LongevityKEDLys-Glu-Asp

Vesugen (KED)

Khavinson 'Cytogen' synthetic tripeptide · claimed vascular/endothelial bioregulator · single-school evidence

Vesugen is a synthetic tripeptide — Lys-Glu-Asp (KED) — from the 'Cytogen' line of short 'peptide bioregulators' developed by Vladimir Khavinson and the St. Petersburg Institute of Bioregulation and Gerontology in Russia. Within that family it is positioned as the 'vascular' peptide, marketed for endothelial function and anti-atherosclerotic, 'geroprotective' effects on blood vessels. The chemistry is real and verifiable: KED is a well-defined molecule with a clear formula, weight and structure in the primary chemical database. The biology is the cautious part. Every primary study traces back to Khavinson's own network — and even the papers with international (Italian) or Moscow co-authors are joint publications with that network, not independent replications by an unrelated group. No genuinely arm's-length team has reproduced the vascular or anti-atherosclerotic claims. The headline findings — that KED 'normalises' endothelin-1, restores endothelial cell-to-cell connections, and raises the longevity-associated protein SIRT1 — come from in-vitro (cell-culture) work and small or Russian-language reports, not from controlled human trials. And the proposed mechanism, that a three-amino-acid peptide enters the nucleus and directly regulates genes, is a single-school hypothesis rather than settled biology. The honest framing: a real, well-characterised little peptide with an internally consistent but unreplicated vascular story — promising on paper, unproven in people.

The short version

Vesugen is a trade name for KED, a synthetic peptide made of three amino acids (lysine, glutamic acid, aspartic acid). It belongs to a Russian family of tiny 'bioregulator' peptides designed by Vladimir Khavinson's group, where each peptide is assigned a target tissue. Vesugen's assigned tissue is the blood-vessel lining (the endothelium).

The molecule itself is real and well-defined — the chemistry checks out in the primary database. The question is whether its blood-vessel claims hold up, and there the picture is weak. All of the research comes from Khavinson's network. Even the studies with Italian or Moscow co-authors were done together with that network, so they are not the independent confirmations they might appear to be at first glance. No unrelated team has reproduced the headline vascular results.

What the studies report is mostly cell-culture work: KED changing the levels of certain proteins (like endothelin-1, involved in blood-vessel tone) and raising SIRT1, a protein often linked to longevity research. Some reports describe effects on memory and attention in elderly people, but without a controlled, citable dosing trial behind them. The big claims — that Vesugen protects arteries, prevents atherosclerosis, or rejuvenates the vascular system — are not backed by independent human trials. So Vesugen is best read as an experimental peptide with an interesting but unproven vascular story, not an established treatment for the heart or blood vessels.

Molecular identity

Specs

Molecular formula: C₁₅H₂₆N₄O₈
Molecular weight: 390.39 g/mol
Monoisotopic mass: 390.1751 Da

Sequence (3 AA): Lys-Glu-Asp (KED) — H-Lys-Glu-Asp-OH, all-L (free acid)PubChem CID 87571363
Structure / class: Synthetic tripeptide; Khavinson 'Cytogen' bioregulatorPubChem CID 87571363; Khavinson-school literature
PubChem CID: 87571363PubChem (peptide record; not the unrelated bare-'KED' CID 130427306)
CAS / UNII: Unverified — not assertedNo CAS or UNII in the PubChem synonym list for CID 87571363
Water solubility: Freely water-soluble (small, highly polar free-acid tripeptide; reconstituted in bacteriostatic water)Structural inference (ionizable Lys/Glu/Asp side chains)
Molecular target: No classic receptor identified; claimed vascular/endothelial gene-expression modulator — endothelin-1, connexins, SIRT1 (single-school positioning)Khavinson-school 'tissue-specific peptide' framework (not independently established)
Half-life: Not established (no published human pharmacokinetics)Not established
Regulatory status: Not approved by any major drug regulator; no independent controlled human trials locatedNo NDA/BLA/EMA record located

Plain English

Mechanism

The Khavinson school proposes that ultra-short peptides like KED act as direct 'epigenetic' gene regulators: the peptide enters the cell, reaches the nucleus, binds specific DNA or chromatin regions, and turns target genes up or down — what the school calls 'peptidergic regulation of homeostasis.' For KED specifically, the claimed downstream effects are normalisation of endothelin-1 (a vasoconstrictor that is elevated in atherosclerosis and restenosis), restoration of connexin-mediated coupling between endothelial cells, and induction of sirtuin-1 (SIRT1), framed as a DNA-repair / geroprotective signal.

