Vesugen
Lys-Glu-Asp (vascular)
Vesugen is Lys-Glu-Asp, a three-residue peptide aimed at the vessel wall. It is the compound in this cohort where the honest comparison is least flattering and most useful, because vascular ageing is the one area where the alternatives have hard outcome data and this does not.
Vesugen quick facts
| Reported research dose | 2mg-5mg |
| Route | Subq |
| Frequency | 1x Daily · Daily (course) |
| Half-life | ~30 min |
| Forms | Injectable |
| Evidence level | Russian studies; limited |
The 'vascular' peptide of the Khavinson set — run in short courses. The vascular peptide of the set — overlapping with Ventfort closely enough that most protocols pick one. Course pattern: roughly 10 days on, then off, once or twice a year. To know whether it did anything, hs-CRP and blood pressure, alongside how you actually feel on exertion. Run it as an experiment you measure, not a protocol you trust.
How Vesugen works — what 3 residues can and cannot do
Vesugen is Lys-Glu-Asp — a tripeptide, molecular weight 390.4 g/mol, isoelectric point 4.18, net charge about -1.1 at blood pH. Those four numbers are computed from the sequence, not quoted from a vendor.
Lys-Glu-Asp. A tripeptide sold for the vascular system, and the first thing worth saying is what it is not: it is not the same molecule as Cartalax. This Vault recorded Cartalax as Lys-Glu-Asp until these pages were written — two different products carrying one sequence — and the correction is documented on Cartalax's own page. Vesugen is KED. Cartalax is AED, Ala-Glu-Asp. One residue apart, sold for different organs, and the difference between them is a hydrocarbon side chain versus a positively charged one.
That one residue is the whole mechanistic argument. Swapping alanine for lysine adds a positive charge to a peptide otherwise dominated by two acidic residues, taking the net charge at blood pH from about −2 to about −1. Since the proposed partner is a polyanionic DNA backbone, less negative means less electrostatic repulsion. If the sequence-specific DNA story is true, then KED and AED should behave measurably differently, and in a predictable direction. Nobody has tested that, and it is the cleanest structure-activity experiment available anywhere in this family.
What a three-residue peptide can and cannot do. A zinc finger needs about 30 amino acids to read three base pairs. Three side chains cannot encode a promoter address, and the arithmetic is unforgiving: even a six-base site occurs roughly 750,000 times in a 3.1-billion-base genome. What Khavinson's group actually proposes is groove binding and local interaction with base-pair edges and methylation sites — chemistry with chromatin, not recognition of a gene. Their own systematic screen covered dipeptides and found the vast majority cannot bind double-stranded DNA at all; they expect longer peptides to do better and say so — “selective peptide binding to dsDNA can increase dramatically with the peptide length” — but expected is not measured, and no dissociation constant for KED against any DNA sequence has been published.
Lys-Glu-Asp. A tripeptide, which matters for how it could be absorbed — see the pharmacokinetics section.
What the primary literature on Vesugen actually says
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
KED is reported to reduce the senescence markers p16 and p21 in periodontal-ligament and gingival mesenchymal stem cells, and to act on IGF1, FOXO1, TERT, TNKS2 and NFκB in bone-marrow-derived FetMSC cultures. Every one of those is a cell-culture readout.
Transport of Biologically Active Ultrashort Peptides Using POT and LAT Carriers
Khavinson V, Linkova N, Kozhevnikova E, Dyatlova A, Petukhov M · International Journal of Molecular Sciences 2022;23(14):7733 · PMID 35887081
The transporter review, and the reason a tripeptide is a different proposition from a tetrapeptide: PEPT1 and PEPT2 'have a broad substrate pattern that includes basically all di- and tripeptides', with PEPT1 sitting on the brush border of the small intestine.
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
Included for calibration. The systematic docking work was done on dipeptides; a tripeptide's selectivity is expected to be higher, and the authors say so — 'selective peptide binding to dsDNA can increase dramatically with the peptide length' — but expected is not measured.
What is not here. Nothing is indexed under the trade name Vesugen. The KED record is cell and animal work. Searched through Europe PMC, PubMed and Google Scholar on 2 September 2026. Naming the gap is more useful than filling it with a paragraph of hedging.
