their finding, in their words: 'the vast majority of the dipeptides were found to be unable to bind dsDNA.' Around 30.8% bind any sequence at all; 57 complexes were both low-energy and selective. KE had the highest affinity to dsDNA among the selective charged dipeptides, scoring −35.8 against TCGA on a scale where −32 was the cutoff for counting as a binder at all.
Effect of vilon on biological age and lifespan in mice
Khavinson VK, Anisimov VN, Zavarzina NY, Zabezhinskii MA, Zimina OA, Popovich IG, Shtylik AV, Malinin VV, Morozov VG · Bulletin of Experimental Biology and Medicine 2000;130(1):687–690
Female CBA mice, subcutaneous, from the sixth month of life. Reported: increased physical activity and endurance, decreased body temperature, prolonged lifespan, prevented spontaneous neoplasms; no effect on age-related estrous changes or free-radical processes. The abstract gives direction, not effect size — the percentage lifespan change is in the paywalled full text of Bulletin of Experimental Biology and Medicine, and this page will not invent it.
Peptide Regulation of Gene Expression: A Systematic Review
Khavinson VKh, Popovich IG, Linkova NS, Mironova ES, Ilina AR · Molecules 2021;26(22):7053 · PMID 34834147
KE is credited with regulating 36 genes and with binding the TCGA sequence — the same target the docking study picked.
Why the Vilon evidence is weak — and what it still showed
Almost every human result in this class comes from one school — Vladimir Khavinson's institute in St Petersburg and the groups around it. That means single-center data, collected by the people who developed the compound, rarely blinded, never pre-registered, and reported across enough endpoints that something was always going to move. Read anything below against that.
Specific to Vilon. Vilon's record is animal and computational. There is no randomized human trial of Lys-Glu. What there is instead is unusually coherent: a docking result that names a target sequence, a gene-expression claim that names the same sequence, and a lifespan signal in one strain of mouse from one group. Coherent is not the same as confirmed — every one of those is by the same authors, and docking scores are predictions, not measured binding constants. Nobody outside the group has reported a Kd for KE and TCGA.
What the data does support. Khavinson et al. 2000 gave Lys-Glu subcutaneously to female CBA mice from the sixth month of life and reported increased physical activity and endurance, decreased body temperature, prolonged lifespan and prevention of spontaneous neoplasms. That is a coherent geroprotective picture in one strain of one species.
What it does not support, and this matters. The abstract reports direction only. There is no percentage lifespan change, no survival curve, no n stated in the abstract — those numbers are behind a paywall in Bulletin of Experimental Biology and Medicine, and this page will not invent them. Anyone quoting a specific lifespan figure for Vilon is quoting something they did not read. The mechanism review separately credits KE with regulating 36 genes and with binding TCGA, which is the same target the docking study picked — consistent, and both computational.
The specific epistemic position: the best-characterized molecule in the family by computational chemistry, with one mouse lifespan study whose effect size is unavailable and no human trial. Not disproven; barely tested.
What is actually measured, and what is not. Measured: an ICM docking score of −35.8 for Lys-Glu against TCGA, against a binder threshold of −32, out of 108,800 complexes screened; regulation of 36 genes reported by microarray. The threshold is worth its own sentence: only 6.8% of the complexes with free peptide termini reached it, and 4.7% of those with blocked termini. This Vault puts the half-life of Lys-Glu at about 20 minutes, a figure with no study behind it. Not measured: the lifespan effect size in the 2000 mouse study, which the abstract gives only as a direction; plasma half-life; clearance; oral bioavailability; and any binding constant measured rather than computed.
Not proven is not the same as disproven. Everything above says the evidence is weak. None of it says the compound does nothing. There is no adequately powered trial that ran and came back null, because outside Russia there is essentially no trial at all — this class is unfunded, not failed. A reader who leaves thinking “disproven” has learned something false, and so has one who leaves thinking “proven”.
Vilon pharmacokinetics — how much of it actually gets in
What degrades it. One peptide bond, two ordinary residues, no protecting group. Serum aminopeptidases cleave Lys-Glu to lysine and glutamate directly. The quick facts above list “~20 min”; that figure has no traceable human pharmacokinetic study behind it, and no measured plasma half-life for this dipeptide has been published by anyone. The direction, though, is not in doubt — an unmodified dipeptide in serum is a minutes-scale molecule.
