Vesugen (Lys-Glu-Asp): what the published papers report

How much of the Vesugen literature is about Vesugen?

The count collapses under its own query: the largest number attached to this compound is the 27 records a PubMed search for its name returned on 4 August 2026, and it is the number that survives the least scrutiny. The database prints its own translation of what it ran, and for this name it expands the word into the substance concept lysyl glutamyl aspartic acid and searches that too. The same search restricted with [tiab], which demands the name in the title or the abstract, returns 11.

What the expansion swept in: two papers about molecules that are not this one. PMID 29226462 studies a pentapeptide, pyroGlu-Glu-Asp-Cys-Lys, as a growth inhibitor of a rat cell line. PMID 25702411 studies a cyclic heptapeptide built around Lys-Gly-Asp, which carries glycine in the middle position where this compound carries glutamic acid. Neither is about Vesugen, and both sit inside the 27.

Why the sibling rows matter: the restricted counts are the only fair comparison, because the same rewrite would inflate any of these names. Against 62 for epitalon and 62 for vilon, this compound is one of the least written-about members of its own family rather than one of the better studied ones.

What is Vesugen, and how many names does it carry?

The molecule: a three-residue peptide, lysine then glutamic acid then aspartic acid. The PubChem record for Lys-Glu-Asp, CID 87571363, gives the formula C15H26N4O8 and a molecular weight of 390.39. Querying the same database by the trade name returns nothing, because Vesugen is a product name and not a chemical one.

Four names for one thing: the National Library of Medicine's controlled-vocabulary record for lysyl-glutamyl-aspartic acid, MeSH UID 67533570, lists its entry terms as Lys-Glu-Asp, tripeptide t-38, t-38 tripeptide and vesugen. That record is the reason the search behaves the way it does, and it is also the reason the search misses papers.

The lab code hides work: PMID 25408528 is a vascular study of this sequence that never prints the trade name. It reports on tripeptide T-38 in organotypic and dissociated cultures of vascular cells, in vitro, where T-38 raised Ki-67, reduced p53 and reduced E-selectin, alongside a second peptide it calls RR-1. A reader searching the trade name does not find it; a reader searching the concept finds it next to two papers about other molecules entirely.

The one paper that writes both: PMID 22808515, in an English-language journal with a DOI, names the sequence and the trade name in the same breath, reporting that vesugen acted on human prostatic fibroblasts while one tetrapeptide acted on human embryonic pancreatic cells and another on human embryonic bronchial epithelial cells. That is a cell-culture result, not a result in a person, and it is the cleanest confirmation available that the trade name and the sequence are the same thing.

The undercount, measured: 18 of the 27 concept records fall outside that set of 11. All 18 carry the substance heading lysyl-glutamyl-aspartic acid, which is what swept them in, and that heading cannot sort them either, because both records about other molecules carry it too. 16 of the 18 are about this molecule, and they write KED or T-38 rather than the trade name in the title and the abstract, which is the only text the [tiab] restriction reads. Six of the 16 are cited on this page: PMID 28509489, PMID 28539025, PMID 25408528, PMID 32399807, PMID 34173097 and PMID 39518916. One of those six, PMID 39518916, does print the trade name once inside its full text, where the restriction cannot see it. So the trade name loses 16 papers while the concept picks up two that belong to other molecules, and the two errors run in opposite directions at once.

Why a reader should care: a trade name is not a molecule, and this one answers to four labels across two databases. The classification page on cardarine works the same problem from the regulatory end, and an HPLC purity number is the laboratory version of it: a percentage and an identity are two separate measurements.

The seven papers that gave it to people

The whole human record, in one table: seven indexed papers report this compound administered to human beings. Every one is a Russian-language article in Advances in Gerontology, none carries a DOI, none has a copy in PubMed Central, and none is registered on ClinicalTrials.gov. What we read, in every case, is the English abstract attached to the indexed record.

The seventh one the trade name hides: PMID 28509489 writes neither Vesugen nor Vezugen in its English abstract, so a search on the name cannot reach it and the set of 11 does not contain it. It is in this table because the National Library of Medicine filed it under the substance heading lysyl-glutamyl-aspartic acid, next to pinealon, and indexed it with Humans. That is the undercount from the section above arriving inside the human record itself, which is why this table is built from the concept set rather than from the name.

It is rarely given alone: in five of the seven it arrives beside something else, pinealon in four of them and an unrelated supplement in the fifth. Only the two vascular papers report it on its own, and those two came from one team.

Does the human evidence hold together?