Why the Vesugen 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 Vesugen. There is no clinical trial of Vesugen. The vascular claim rests on senescence markers in cultured cells from tissues that are not blood vessels. That is a two-step extrapolation — cell to tissue, and gingival or bone-marrow stroma to endothelium — and each step should cost the claim something. Set against a field where ApoB and Lp(a) have decades of outcome data, this is the weakest position in the cohort.
What the data does support. The gene-regulation review reports that AEDG and KED reduce expression and synthesis of the replicative senescence proteins p16 and p21 in stem cell cultures of the periodontal ligament and in human gingival mesenchymal stem cells, and that AED, KED and KE together modulate expression of IGF1, FOXO1, TERT, TNKS2 and NFκB in bone-marrow mesenchymal stem cells. Those are named genes, named cell types and a coherent senescence story.
Every one of them is a cell-culture readout. Not one is a human outcome, an animal outcome, or a vascular measurement of any kind. The compound is sold for blood vessels; the published gene work is in periodontal ligament, gingival and marrow stem cells. That gap between the tissue studied and the tissue marketed is the specific weakness of this page's evidence, and it is different from the weakness on the pages either side of it.
The specific epistemic position: a defined tripeptide with real senescence-marker data in the wrong tissue, no animal vascular study, and nothing indexed under the trade name at all. There is no negative result here to point at — there is an absence.
What is actually measured, and what is not. Measured, in cell culture: reduced p16 and p21 senescence-protein expression in periodontal ligament and gingival stem cells, and modulation of IGF1, FOXO1, TERT, TNKS2 and NF-kB in marrow mesenchymal cells. Not measured: any endothelial readout; any vascular endpoint in any animal; plasma half-life or clearance; nuclear uptake; a DNA binding constant. The tissue the compound is sold for has never been studied with it.
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”.
Vesugen pharmacokinetics — how much of it actually gets in
What degrades it. Two peptide bonds and no protection. Serum aminopeptidases cleave from the free N-terminal lysine directly. The quick facts list “~30 min”, which is untraceable to any human study but is at least the right order of magnitude for an unmodified tripeptide.
The transporter position. Lys-Glu-Asp sits squarely inside PEPT1's described substrate range — the brush-border transporter of the small intestine covers “basically all di- and tripeptides”. So an oral Vesugen would have the mechanism on its side, and Vesugen is sold here as injectable only. That is a conservative choice rather than a commercial one, and it is worth crediting.
The exposure bound. Subcutaneous injection is 100% bioavailable by definition — no gut wall, no hepatic first-pass. For the endothelial claim to be doing anything, an intact tripeptide has to be present at vascular endothelium in some concentration for some period, and neither number exists for this compound in any species. What can be said is that endothelium is the first tissue an injected peptide meets and the one least dependent on surviving a long circulation, which makes a vascular target the most pharmacokinetically forgiving claim in the entire catalog. That is a real argument in Vesugen's favor and nobody makes it.
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 Vesugen to work
What would have to be true. Lys-Glu-Asp would have to persist at endothelium long enough to act; enter endothelial cells and their nuclei; change transcription of genes that control vascular tone or lipoprotein handling; and shift that enough to move a number you can measure. The first step is more plausible here than anywhere else in the family, because endothelium is where an injected peptide already is. The rest is unaddressed.
The vascular claim is unusually testable, because vascular function has a direct non-invasive measurement.
- Prediction 1 — hs-CRP (High-Sensitivity C-Reactive Protein). should fall if the NFκB claim operates in a whole organism, within one course. NFκB is the specific mechanism named. hs-CRP is its cheapest downstream readout. If NFκB signaling is being damped, this is where it shows.
- Prediction 2 — ApoB (Apolipoprotein B). should not move, over any course. Another deliberate negative. Nothing in the KED literature touches lipoprotein production. If ApoB moves, something else in the protocol did it — and if it does not, that is not a failure of the compound, it is a reason not to run it for a lipid goal in the first place.
- Prediction 3 — Lipoprotein(a) — Lp(a). should NOT move — it is close to genetically fixed, over any course length. This is the negative control for the whole vascular claim. Lp(a) barely responds to diet, training or statins, so a reported fall on a peptide is far more likely to be assay variation than an effect. Anyone selling a bioregulator on an Lp(a) change is describing noise.
