Vesugen Research: The Lys-Glu-Asp (KED) Tripeptide and Its Literature
Vesugen is the KED tripeptide of the Khavinson short-peptide family, assigned by its developers to vascular tissue. Its literature is mostly cell culture and computational docking, with one small uncontrolled human report and — usefully — one published null result. This is a deliberately short page; the family’s evidence problems are set out in full on the peptide bioregulator overview.
What is Vesugen?
What is Vesugen? A synthetic tripeptide — three amino acids, Lys-Glu-Asp, written KED. It is Vilon (Lys-Glu) with an aspartate added, and one residue away from Pancragen (Lys-Glu-Asp-Trp) and Prostamax (Lys-Glu-Asp-Pro). The naming equivalence is worth stating because the newer literature from the originating group mostly writes “KED” and drops the trade name, so a search on one term misses papers indexed under the other.
Its developers assigned it the designation “vasoprotector” — that is a label from the programme described on the overview page, not a conclusion drawn from an independent literature.
Reference data
Identity and form only, from the public chemical record for the all-L Lys-Glu-Asp tripeptide (PubChem CID 87571363). No PubChem record carries “Vesugen” as a listed synonym; the sequence link is made from the primary literature cited below.
| Property | Value |
|---|---|
| Peptide class | Tripeptide (3 residues) |
| Sequence | Lys-Glu-Asp (KED) |
| Also known as | Vesugen, KED peptide |
| Molecular formula | C₁₅H₂₆N₄O₈ |
| Molecular weight | ≈ 390.39 g/mol |
| CAS number | 204271-66-9 |
| Physical form | Lyophilized powder |
| Storage | Kept cold and dry as supplied; protected from light |
No handling quantity, reconstitution procedure or route is given or implied.
What the literature has examined
- Differentiation markers in fibroblast culture — Khavinson et al. (2012, Bull Exp Biol Med, PMID 22808515) examined expression of CXCL12 and WEGC1 in human prostatic fibroblasts across culture passages, reporting a larger effect in late-passage (ageing) cultures. This is the paper that names vesugen as Lys-Glu-Asp.
- Proliferation marker plus molecular docking — Khavinson et al. (2014, Adv Gerontol, PMID 25051766) examined Ki-67 in vascular endothelial cell cultures and used docking to model peptide contact with a 27-base-pair core promoter region of the MKI67 gene. The docking is computational; it predicts an interaction rather than measuring one.
- Vascular disease models — Kozlov et al. (2016, Adv Gerontol, PMID 28539025, Russian-language) examined markers relating to atherosclerosis and restenosis. Only the English abstract was available for this page.
- Neuronal ageing in vitro — Kraskovskaya et al. (2024, Int J Mol Sci, PMID 39518916) examined KED alongside EDR and AEDG in neurons transdifferentiated from the dermal fibroblasts of elderly donors, reporting increased dendritic branching and, for the tripeptides, no effect on mitochondrial or lysosomal activity or on p16.
- Review of gene-expression claims — Khavinson et al. (2021, Bull Exp Biol Med, PMID 34173097) is a narrative review from the originating group collating reported effects of KED on p16, p21, NES, GAP43, SUMO, APOE and IGF1. It reports rather than tests.
A null result also belongs here: Linkova et al. (2011, PMID 22803057) reported that vesugen had no effect on the differentiation capacity of pineal immune cells, where Vilon and Epitalon did.
Evidence status — what is not established
The human evidence is the part most often overstated elsewhere, so it is worth being precise. Meshchaninov et al. (2015, PMID 26390612) assessed 32 people aged 41–83 with chronic polymorbidity, receiving Vesugen or Pinealon, with no control group and no blinding. The authors themselves report mixed signals — a prooxidant effect by chemiluminescence and a decrease in circulating CD34+ haematopoietic cells — alongside their positive findings. That is not a study design capable of establishing an effect, and it is the only human study of Vesugen located in indexed sources.
What is not established: any clinical effect; the “vasoprotector” designation, which is the developers’ label rather than an independently demonstrated property; and the mechanism, which rests on the family-wide peptide–DNA hypothesis plus one computational docking result rather than on a measured interaction in a cell. Independent replication outside the originating network was not found. Nothing here is a claim about what this compound does in a person.