Read one at a time, the two vascular papers look like two trials. Read side by side, they look like one team working twice. PMID 28976154 reports Vezugen as monotherapy in 41 patients after surgery for chronic lower-limb ischemia, with blood flow measured before and after. PMID 25051774 reports Vezugen as monotherapy in 41 patients with vasculogenic erectile dysfunction, with blood flow measured before and after. Same cohort size, same design language, consecutive volumes of the same journal, and five of the six author surnames on each paper appearing on the other in slightly different transliterations.

The 2014 record disagrees with itself: its title is about lower-limb chronic arterial insufficiency in old and elderly people, and its abstract is about erectile dysfunction. We are reporting what the indexed record contains, which is a mismatch a reader should know about before treating the two papers as independent findings. It is not an accusation about anyone's conduct.

The friendliest human paper carries its own bad news: PMID 26390612 concludes that vesugen produced a more visible geroprophylactic effect than pinealon on biological-age indicators, and the same abstract reports prooxidant activity on chemiluminescence and a fall in CD34-positive cells that it describes as significant inhibition of hemopoiesis. It reports the two together, in one paragraph, and still closes by recommending both peptides.

An arithmetic problem in the same abstract: it states 32 people and then breaks them down as 18 men and 12 women, which sums to 30. We print both numbers rather than quietly picking the one that reads better, because there is no full text to settle it against.

What none of the seven abstracts reports: a control arm that received nothing, a placebo, blinding, or a registered protocol, and not one of the seven has a retrievable full text. Improvement measured before and after in patients recovering from vascular surgery has more than one available explanation, and an uncontrolled design cannot separate them.

What the cell and animal work measured

The vascular mechanism story, and its species: PMID 28539025 reports that KED normalized the endothelin-1 expression raised in atherosclerosis and restenosis, restored cell-to-cell interaction through connexin expression, and increased sirtuin-1, in normal, atherosclerotic and restenotic endothelium. That is an in vitro result in a Russian-language paper with no DOI, and it is the closest thing this compound has to a mechanism.

The docking result, and what it actually is: PMID 25051766 reports that vesugen and a second peptide the paper calls D-7 raised Ki-67 in vascular endothelial cell cultures taken from young and old animals, and that molecular docking placed both peptides at the MKI67 core promoter, the sequence 5'-agcctcaaccatcaggaaaacaagagt-3', spanning positions -14 to +12 relative to the transcription start site of gene ENSG00000148773. Docking is a computation, not a measurement, and the cells were animal-derived.

The one open-access full text: PMID 39518916 applied KED at 10 mcg/mL for 10 days to induced cortical neurons, transdifferentiated from skin fibroblasts of three women aged 61, 66 and 68. Primary processes rose 32% to 6.06 plus or minus 0.3 (p equals 0.0093) and total dendrite length rose 42%, from 270.2 plus or minus 25.5 in the control to 384 plus or minus 27 (p equals 0.0148), in a unit the results text never names. This is human-derived tissue in a dish, which is not a human trial.

What the same paper found no effect on: branching points, terminal processes, mitochondrial activity, lysosomal activity, LaminB1 and oxidative DNA damage. LaminB1 moved down 7% and the DNA damage marker down 15%, neither reaching significance, and the paper reports the aging marker p16 unchanged, at 7021 plus or minus 352.4 in the control against 7179 plus or minus 458.1 after the peptide. The authors close by recommending the peptides as neuroprotective agents. That is their recommendation, and this page reports their measurements instead.

Gene expression, and a contradiction worth keeping: PMID 32399807 reports that KED at nanomolar concentrations inhibited FOXO1 expression 1.6 to 2.3 fold in a human embryonic bone-marrow stem cell line, and that its effect on TNKS2 ran in opposite directions in the paper's two aging models, inhibition in one and stimulation in the other. Both figures are in vitro.

Where the mechanism story outruns the record: PMID 34173097 is a narrative review written by the originating laboratory. Its abstract states that oral KED improved memory and attention in elderly people with functional central-nervous-system disorders, and cites nothing for that sentence in the abstract itself. The same abstract closes by calling a test of the peptide in animal models of Alzheimer's disease very important, which is a plain statement that the test had not been done.

Where Vesugen loses a head-to-head

Why this section exists: the same laboratory group published direct comparisons between these peptides, and in three of them this one is not the winner. A result that runs against the compound earns the same space here as a result that runs for it, which is the only way a summary of a small literature stays honest.