- Prediction 4 — flow-mediated dilation. should improve if the endothelial claim is real, over a course, measured before and after. This is the study that would change the picture and it has never been published for any bioregulator. It is non-invasive, standardized, and answers the question directly.
Run these before and after, not after alone. A single post-course number tells you what your body is doing, not what Vesugen did to it — and that difference is the entire point of testing.
Vesugen versus the alternatives
Vesugen versus Ventfort. Ventfort is the vascular tissue extract; Vesugen is the defined tripeptide the extract is claimed to work through. The extract has whatever human record exists for the class and cannot be chemically identified; the peptide has a sequence, a mass and a purity number and no clinical record of its own. Nobody has compared them.
Vesugen versus Cartalax — the comparison this Vault got wrong. These two were recorded as the same sequence here until this rebuild. They are not. KED and AED differ by one residue and by roughly one unit of net charge, and they are sold for different tissues on the basis of that difference. If tissue specificity in this family is real, these two compounds are the experiment that demonstrates it; if it is not, the distinction between most of this catalog collapses.
And against the credible alternative. For vascular risk the comparators have decades of hard-outcome trial data: lipid-lowering, blood pressure control, not smoking, exercise. Those move ApoB and events, and they win on evidence by a margin that is not arguable. A tripeptide with cell-culture senescence data is not in that conversation, and the only honest reason to consider it is that the proven things are already done.
What you are actually buying when you buy Vesugen
Defined peptide, so the certificate means something: one correct mass, confirmable by mass spectrometry, with HPLC purity alongside it.
What the certificate cannot do is settle the name. KED is peer-reviewed as a peptide — the gene-regulation review reports it acting on p16 and p21 — but the mapping from the trade name Vesugen to Lys-Glu-Asp is vendor consensus, not something any indexed paper states. This repo now records that sequence as claimed rather than verified, and the Cartalax mix-up is what that distinction is for: when the mapping is convention rather than citation, errors propagate silently and nobody has a document to check them against.
Expect/mol — which is almost exactly Epitalon's 390.35, from a completely different sequence. Mass alone cannot tell Vesugen from Epitalon. Ask for sequencing or a retention time against a reference standard, not just a mass number.
Where to get Vesugen
Buy Vesugen at Biolongevity Labs →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 Vesugen
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 defined-sequence vascular bioregulator, used in place of Ventfort where people want a known peptide rather than an extract.
- Beyond that the record is self-reported: community dosing logs are real information about tolerability and almost none about efficacy.
🧪 Theoretical / extrapolated
- Lys-Glu-Asp — a synthetic tripeptide targeting vessel wall cells, proposed to normalize protein synthesis in endothelium and smooth muscle.
- 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.
- The endothelium is the tissue where a normalizing mechanism would be easiest to detect if it were real — flow-mediated dilation is a cheap, non-invasive, well-validated readout. Nobody in the series has published one.
What that tier rests on here. The tier above rests on cell-culture senescence markers measured in periodontal-ligament, gingival and bone-marrow stem cells — not in vascular tissue, which is what the product is sold for.
What community dosing logs are worth → · 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
Lys-Glu-Asp, 390.4 g/mol, computed net charge about −1.1 at blood pH. The vascular claim attached to it has one on-tissue paper: Khavinson 2014, on epigenetic aspects of peptidergic regulation of vascular endothelial cell proliferation during aging. Endothelial cells in culture, proliferation as the endpoint, published in the group's own gerontology journal in Russian.
That is the whole of the tissue-specific record. A search of NCBI PubTator3 for this peptide against vascular endpoints on 6 September 2026 returned nothing further — no rodent study with a vessel endpoint, no blood pressure measurement, no imaging, no human data of any kind. What surrounds it is class-level: Kolchina 2019 on how a short peptide might bind DNA at all, Khavinson 2021 as the systematic review of the gene-expression claim, Khavinson 2012 as the tissue-specificity assertion.