The transporter case is at its strongest here. PEPT1, on the brush-border membrane of the small intestine, is described by this research group's own review as handling “basically all di- and tripeptides”, with dipeptides preferred. Lys-Glu is a dipeptide with an unblocked N-terminus, which is the canonical PEPT1 substrate shape. If any compound in this catalog can cross the gut wall intact, it is this one.
And the reason that still does not get it into the blood. PEPT1 delivers peptides into the enterocyte cytosol, where cytosolic peptidases hydrolyze most of them to free amino acids before they reach portal circulation. Transport across the brush border and appearance intact in plasma are two different measurements, and only the first has been characterized. Vilon is sold here as injectable only — subcutaneous injection is 100% bioavailable by definition and skips gut wall and hepatic first-pass altogether — so the route matches the pharmacology rather than fighting it. That is worth noticing, because several of its siblings are sold orally on an argument that applies better to this one.
The ratio the catalog itself implies. Across this class, the oral products carry a median of roughly 29x more material per day than the injectable ones. Nobody arrived at that by measuring absorption — no oral bioavailability figure has been published for any compound in this family — but the gap is the vendors' own implicit answer to the question: swallowing it is assumed to deliver a small fraction of what an injection delivers, and an injection is fully bioavailable by definition. Treat that as a bound on the plausible exposure, not as a measurement, because a measurement is exactly what is missing.
What would have to be true for Vilon to work
What would have to be true. Lys-Glu would have to survive a minutes-scale serum residence long enough to reach thymus or marrow; enter cells; enter nuclei; and interact with chromatin strongly enough to change transcription. The docking work addresses only the last step, and only in silico. Because Vilon is named as a constituent of Thymalin — which does have a randomized trial with lymphocyte endpoints — the sharpest test is whether the dipeptide alone reproduces any part of that response.
These are cheap, standard tests, and a null result on all three would be genuinely informative rather than explainable away.
- Prediction 1 — Complete Blood Count (CBC) with Differential. lymphocyte count should respond in someone who starts low, by the end of a course. The immune claim is the oldest one attached to this molecule. It is also the cheapest to check, and a null result in a lymphopenic person is a real argument against.
- Prediction 2 — hs-CRP (High-Sensitivity C-Reactive Protein). should fall if the immune-modulation framing is right, within one course. Non-specific, and that is the point — a compound proposed to normalize immune function should move the cheapest inflammatory marker there is, and if it never does, the framing is doing no work.
- Prediction 3 — telomerase activity. no prediction — and that is deliberate. Vilon is routinely sold alongside telomerase language borrowed from Epitalon. Nothing in the KE literature supports it. If you are told to expect a telomere effect from a dipeptide, the person selling it has swapped compounds.
Run these before and after, not after alone. A single post-course number tells you what your body is doing, not what Vilon did to it — and that difference is the entire point of testing.
Vilon versus the alternatives
Vilon versus Thymalin. Vilon is Lys-Glu; Thymalin is the calf thymus extract that Kuznik et al. say works because of KE, EW and EDP. So this is the same hypothesis-and-test pairing as Thymogen, from the other side. Thymalin carries the randomized trial and cannot be chemically verified; Vilon can be verified to the milligram and carries no trial of its own. Nobody has compared them in a human, which means the central claim of the entire bioregulator program — that the extracts work through these short peptides — has never been tested in the one experiment that would test it.
And against the credible alternative — thymosin alpha-1. Defined 28-residue peptide, registered clinical use in several countries, independent trials. On evidence it is not close. Vilon's argument is mechanistic elegance and a docking score; thymosin alpha-1's argument is outcomes in patients. Evidence beats elegance, and saying so is the reason to trust the rest of this page.
What you are actually buying when you buy Vilon
A defined dipeptide is the easiest thing in this catalog to verify. One correct mass, one correct sequence; mass spectrometry confirms identity outright and HPLC quantifies purity. Both claims are falsifiable.
What that verification cannot cover. Lys-Glu is two of the commonest amino acids joined by one bond — it is chemically trivial and cheap to make correctly, which removes the usual purity worry and replaces it with a different one: there is very little in the synthesis for a vendor to get wrong, and therefore very little for a certificate of analysis to distinguish between suppliers. The meaningful question for this compound is not purity, it is whether the pharmacology exists at all.
A dipeptide is the easiest thing in this catalog to verify and the easiest to fake convincingly. Mass spectrometry should show/mol. Anything else in the vial is not Lys-Glu.
Where to get Vilon
Buy Vilon at Soma Chems →Bacteriostatic water is the diluent — sterile water with 0.9% benzyl alcohol, which is what lets a vial be drawn from more than once. It does not come with the vial, and unlike the compound it is bought again every time.