It needs to be stated plainly: this 'short peptide = direct epigenetic gene regulator' model is a single-school hypothesis. It is plausible-sounding and internally consistent across the network's own papers, but it has not been independently validated outside the Khavinson network. It should be presented as the school's proposed mechanism, never as settled biology.

What is actually demonstrated is narrower: reported in-vitro changes in gene and protein expression in cultured cells — endothelial cells, fibroblasts, mesenchymal stem cells, neuronally differentiated stem cells. What is not demonstrated to any independent standard is the proposed direct peptide-to-DNA binding event, or clinical vasoprotection / anti-atherosclerotic efficacy in controlled human trials. The gap between 'changes a protein level in a dish' and 'protects human arteries' is exactly where the evidence runs out.

Sources:PMID 28539025 PMID 34173097 PMID 32399807

Why people reach for it

Potential benefits

Vesugen (KED) is the Khavinson family's vascular peptide, positioned around the blood-vessel lining. Here's what draws people to it — kept modest, because the evidence is cell-culture work from a single research network, not human proof.

A vascular / endothelial angle people pursue — Vesugen's core result is in cultured vascular cells, where it was reported to normalise endothelin-1 (a vessel-tone protein), restore connections between endothelial cells, and raise SIRT1 — the endothelial-support story people reach for it on, with the caveat that it's in-vitro and single-school, not human proof.
A longevity / 'healthy aging' angle — Because that same work raised SIRT1 — a protein often tied to longevity research — and modulated aging-related genes in stem-cell cultures, it's used in pursuit of vascular and cellular aging goals, framed honestly as a cell-culture signal rather than a clinical outcome.
The 'vascular' tile of the bioregulator set — Within Khavinson's one-peptide-per-tissue concept, Vesugen is the vessel-wall-assigned member, which is why users add it when the goal is vascular tissue specifically rather than a whole-body effect.
Runs as a short, defined course — Like the rest of the family, Vesugen is used in brief pulsed courses (10–20 days) rather than daily indefinitely — a contained pattern that suits the bioregulator approach.
The honest vascular levers, named — If the real goal is vascular health, the cofactor work on this page (nitric-oxide precursors, omega-3, and especially exercise, not-smoking, and blood-pressure control) is far better-evidenced than the peptide it sits alongside.

Sources:PMID 28539025 PMID 32399807 PMID 34173097

What people reach for Vesugen for, drawn from what the research reports (single-school, cell-culture only) and how it's used — not proven human outcomes or medical claims.

Implied timing

Best time to dose

Implied best time

Anytime (consistent)

Time of day isn't critical for Vesugen — pick one daily time you'll actually keep, and hold it across the course.

Vesugen is positioned as a vascular/endothelial bioregulator, not a circadian one. Nothing in its proposed mechanism (gene- and protein-expression changes in cultured vascular cells) ties its effect to a specific time of day.
Unlike the pineal members of this family (Epitalon, Pinealon), there's no melatonin or body-clock logic anchoring the dose — morning is a sensible default that lines up loosely with daytime activity and blood-pressure rhythms, but it isn't a mechanistic requirement.
No published human pharmacokinetic or chronobiology data exist for Vesugen, so consistency is the only defensible timing guidance rather than a specific hour.
Vesugen is run in short pulsed courses (10–20 days), so holding the same daily time across the course is what actually matters.