The transport step is explicitly unmeasured. Khavinson 2023 scored 26 ultrashort peptides against LAT1, LAT2 and PEPT1 by docking and states its comparison set: all possible di- and tripeptides. No living cell was asked to transport anything. For a molecule whose target tissue is the vessel wall, this matters less than usual — the endothelium is the first surface a circulating peptide meets, so it is the one tissue that needs no transporter to reach. That is the strongest structural argument Vesugen has, and no vendor makes it.
The odd sibling result. Linkova 2023 reports that the dipeptide EW — a different molecule, sold here as Thymogen — reduces angiotensin-induced vasoconstriction and preserves endothelium-dependent relaxation. The vascular result in this family belongs to the thymus peptide, not the vascular one.
What nobody has tested yet
Flow-mediated dilation is the measurement this compound exists for and nobody has published one. It is a non-invasive ultrasound of the brachial artery, it is the standard index of endothelial function, it is used in hundreds of nutrition and drug trials, and it is repeatable in the same person before and after a course. Zero studies of any peptide in this class have reported it.
Two blood markers are almost as good and much easier. Asymmetric dimethylarginine and hs-CRP both track endothelial health and are orderable. A product sold for vascular aging with no published value for either has not engaged with its own claim.
Extrapolation, labeled as such. The endothelium argument cuts both ways. If KED genuinely promotes endothelial proliferation, the same signal that repairs a vessel wall is the signal that feeds angiogenesis, and angiogenesis is not universally good — it is how a tumor and a diabetic retina both get worse. No study in this class has looked at a proliferative endpoint in a setting where proliferation is the problem. That is a hypothesis about risk, not a reported harm, and the distinction matters: nobody has looked, which is different from having looked and found nothing.
Sources read for this page
- Khavinson VKh. Epigenetic aspects of peptidergic regulation of vascular endothelial cell proliferation during aging. Advances in Gerontology 2014 [Russian] · PMID 25051766
- Khavinson VK, Linkova NS, Rudskoy AI, Petukhov MG. Feasibility of Transport of 26 Biologically Active Ultrashort Peptides via LAT and PEPT Family Transporters. Biomolecules 2023;13(3):552 · PMID 36979488
- 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 VKh, Popovich IG, Linkova NS, Mironova ES, Ilina AR. Peptide Regulation of Gene Expression: A Systematic Review. Molecules 2021;26(22):7053 · PMID 34834147
- Khavinson VKh. Peptides tissue-specifically stimulate cell differentiation during their aging. Bulletin of Experimental Biology and Medicine 2012 · PMID 22808515
- 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
Vesugen — 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.
Vesugen — safety specifics for this compound
Specific to Vesugen: the claimed target is endothelium, which is also the tissue that controls coagulation and vascular tone — the two systems where an unmeasured effect would matter most. Nothing in the literature examines interaction with anticoagulants or antiplatelet therapy, and the cell-culture work reports NFκB modulation, which sits directly upstream of inflammatory and thrombotic signaling. That is not a warning about a known harm; it is a specific, named gap that a person on blood thinners should know exists before deciding.
Vesugen — interference & stacking
Predicted from mechanism, not from an interaction study. How mechanism-predicted claims are made →
What Vesugen 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 — Vesugen in an order, with the rest of what you're running.
Unlock in Skool — $10/mo →Bloodwork to run alongside Vesugen
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
Vesugen — frequently asked questions
What is the amino acid sequence of Vesugen?
Vesugen is Lys-Glu-Asp — 3 residues, 390.4 g/mol, isoelectric point 4.18. 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 Vesugen?
Nothing is indexed under the trade name Vesugen. The KED record is cell and animal work.
What should I measure if I run Vesugen?
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
- 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
- Khavinson V, Linkova N, Kozhevnikova E, Dyatlova A, Petukhov M — Transport of Biologically Active Ultrashort Peptides Using POT and LAT Carriers · International Journal of Molecular Sciences 2022;23(14):7733 · PMID 35887081
- 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
Vesugen inside a finished plan
One arm of 2 Protocol Blueprints, free to read in full.
What Vesugen is used for
Vesugen appears under 1 goal in the goal router.
Related Longevity & Bioregulators compounds
Where this goes next
Vesugen is the cardiac & vascular 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.