• Pineal immune cells, in vitro: PMID 22803057 reports that vesugen had no effect on the differentiation capacity of these cells, while vilon drove precursors towards T-helpers, cytotoxic T lymphocytes and B cells and epithalon drove them towards B cells. Vesugen raised proliferation potential only. Organotypic culture of rat pineal tissue: the abstract names no species, the indexed record does.
• Low-oxygen stress, animals in vivo: PMID 18546825 reports that vilon, epitalon, vesugen and pinealon all showed antihypoxic properties in a hypobaric hypoxia model, and that pinealon had the most pronounced effect of the four.
• Antioxidant activity, in vitro: PMID 18546826 reports that pinealon, vesugen, vilon and epitalon showed no direct antioxidant activity, though they limited peroxidation of human lipoproteins by modifying their structure and raised the resting level of reactive oxygen species inside cells.
• Aging markers in human-derived neurons, in vitro: PMID 39518916 found the dendrite changes above and no significant movement in p16, LaminB1, mitochondrial activity, lysosomal activity or oxidative DNA damage.

How to read that set: a compound can be real, measurable and still be the weaker option in the comparisons its own developers ran. Nothing in the four results above says the peptide does nothing. They say the published comparisons put it behind its siblings on the specific endpoints those papers chose.

Is Vesugen approved as a medicine anywhere?

We found no US approval and no registered trial. On 4 August 2026 the openFDA drug endpoints for approvals, labels, adverse events and enforcement all return NOT_FOUND for this compound, while a control query for semaglutide on the approvals endpoint returns records, so the zero is a real answer rather than a broken request. On the same day the ClinicalTrials.gov API returns zero studies for the trade name and zero for Khavinson, the surname carried by nine of the nineteen papers listed below, against 757 for the same control.

What we could not check, stated as such: two registers refused us. The European regulator's search returned an authorization error for this compound and for our control alike, and the Russian state medicines register denied access for this compound and for two positive controls alike. A register that will not answer is not a register that answered no, and we are not going to report a blocked query as an absence.

What that leaves: a compound with a trade name, an entry in a controlled medical vocabulary, and an indexed literature we measure at twenty-seven papers genuinely about it, the 27 concept records minus the two other molecules, plus the two that name it in their abstracts and sit outside the concept set entirely. That it lands on the same figure as the raw search is a coincidence and not an agreement; it is a different set of papers. Seventeen of the twenty-seven are cited below, beside the two that are not about it at all, and not one of the twenty-seven is an approval and not one is a registered trial. That is a different position from illegal and a different position from approved, and the honest description is that we could not find a marketing authorization in any register that answered us.

What the record still leaves open

The gaps that survive the whole file:

• Whether the vascular effect is real. Two uncontrolled before-and-after series from one team, in one journal, with no full text, is the entire human vascular case.
• What happens over time. No paper in this set follows anyone beyond the treatment period, so durability is unmeasured rather than unclear.
• Whether the safety signal repeats. One human abstract reports prooxidant activity and reduced CD34-positive cells. One report is not a finding, and no second paper in this set looked.
• What is in a given vial. Identity for a three-residue peptide is a laboratory question rather than a label question.
• Whether any powder matches the papers. The published work used defined material under defined conditions, and a vial is not a paper.

The last two are questions about an object rather than about a literature: identity is a laboratory result, and a certificate of analysis answers only the parts somebody paid to have tested, while the freeze-dried solid in a vial is a formulation whose composition the glass does not disclose.

How this page is sourced

What we opened ourselves: every record named on this page was pulled through the NCBI E-utilities interface on 4 August 2026 and read, along with one open-access full text, two reference-database records, and two live queries against regulator and registry interfaces with their positive controls run beside them. The search counts printed above were reproduced on that date, not copied from anywhere.

The limit on eleven of them: eleven of the nineteen papers in the list below are Russian-language articles with no DOI, no copy in PubMed Central, and no full text we could reach. For those the indexed English abstract is the whole of what we read, and every number this page takes from them is labeled as an abstract figure at the point where it appears. That is a real limit on this page, and it is not one that better writing can fix.

What was deliberately left out: one 2026 item that names the compound in a publication we could not place, and every figure we could not trace back to a document we had opened ourselves. A claim that cannot be tied to a retrievable record is cut rather than softened.

Twenty-three sources: nineteen indexed papers, two reference-database records, and two live database queries printed with their exact strings and their controls.

The standard: the full sourcing and citation-verification standard for this site, including who checks a page before it ships, lives on the methodology page.

Last reviewed: 4 August 2026.

1. 1

   National Library of Medicine. MeSH Supplementary Concept Record, lysyl-glutamyl-aspartic acid. Entry terms Lys-Glu-Asp, tripeptide t-38, t-38 tripeptide, vesugen; heading mapped to Oligopeptides. Retrieved 4 August 2026. MeSH UID 67533570.