No study establishes an ideal time of day for Vesugen — this is reasoned from its vascular (non-circadian) mechanism and how it's used. As a rule of thumb most peptide dosing lands in the midday-to-evening window; for Vesugen the time of day isn't critical, so consistency is the verdict.

How to run it

Dosing & protocol

Vesugen is used here as a subcutaneous injection — the form sold as a research peptide and the route the on-page calculator is built for. No human clinical trial has established a dose, so every number and schedule below is community-and-practitioner convention, extrapolated from its proposed vascular/endothelial mechanism. Read it as a map of how people actually run injectable Vesugen — not a validated prescription.

No established human dose: Vesugen has no controlled human trials, no published pharmacokinetics, and is not approved by any drug regulator. Its entire research base is in cultured cells (almost all from one network). Every number and schedule here is convention — not evidence.

Dose — no established human dose

Because no human trial has been run, the ranges below are inferred from the broader Khavinson 'Cytogen' course conventions — stated as convention throughout.

Convention range:: 100–500 mcg per injection, once daily — the range most commonly cited by users and practitioners working with the Cytogen bioregulator family. No single figure is evidence-backed; treat the entire range as a usage pattern.
Route:: Subcutaneous injection — the standard research-peptide delivery form and the route the on-page calculator is built for. The primary literature used cell-culture application; subcutaneous use for systemic vascular goals is mechanistic reasoning, not a studied route.

Subcutaneous administration

Inject into subcutaneous fat; site selection, rotation, and timing are the actionable choices.

Injection site:: The abdomen (2–3 cm clear of the navel), the love-handle area, or the outer thigh. Rotate sites between injections so the same spot isn't used repeatedly — preventing local irritation and lipohypertrophy (fatty lumps).
Measuring the dose:: Drawn from the reconstituted vial on a U-100 insulin syringe. Using the calculator default (10 mg vial + 2 mL BAC water = 5,000 mcg/mL): 100 mcg = 2 IU · 250 mcg = 5 IU · 500 mcg = 10 IU. Use the on-page calculator for any vial size.
Time of day:: Time of day isn't critical for Vesugen — see Best time to dose above. Most users dose in the morning (loosely aligning with daytime activity and blood-pressure rhythms), but there is no published circadian rationale specific to Vesugen, so a consistent daily time across the course matters more than the exact hour.
Food window:: Subcutaneous injection is independent of meals — no food-timing constraint for this route.

Cycle & washout

Khavinson bioregulators are conventionally run as pulsed courses — short on, then off — rather than continuously.

Standard course:: 10–20 days of daily dosing, then a break — the typical Cytogen family convention. Some protocols run 3–4 weeks; no controlled trial has compared durations.
Washout:: 2–4 weeks off between courses is the common pattern. Users sometimes check cardiovascular markers (blood pressure, basic lipid panel) during the break to track any directional change — noting that these are not validated Vesugen biomarkers, just general vascular housekeeping.
Repeat courses:: Some users run 2–3 courses per year, aligned with the Cytogen framework's seasonal-course logic. There is no evidence base comparing continuous vs pulsed use for this compound.

Reconstitution at a glance

The on-page calculator handles any vial size live. Quick reference for the calculator-default 10 mg vial + 2 mL BAC water:

Mixing:: 10 mg vial + 2 mL bacteriostatic water = 5,000 mcg per mL. On a 100-unit (1 mL) U-100 insulin syringe: 100 mcg = 2 IU · 250 mcg = 5 IU · 500 mcg = 10 IU · 1,000 mcg = 20 IU.
Higher dilution option:: Adding 5 mL instead of 2 mL gives 2,000 mcg/mL, spreading smaller doses across more syringe units for easier measurement: 100 mcg = 5 IU · 250 mcg = 12.5 IU · 500 mcg = 25 IU. Either dilution is standard — choose based on your dose.

