Vesugen

Lys-Glu-Asp, KED, "vascular tripeptide"

Immune & bioregulators

Awaiting medical reviewEN ES DE FR PT ZH+ Follow for updates

Summary

Class: Synthetic tripeptide (3 amino acids: lysine-glutamate-aspartate) from the Khavinson "cytogen" family
Mechanism: Proposed to regulate gene expression in vascular endothelium and smooth muscle — and, in later work, in neurons — through DNA binding; cell and rodent evidence from one group
Routes studied: Injection (rodents); oral capsules (marketed form in Russia); intranasal in some rodent neuro work †
Dose range reported: In vitro: ~20 ng/ml typical. Rodent: microgram/kg. Community-reported: 1–2 capsules/day for 10–30 days. No validated human dose
Half-life: Not characterised; tripeptides are expected to be degraded in plasma within minutes
Storage: Lyophilised: refrigerate, protect from light. Capsules: room temperature, dry
Regulatory status: Not approved as a medicine anywhere. Sold in Russia as a food supplement †

Doses are as reported in studies or by the community — never recommendations.

1What it is

Vesugen is the Khavinson group's three-amino-acid "vascular" peptide, Lys-Glu-Asp. The name has no chemical meaning. It was designed as the short-peptide successor to the group's blood-vessel organ extracts and is marketed in Russia for "vascular ageing". In the 2010s the group also began reporting effects of KED on neurons and in rodent models of Alzheimer's disease, so it now appears in both vascular and brain contexts.

Synthetic compound; one originating group; mostly Russian-language primary literature; no independent replication to our knowledge; no human trial.

2How it's thought to work

Gene-expression model. as for the whole family — cell penetration, nuclear entry, preferential binding at promoter regions (Khavinson 2014).

Endothelium. the group reports that KED increases proliferation and reduces apoptosis markers in cultured endothelial cells, and shifts expression of adhesion molecules and signalling proteins associated with vascular ageing and atherosclerosis.

Neurons. in cultured neurons and in a mouse Alzheimer's model, the group reported that KED (with EDR and AEDG) reduced markers of neurodegeneration and improved behaviour, and attributed this to effects on genes for neuronal differentiation and synaptic function (Khavinson 2021, Pharmaceuticals).

Haemostasis. older Russian work from a collaborating group (Kuznik and colleagues) describes effects of Vesugen on endothelial function and clotting indices in elderly subjects; these are uncontrolled observations.

Proposed: a tripeptide directed at vascular tissue, reported in cell work to affect endothelial gene expression. No human data.Schematic — not to scale

3What the research shows

Endothelial cell biology

Culture studies from the originating group report pro-proliferative, anti-apoptotic and "anti-ageing" expression changes in endothelial cells exposed to KED (Khavinson 2012; Khavinson 2020, Stem Cell Rev Rep). only. [2][4]

Neuroprotection in a mouse Alzheimer's model

A 2021 paper reported that KED and related tripeptides reduced amyloid-associated pathology markers and improved behavioural scores in 5xFAD mice, with accompanying gene-expression changes (Khavinson 2021, Pharmaceuticals). Single group; not independently replicated. [5][6]

Graded B (uncontrolled)

Vascular and clotting indices in elderly people

Russian-language reports from the Kuznik/Khavinson collaboration describe improved endothelial-function and haemostasis indices in elderly volunteers given Vesugen (and the related Vesilute). Small, uncontrolled, unblinded †. This is the only human data in the family for this compound and it should be treated as hypothesis-generating.

Hypertension, atherosclerosis, cognitive outcomes in humans

No controlled trial. Community reports are anecdotal.

4Reported side effects and interactions

Literature-reported

No adverse effects reported in animal or cell work; no controlled human safety data.

Community-reported

Very few; occasional mentions of mild headache or flushing early in a course, which may be unrelated.

Theoretical. Any compound said to act on endothelium and clotting indices could in principle affect bleeding or thrombosis risk; nothing measured. Pro-proliferative effects carry the usual malignancy caution.

Interactions. None established. The reported haemostasis effects mean anyone on anticoagulants or antiplatelets is in genuinely uncharted territory.

Markers researchers commonly monitor

No compound-specific markers are established. Commonly discussed:

Marker	Why it's watched
Blood pressure (home cuff, seated, same time daily)	the claimed target is the vasculature; this is the cheapest objective measure.
Lipid panel and ApoB	relevant to the atherosclerosis framing; unlikely to move, but establishes a baseline.
hs-CRP	vascular inflammation.
Coagulation screen (PT/INR, aPTT, fibrinogen)	only because the uncontrolled human reports describe haemostasis changes; important for anyone on blood thinners.
CBC and CMP	general baseline.

Free for everyone. Safety information is never behind a paywall.

5Reconstitution and handling

Marketed in Russia as oral capsules; injectable vials (10–20 mg) circulate. For vials, with , swirl gently, refrigerate, protect from light.

Open in calculator, pre-loaded →

6Commonly studied alongside

Cardiogen (#81) — the group's cardiovascular pairing; Vesilute (bladder/vascular); Pinealon (Glu-Asp-Arg) and Epitalon (#13) in the neuro work; occasionally discussed with Humanin (#15) or MOTS-c in community "vascular ageing" stacks, without any combined study.

Informational cross-links. Not stack recommendations.

7Regulatory status by region

Region	Status (checked —)
United States	Not FDA-approved; not a permitted supplement ingredient. Not on the 2023 Category 2 list to our knowledge †
European Union	Not authorised
United Kingdom	Not licensed
Australia	Not approved †
South Africa	Not registered
Sport (WADA)	Not specifically named; S0 as a non-approved substance †

8Open questions

Can any of the endothelial or neuro findings be replicated outside the originating network?
Does oral KED have any bioavailability?
Are the reported haemostasis changes real, and in which direction do they move risk?

9References

1Khavinson VKh, Malinin VV (2005). Gerontological Aspects of Genome Peptide Regulation. Karger, Basel. DOI
2Khavinson VKh, Linkova NS, Polyakova VO, Kheifets OV, Tarnovskaya SI, Kvetnoy IM (2012). Peptides tissue-specifically stimulate cell differentiation during their aging. Bull Exp Biol Med. PubMed · DOI
3Khavinson VKh, Solov'ev AYu, Tarnovskaya SI, Linkova NS (2014). Mechanism of biological activity of short peptides: cell penetration and epigenetic regulation of gene expression. Biology Bulletin Reviews. DOI
4Khavinson V, Linkova N, Diatlova A, Trofimova S (2020). Peptide regulation of cell differentiation. Stem Cell Rev Rep. PubMed · DOI
5Khavinson V, Ilina A, Kraskovskaya N, Linkova N, Kolchina N, Mironova E, Erofeev A, Petukhov M (2021). Neuroprotective effects of tripeptides — epigenetic regulators in mouse model of Alzheimer's disease. Pharmaceuticals. PubMed · DOI
6Khavinson VKh, Popovich IG, Linkova NS, Mironova ES, Ilina AR (2021). Peptide regulation of gene expression: a systematic review. Molecules. PubMed · DOI

† Being confirmed by our reviewers against current sources.

10Community

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Self-reported side effects Phase 2

Not enough data yet. 0 of the 50 members needed have logged this compound for 4+ weeks. We don't show anything below 50, so no one can be identified.

11Page history

26 Oct 2026Profile published — awaiting medical review

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