Need bacteriostatic water? Get it at AminoWell USA (my company) → Code CAMERON.
The evidence for Vilon
Graded by what exists behind each claim.
Human clinical evidence
- The human record is Soviet and post-Soviet clinical work — real patients and real endpoints, published in Russian and rarely replicated to Western standards.
📊 Correlative data
- The most-studied of the synthetic dipeptides within the Khavinson literature, with reported lifespan extension in mice and rats and immune effects in aged animals. Human use is longstanding in Russia and negligible elsewhere.
🧪 Theoretical / extrapolated
- Lys-Glu — a two-amino-acid peptide, the simplest bioregulator there is. Proposed to modulate immune function and, in the animal work, to shift gene expression in aged tissue.
- The shared claim across the Khavinson series: peptides this short are proposed to enter the cell nucleus and bind promoter regions of DNA, shifting tissue-specific gene expression.
- A dipeptide is where the mechanism is most plausible and least impressive at once: it is small enough to conceivably reach the nucleus, and too small to carry much sequence-specific information. That tension is the honest state of the hypothesis.
What that tier rests on here. The tier above rests on one mouse lifespan study whose effect sizes are not in the public abstract, plus computational DNA-docking work. No human data of any kind.
How to read the Soviet clinical series → · The Khavinson series, in full →
How to read these tiers: they say how much human evidence exists, not how well something works — and ✗ flags harm, never a disappointing trial. How the evidence tiers work →
Cell, rodent, human — and where it stops
The chemistry first, because Vilon is the odd one out. Lys-Glu is two residues and 275.3 g/mol, and its computed net charge at blood pH is about −0.06 — the lysine cancels the glutamate. Every other peptide in this catalog is an anion in plasma; this one is very close to neutral. That single number is why the membrane argument that sinks most of these molecules is weakest here, and no vendor page mentions it.
In cells. Khavinson 2023 reports that KE changes SIRT1, PARP1 and PARP2 gene expression and protein synthesis in aging human mesenchymal stem cells — named genes, a named cell type, and human tissue rather than rodent. Raikhlin 2004 co-cultured human thymocytes and thymic epithelial cells with Vilon and with Epithalon and scored argyrophilic nucleolar organizer proteins, a stain for ribosomal transcription. Khavinson 2002 places it on the sphingomyelin signaling pathway in thymocytes. Kolchina 2019, in Nucleic Acids Research, is the structural attempt to say how a peptide this short could recognize DNA at all.
In animals. Pliss 2001 is the one that deserves attention: chemically induced bladder tumors in rats, with Vilon reported to inhibit their development. A tumor-count endpoint is hard, countable and hard to talk yourself into. Khavinson 2000 reports effects on biological age and lifespan in mice.
Where it stops. There is no human trial of Vilon. The closest thing to human evidence is that Linkova 2023 names KE as one of the two active substances of Thymalin — which means the clinical record people cite for Vilon is, at best, borrowed from a mixture in which KE is one component of unknown share.
What nobody has tested yet
Whether the neutral charge actually buys anything. The computed charge says Lys-Glu should partition into a lipid membrane far more readily than Ala-Glu-Asp-Gly or Lys-Glu-Asp. That is a prediction about a physical constant, it is measurable in an afternoon with a standard octanol-water or PAMPA assay, and it has never been reported for any peptide in this family. If it came back flat, the entire oral case for the class would weaken at once.
The SIRT1 and PARP result has an obvious human read-out and nobody has taken it. PARP activity consumes NAD+. If KE genuinely moves PARP1 and PARP2 expression in human cells, then whole-blood NAD+ or its metabolites should be measurable and directional in a person taking it — a hypothesis, not a finding, and one that a single small self-experiment series could support or kill.
Extrapolation, labeled as such. The bladder tumor result Pliss 2001 was never followed up in any second species or second tumor model, and a cancer-inhibition claim that sits unreplicated for a quarter of a century is not evidence of an anticancer drug. It is, however, a specific and cheap experiment: the same carcinogen protocol, a second laboratory, a countable endpoint.