Sources:PMID 28539025 PMID 34173097

Substrate the signal needs

Nutritional cofactor precision

Vesugen's proposed target is the blood-vessel lining, so the most sensible cofactors are the nutrients vascular biology actually runs on. These are reasoned from vascular physiology and basic nutrition — not a Vesugen cofactor study. Worth saying up front: the inputs below (nitric-oxide precursors, vitamin C, omega-3, and especially exercise) are the better-evidenced vascular levers. Vesugen's own vascular story is single-school and unreplicated.

Reasoned from vascular and endothelial physiology — not a Vesugen cofactor study. Supplement doses are established nutrition ranges, not Vesugen-specific findings. Exercise is the best-evidenced endothelial input; the peptide's contribution is unproven.

Supply the substrate — nitric oxide precursors + dietary nitrate

The endothelium (the vessel lining Vesugen supposedly targets) produces nitric oxide to relax and widen vessels. Give it the raw material.

L-citrulline:: 3 g once daily — converts to L-arginine in the kidney with better oral survival than arginine itself, raising plasma arginine for eNOS (endothelial nitric-oxide synthase) substrate. Take on an empty stomach or between meals.
L-arginine (alternative):: 3–6 g/day if not using citrulline — the direct eNOS substrate. Citrulline is often preferred because arginine is more extensively degraded in the gut before reaching the bloodstream.
Dietary nitrate:: Beets, leafy greens (rocket/arugula, spinach, chard), and beet-root powder — these supply inorganic nitrate, which bacteria on the tongue reduce to nitrite and then to nitric oxide via a non-eNOS pathway. A meaningful dose comes from ~200–300 mL beet juice or a large serving of leafy greens.

Supply the substrate — vessel-wall integrity (vitamin C + collagen substrate)

Vessel walls are built from collagen. Vitamin C is a required cofactor for hydroxylating proline and lysine during collagen synthesis — without it the structure weakens.

Vitamin C:: 500 mg once or twice daily — the minimum effective range for collagen-synthesis support; 1,000 mg/day is used in higher-requirement contexts. Take with a collagen-containing meal or a collagen supplement to co-deliver the substrate.
Mechanism:: Vitamin C is a cofactor for prolyl-4-hydroxylase and lysyl hydroxylase, the enzymes that stabilise the collagen triple-helix. In vessel walls this supports structural integrity of the tunica intima and media — the layers atherosclerosis damages.

Amplify — omega-3 EPA/DHA for endothelial health

Omega-3 fats are among the best-studied nutritional inputs for endothelial function and vascular inflammation — the biology Vesugen is claimed to touch.

EPA/DHA:: 1–2 g combined EPA + DHA daily — from fish oil, krill oil, or algae (the vegan source). Take with a fat-containing meal for best absorption. This is a cardiovascular nutrition mainstream recommendation, not Vesugen-specific.
Mechanism:: EPA and DHA are incorporated into endothelial cell membranes, modulating eicosanoid signaling, reducing adhesion-molecule expression (VCAM-1, ICAM-1), and lowering triglycerides — all relevant to the vascular biology Vesugen is positioned around.

Amplify — the proven vascular levers (exercise, not-smoking, blood-pressure control)

These are not optional extras — they are the strongest established inputs for endothelial function. Framed here because anyone pairing a peptide with vascular goals should know the hierarchy of evidence.

Exercise:: Aerobic exercise (walking, cycling, swimming) is the single best-evidenced driver of endothelial nitric-oxide production and vascular adaptation. Even 30 minutes of moderate-intensity exercise 5 days/week produces measurable improvement in flow-mediated dilation (FMD) — the standard endothelial-function metric. No peptide has evidence at this level.
Not smoking:: Cigarette smoke directly damages the endothelium — impaired eNOS, oxidised LDL, elevated endothelin-1 (the same marker Vesugen reportedly modulates in cultured cells). Stopping smoking is the single most impactful vascular intervention most users can make.
Blood-pressure control:: Chronic hypertension mechanically damages endothelial cells through shear stress. If blood pressure is elevated, dietary sodium reduction, DASH diet, and physician management produce vascular benefits that are orders of magnitude better-evidenced than any experimental peptide.