How to verify this compound yourself
Mass spectrometry is the decisive test in this family: the measured mass should match the expected ≈ 390 Da, which separates KED from Vilon (KE, ≈ 275 Da), Prostamax (KEDP, ≈ 488 Da) and Pancragen (KEDW, ≈ 577 Da) — all of which share the same N-terminal Lys-Glu-Asp. HPLC purity is reported as a percentage. See how to read a COA and how to verify peptide purity, and check a specific batch on the verify tool.
Research-grade sourcing and verification
Vesugen is not held in stock. It is listed on our sourcing catalogue as available to order — our supplier lists it, we have not bought it, and material of this kind typically takes about two to three weeks to reach us. For laboratory research use only, it is supplied with a per-batch Certificate of Analysis reporting HPLC purity (%) and mass-spec identity confirmation. Related pages: the bioregulator overview, Vilon, Pancragen, Prostamax and Pinealon. This is sourcing and quality-assurance framing only.
Verify a batch
Every order ships with a per-batch Certificate of Analysis. Have a vial in hand? Enter its lot number to look up the COA for that exact batch.
Frequently asked questions
What is Vesugen?
Is KED the same as Vesugen?
What did the Vesugen studies actually measure?
Is there controlled human evidence for Vesugen?
Literature cited
- Khavinson VKh, Linkova NS, Polyakova VO, et al. “Peptides tissue-specifically stimulate cell differentiation during their aging.” Bull Exp Biol Med. 2012;153(1):148–151. PMID 22808515. pubmed.ncbi.nlm.nih.gov/22808515 (names vesugen = Lys-Glu-Asp).
- Khavinson VKh, Tarnovskaia SI, Lin’kova NS, et al. “Epigenetic aspects of peptidergic regulation of vascular endothelial cell proliferation during aging.” Adv Gerontol. 2014;27(1):108–114. PMID 25051766. pubmed.ncbi.nlm.nih.gov/25051766 (Russian-language; English abstract only).
- Kozlov KL, Bolotov II, Linkova NS, et al. “Molecular aspects of vasoprotective peptide KED activity during atherosclerosis and restenosis.” Adv Gerontol. 2016;29(4):646–650. PMID 28539025. pubmed.ncbi.nlm.nih.gov/28539025 (Russian-language; English abstract only).
- Khavinson VK, Lin’kova NS, Umnov RS. “Peptide KED: Molecular-Genetic Aspects of Neurogenesis Regulation in Alzheimer’s Disease.” Bull Exp Biol Med. 2021;171(2):190–193. PMID 34173097. pubmed.ncbi.nlm.nih.gov/34173097 (review from the originating group).
- Kraskovskaya N, Linkova N, Sakhenberg E, et al. “Short Peptides Protect Fibroblast-Derived Induced Neurons from Age-Related Changes.” Int J Mol Sci. 2024;25(21):11363. PMID 39518916. pubmed.ncbi.nlm.nih.gov/39518916.
- Linkova NS, Khavinson VKh, Chalisova NI, et al. “Peptidergic stimulation of differentiation of pineal immune cells.” Bull Exp Biol Med. 2011;152(1):124–127. PMID 22803057. pubmed.ncbi.nlm.nih.gov/22803057 (null result for vesugen).
- Meshchaninov VN, Tkachenko EL, Zharkov SV, et al. “Effect of synthetic peptides on aging of patients with chronic polymorbidity and organic brain syndrome of the central nervous system in remission.” Adv Gerontol. 2015;28(1):62–67. PMID 26390612. pubmed.ncbi.nlm.nih.gov/26390612 (32 subjects, uncontrolled, unblinded; Russian-language).
- National Center for Biotechnology Information. “PubChem Compound Summary for CID 87571363, Lys-Glu-Asp.” pubchem.ncbi.nlm.nih.gov/compound/87571363 (formula, mass, CAS 204271-66-9).
RESEARCH USE ONLY — NOT FOR HUMAN CONSUMPTION. All products are sold strictly for in-vitro laboratory research and are not intended for human or veterinary use, ingestion, or administration. Nothing on this page is a medical or efficacy claim. You must be 21 or older to browse this catalog.