Sources read for this page
- Khavinson VK. KE peptide regulates SIRT1, PARP1, PARP2 gene expression and protein synthesis in human mesenchymal stem cells aging. Advances in Gerontology 2023 [Russian] · PMID 37782636
- Pliss GB. Inhibitory effect of peptide vilon on the development of induced rat urinary bladder tumors in rats. Bulletin of Experimental Biology and Medicine 2001 · PMID 11586406
- Raikhlin NT. Expression of argyrophilic proteins in the nucleolar organizer regions of human thymocytes and thymic epitheliocytes under conditions of coculturing with vilon and epithalon peptides. Bulletin of Experimental Biology and Medicine 2004 · PMID 15455093
- Linkova N. The Influence of KE and EW Dipeptides in the Composition of the Thymalin Drug on Gene Expression and Protein Synthesis Involved in the Pathogenesis of COVID-19. International Journal of Molecular Sciences 2023 · PMID 37686182
- Kolchina N, Khavinson V, Linkova N, Yakimov A, Baitin D, Afanasyeva A, Petukhov M. Systematic search for structural motifs of peptide binding to double-stranded DNA. Nucleic Acids Research 2019;47(20):10553–10563 · PMID 31598715
- Khavinson VK, Anisimov VN, Zavarzina NY, Zabezhinskii MA, Zimina OA, Popovich IG, Shtylik AV, Malinin VV, Morozov VG. Effect of vilon on biological age and lifespan in mice. Bulletin of Experimental Biology and Medicine 2000;130(1):687–690
- Khavinson VKh, Rybakina EG, Malinin VV, Pivanovich IY, Shanin SN, Korneva EA. Effects of short peptides on thymocyte blast transformation and signal transduction along the sphingomyelin pathway. Bulletin of Experimental Biology and Medicine 2002;133(5):497-499 · PMID 12420072
Vilon — safety, predicted from mechanism
Predicted from mechanism, not from a human safety trial. How that reasoning works →
What the mechanism predicts
Derived from the molecule, not a trial.
- These are short peptide fragments of organ extracts, and the honest starting point is that the mechanism itself is not established in a way that lets anyone predict harm precisely. The proposal is gene-regulatory — short peptides binding DNA and modulating transcription in a tissue-specific way. If that is what they do, the theoretical concern is influencing transcription in tissue you were not aiming at.
- In practice the doses are tiny, the peptides are short, and they are degraded quickly — which is also the argument that they may do very little at all. Those two possibilities are the same uncertainty viewed from opposite ends, and you should hold both.
What has actually been reported
- Decades of Russian clinical use with a strikingly clean tolerability record — injection-site reactions and little else reported.
- That record comes almost entirely from one research school, is largely unreplicated outside it, and safety data from a group with an interest in the outcome is worth less than the same data from a skeptic. This is not an accusation; it is how evidence weighting works.
How to reduce the risk
Same mechanism as the prediction.
- Follow the course printed on the label rather than running continuously. These are the one class in the Vault where a duration is STATED rather than inferred, and it is typically 10–20 days repeated a few times a year. Read the box.
- Run one at a time. They are cheap and it is tempting to stack six. If something changes, a stack of six tells you nothing about which one did it — and given the evidence base, attribution is the entire value of your own experiment.
- Decide your endpoint before you start, and make it a marker or a measurable symptom rather than a feeling. With a compound class this under-evidenced, an unfalsifiable endpoint means you will conclude it worked no matter what happened.
- Buy from a source that publishes third-party testing. Where the molecule itself is uncertain, identity and purity are the only variables you can actually control.
What it does to your bloodwork
A fact about the assay.
- Test the ORGAN, not the peptide. A thymic peptide is judged on immune markers, a pineal one on sleep and IGF-1, a vascular one on lipids and inflammatory markers. There is no assay for the compound itself.
Don't run this if
- Pregnancy — not because of a specific finding, but because nobody has studied it and the mechanism claim is transcriptional.
- Active malignancy, on the same reasoning as any tissue-growth signal: unproven, mechanistically arguable, and not worth finding out.
The honest unknown
- Essentially everything a skeptic would want: independent replication, pharmacokinetics, and whether the oral forms survive digestion at all. Unproven is not the same as ineffective — but here it is a large unproven.
Not medical advice. If you take prescription medication or have a diagnosed condition, check this with a pharmacist or doctor.
Vilon — safety specifics for this compound
Specific to Vilon: the degradation products are lysine and glutamate, both ordinary dietary amino acids at the quantities involved, which makes acute toxicity an implausible failure mode. The mechanistic concern is the opposite of dramatic — it is that a compound proposed to act on marrow and lymphoid tissue is being used without any measurement of those tissues. Anything that genuinely moves lymphocyte subsets is doing something worth monitoring, and if it moves nothing then the safety question was never the interesting one. What the animal work does not answer is the one thing a safety reader wants: Khavinson et al. 2000 ran female CBA mice from month 6 of life and reported prevention of spontaneous neoplasms, which is the opposite of a harm signal — in one strain, one sex, one species. No human has been followed on Lys-Glu for any period, so 0 adverse-event tables exist. Marrow and lymphoid tissue are also exactly where an unexplained cytopenia hides; a CBC with differential before and after is the cheapest way to keep an unstudied compound from masking one.