Combinations + timing

Stacking notes + timing windows

Vesugen is one tile in Khavinson's 'one short peptide per tissue' mosaic, so community stacking follows that logic — not any head-to-head trial. The honest caveat is foregrounded: combining two single-school, unreplicated peptides does not produce synergy evidence, it multiplies speculation. The better-supported 'stack' for vascular health remains the unglamorous one — the dietary, lifestyle, and cofactor inputs above, where the actual evidence lives.

Single-school caveat: every stack partner here is also from the Khavinson network — pairing them compounds the evidence problem rather than solving it. These are user-framework combinations, not studied regimens. Convention only.

Vesugen + Ventfort — the two 'vascular' Khavinsons

Ventfort is the other Khavinson peptide positioned for vascular function; the community pairs them on a 'cover the vascular system from two sides' rationale.

Why it is used:: Ventfort is assigned to the heart and blood vessels in the Khavinson tissue-specific framework; Vesugen is assigned to the vessel wall/endothelium specifically. Users combine them under the logic of complementary vascular targets within the same family.
The protocol:: Both peptides typically at their individual convention doses — commonly 100–500 mcg each, subcutaneous, once daily — on the same pulsed Cytogen course schedule (10–20 days on, 2–4 weeks off).
Honest caveat:: Both Ventfort and Vesugen are single-school evidence only. The pairing has no independent study behind it and no human-trial evidence. If the goal is vascular health, the evidence for exercise and diet is thousands of times stronger than either of these peptides, let alone the combination.

Vesugen + Epitalon — the vascular + longevity pair

Epitalon is the most widely studied of the Khavinson bioregulators (pineal/telomere axis); users combine it with Vesugen on a 'cover the aging biology from multiple tissues at once' rationale.

Why it is used:: Epitalon is the Khavinson peptide with the broadest evidence base within the school (telomere-length data in small human cohorts, melatonin induction, longevity-related gene expression). Pairing it with Vesugen is the 'systemic aging + vascular aging' combination in the school's framework.
The protocol:: Epitalon 5–10 mg daily SubQ on a 10–20-day course, run alongside Vesugen at its convention dose. Many users run the two simultaneously on the same Cytogen course calendar.
Honest caveat:: Epitalon has more Khavinson-school papers than Vesugen, but the same independence problem applies — its evidence is still almost entirely single-network. Adding it to a Vesugen course is an experiment in single-school speculation, not a validated protocol.

Reconstitution math

Reconstitution calculator

Calculated for a 1 mL U-100 insulin syringe (100 units/mL).

Peptide per vial

BAC water added

Desired dose

Units per dose

Draw to this mark on a U-100 syringe

Volume per dose: 0.2 mL
Doses per vial: 10
Concentration: 5 mg/mL

One vial lasts

Daily: 10 days
Every other day: 20 days
5×/week: 14 days

Research use only. Not for human consumption. Outputs are reference values based on research literature — verify all measurements independently.

From the studies

Side effects from research

There is no meaningful human safety database for Vesugen. The research is in-vitro cell work and small or Russian-language reports, which cannot characterise side effects, rare events, or long-term risk in people. Absence of reported harm in such studies is not the same as a demonstrated safety profile.

Because the molecule is claimed to act on the vascular system, the lack of controlled human safety data is particularly worth flagging for anyone with cardiovascular conditions — there is simply no reliable evidence about how it behaves in people at any dose or duration.

Gray-market sourcing adds purity and identity risk independent of the peptide. The honest summary: Vesugen's human safety is uncharacterised, not established.

Sources:PMID 28539025

As reported in literature

Research dosing ranges

These are experimental settings from cell-culture studies — all from the Khavinson network — shown for reference only. There is no human dose, no approved regimen, and no independent replication. Read the table for what was actually tested (mostly cells) versus what is claimed (protected human arteries): the distance between them is the point.