Vilon — interference & stacking
Predicted from mechanism, not from an interaction study. How mechanism-predicted claims are made →
What Vilon moves on your bloodwork
Expected direction, not a measured one.
- Comprehensive Metabolic Panel (CMP) — ◆ worth watching
These are short peptide fragments given in microgram amounts and there is no mechanism predicting a specific marker shift. Listing markers here would be padding.
What to do: Test the organ system the bioregulator is aimed at, not a generic panel — that is the only measurement that would tell you anything.
The evidence base here is almost entirely one research group's, largely in Russian, and rarely replicated independently. That is the single most important thing to know before running a course, and it is more useful than any interaction list.
- How to work up to it, and when not to
- When to take it, and why that window
- Cycle length
- Time off between cycles
- Fasted or fed, and when in the day
- Needle gauge and injection site
- Coach Cam's personal notes
- Which compounds push the same lever, and why the dose adds up faster than people count
- What blunts it — the stacks that waste your money
- What compounds the risk, so a side effect arrives sooner than any one of them suggests
- Coach Cam's read on running it alongside the rest of your protocol
Everything above is free and stays free. Skool is where it becomes a plan — Vilon in an order, with the rest of what you're running.
Unlock in Skool — $10/mo →Bloodwork to run alongside Vilon
Baseline first, then again at 8–12 weeks.
| Marker | What it’s watching for |
|---|---|
| hs-CRP (High-Sensitivity C-Reactive Protein) | Chronic low-grade inflammation is the process most of these target |
| ApoB (Apolipoprotein B) | Counts the particles that actually cause plaque, unlike LDL-C |
| HbA1c (Hemoglobin A1c) | Glycation, which is the other half of the ageing story |
| Comprehensive Metabolic Panel (CMP) | Liver and kidney — the two organs that clear everything you take |
| Complete Blood Count (CBC) with Differential | The cheapest broad screen there is |
The Longevity Baseline panel covers these in one order — 13 markers, $219.10 with the discount applied.
Check results you already have → · All 103 markers A–Z
Vilon — frequently asked questions
What is the amino acid sequence of Vilon?
Vilon is Lys-Glu — 2 residues, 275.3 g/mol, isoelectric point 6.41. Those figures are computed from the sequence rather than quoted.
Can a peptide that short really bind DNA?
Not the way a transcription factor does. A zinc finger needs about 30 residues to read three base pairs. When Khavinson's group docked all 400 dipeptides against DNA, the vast majority could not bind double-stranded DNA at all. The claim is a computational prediction supported by gene-expression readouts in cells, not a measured binding event.
Is there a human trial of Vilon?
See the literature section above — the record is named study by study.
What should I measure if I run Vilon?
Before and after, not after alone. The falsifiability section on this page names the specific markers, the direction each should move and the timescale — and says what a null result would rule out.
References & further reading
- Kolchina N, Khavinson V, Linkova N, Yakimov A, Baitin D, Afanasyeva A, Petukhov M — Systematic search for structural motifs of peptide binding to double-stranded DNA · Nucleic Acids Research 2019;47(20):10553–10563 · PMID 31598715
- Khavinson VK, Anisimov VN, Zavarzina NY, Zabezhinskii MA, Zimina OA, Popovich IG, Shtylik AV, Malinin VV, Morozov VG — Effect of vilon on biological age and lifespan in mice · Bulletin of Experimental Biology and Medicine 2000;130(1):687–690
- Khavinson VKh, Popovich IG, Linkova NS, Mironova ES, Ilina AR — Peptide Regulation of Gene Expression: A Systematic Review · Molecules 2021;26(22):7053 · PMID 34834147
Vilon inside a finished plan
One arm of 2 Protocol Blueprints, free to read in full.
What Vilon is used for
Vilon appears under 1 goal in the goal router.
Related Longevity & Bioregulators compounds
Where this goes next
Vilon is the nutrient-sensing arm of this plan. The page above is the free breakdown of one compound; the plan it belongs to — the dosing, the order to correct things in, the week-by-week schedule and what to retest — is a lesson inside Skool.