Dose	Route	Model	Outcome	Sources:
In vitro	Cell culture	Cultured vascular/endothelial cells (Kozlov 2016, Advances in Gerontology — the core 'vascular' paper)	KED reportedly normalised endothelin-1 expression, restored connexin-mediated endothelial cell interactions, and increased SIRT1; the 'anti-atherosclerotic substance' label is an author claim, not a trial outcome	PMID 28539025
In vitro	Cell culture	Aging human mesenchymal stem cell cultures (Ashapkin 2020, Mol Biol Rep)	KED (with related peptides) modulated IGF1 / FOXO1 / TERT / NF-κB expression; IGF1 reported up several-fold — a gene-expression signal in cultured cells, not a clinical result	PMID 32399807
In vitro	Cell culture	Human periodontal-ligament stem cells, neuronal differentiation (Caputi 2019, Int J Immunopathol Pharmacol)	KED (with related peptides) increased GAP43 and Nestin during neuronal differentiation — a cell-marker signal from a network collaboration, not independent replication	PMID 30791821
Oral (unspecified)	Review claim	Elderly individuals with functional CNS disorders, as summarised in a Khavinson review (Khavinson 2021, Bull Exp Biol Med)	Review states oral KED 'improved memory and attention' — reported without a controlled, citable dosing regimen; treat as a single-school review claim, not trial evidence	PMID 34173097

Quick answers

Frequently asked

What is Vesugen?

It is a trade name for KED, a synthetic tripeptide (Lys-Glu-Asp) from Vladimir Khavinson's Russian 'Cytogen' line of short peptide bioregulators, positioned as the 'vascular' peptide. The molecule is well-defined chemically; the blood-vessel and anti-aging claims are single-school and unproven.

Does Vesugen protect blood vessels or prevent atherosclerosis?

That is not established. The evidence is mostly cell-culture work (changes in endothelin-1, connexins and SIRT1) from one research network, with no independent replication and no controlled human trials. The 'anti-atherosclerotic' label comes from the authors' own framing, not a clinical outcome. Treat the vascular claims as hypotheses, not facts.

How does it supposedly work?

The Khavinson school proposes that this three-amino-acid peptide enters the cell nucleus and directly regulates genes. That is a single-school hypothesis, not independently established biology. What is actually shown is changes in protein/gene levels in cultured cells.

Is there a known dose?

No. There is no citable, trial-grounded human dose. A review mentions oral KED improving memory and attention in elderly subjects but gives no controlled dosing regimen. Any mg amounts or 'courses' from vendors are unverified convention.

Is Vesugen approved or independently validated?

No. It is not approved by any major drug regulator, and no independent group outside the Khavinson network — including its international collaborators — has reproduced the vascular claims. Vendor marketing is not evidence of Western or independent validation.

Primary sources

References

PMID 28539025Kozlov KL et al., Advances in Gerontology 2016 — the core 'vascular' paper: KED normalised endothelin-1, restored endothelial connexin coupling, increased SIRT1 (in vitro; Russian)
PMID 34173097Khavinson VK et al., Bull Exp Biol Med 2021 — review; states oral KED improved memory/attention in elderly and restores synaptic plasticity in an in-vitro AD model
PMID 32399807Ashapkin V et al., Mol Biol Rep 2020 — KED (with AED, KE) modulated IGF1/FOXO1/TERT/NF-κB in aging human MSC cultures (network collaboration, not independent replication)
PMID 30791821Caputi S et al., Int J Immunopathol Pharmacol 2019 — KED (and related peptides) increased GAP43 and Nestin in neuronal differentiation of human periodontal-ligament stem cells (Italian–St. Petersburg collaboration)
PMID 27259496Lin'kova NS et al., Bull Exp Biol Med 2016 — peptide regulation of skin fibroblast function during in-vitro aging (KED among peptides studied)
PubChem CID 87571363PubChem record — identity (CID, formula, MW, sequence). Note: the bare 'KED' name search returns an unrelated molecule (CID 130427306); the correct peptide CID is 87571363

Research use only · Not medical advice · Updated 2026-06-01