2. 2

   National Center for Biotechnology Information. PubChem Compound Summary for CID 87571363, Lys-Glu-Asp. Molecular formula C15H26N4O8, molecular weight 390.39. Retrieved 4 August 2026. PubChem CID 87571363.

3. 3

   Kitachov KV, Sazonov AD, Kozlov KL, Petrov KY, Slusarev AS, Sedova EV. [The role of vasoactive peptid in lower limbs chronic arterial insufficiency treatment]. Adv Gerontol. 2013;26(2):292-296. Russian, English abstract only, no DOI. PMID 28976154.

4. 4

   Kitachev KV, Sazonov AB, Kozlov KL, Petrov KIu, Sliusarev AS, Khavinson VKh. [The efficacy of peptide bioregulators of vessels in lower limbs chronic arterial insufficiency treatment in old and elderly people]. Adv Gerontol. 2014;27(1):156-9. Russian, English abstract only, no DOI, indexed publication type Clinical Trial. PMID 25051774.

5. 5

   Meshchaninov VN, Tkachenko EL, Zharkov SV, Gavrilov IV, Katyreva IuE. [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):62-7. Russian, English abstract only, no DOI. PMID 26390612.

6. 6

   Myakotnykh VS, Torgashov MN, Egorin KV, Meshchaninov VN, Gavrilov VI, Borovkova TA, et al. [Comparative analysis of different methods of geroprotective]. Adv Gerontol. 2016;29(4):594-601. Russian, English abstract only, no DOI. PMID 28539017.

7. 7

   Bashkireva AS, Artamonova VG. [The peptide correction of neurotic disorders among professional truck-drivers]. Adv Gerontol. 2012;25(4):718-28. Russian, English abstract only, no DOI, indexed publication type Clinical Trial. PMID 23734521.

8. 8

   Filippova EV. [Treatment of chemical stomatitis in people of advanced and senile age]. Adv Gerontol. 2013;26(2):288-291. Russian, English abstract only, no DOI. PMID 28976153.

9. 9

   Bashkireva AS, Kachan EY. [Assessment of work ability index in evaluation of small peptides geroprotective effect]. Adv Gerontol. 2015;28(3):510-512. Russian, English abstract only, no DOI, no copy in PubMed Central. The abstract names no compound; the indexed record carries the chemical substance headings lysyl-glutamyl-aspartic acid and pinealon, and the MeSH headings Humans, Male, Adult and Middle Aged. PMID 28509489.

10. 10

    Kraskovskaya N, Linkova N, Sakhenberg E, Krieger D, Polyakova V, Medvedev D, et al. Short Peptides Protect Fibroblast-Derived Induced Neurons from Age-Related Changes. Int J Mol Sci. 2024;25(21):11363. Open-access full text read in full. doi:10.3390/ijms252111363. PMC11546785. PMID 39518916.

11. 11

    Kozlov KL, Bolotov II, Linkova NS, Drobintseva AO, Khavinson VK, Dyakonov MM, et al. [Molecular aspects of vasoprotective peptide KED activity during atherosclerosis and restenosis]. Adv Gerontol. 2016;29(4):646-650. Russian, English abstract only, no DOI. PMID 28539025.

12. 12

    Khavinson VKh, Tarnovskaia SI, Lin'kova NS, Guton EO, Elashkina EV. [Epigenetic aspects of peptidergic regulation of vascular endothelial cell proliferation during aging]. Adv Gerontol. 2014;27(1):108-14. Russian, English abstract only, no DOI. PMID 25051766.

13. 13

    Khavinson VKh, Lin'kova NS, Evlashkina EV, Durnova AO, Kozlov KL, Gutop OE. Molecular aspects of anti-atherosclerotic effects of short peptides. Bull Exp Biol Med. 2014;158(1):159-63. doi:10.1007/s10517-014-2713-8. PMID 25408528.

14. 14

    Khavinson VKh, Linkova NS, Polyakova VO, Kheifets OV, Tarnovskaya SI, Kvetnoy IM. Peptides tissue-specifically stimulate cell differentiation during their aging. Bull Exp Biol Med. 2012;153(1):148-51. doi:10.1007/s10517-012-1664-1. PMID 22808515.

15. 15

    Ashapkin V, Khavinson V, Shilovsky G, Linkova N, Vanuyshin B. Gene expression in human mesenchymal stem cell aging cultures: modulation by short peptides. Mol Biol Rep. 2020;47(6):4323-4329. doi:10.1007/s11033-020-05506-3. PMID 32399807.

16. 16

    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. Narrative review by the originating laboratory, not primary data. doi:10.1007/s10517-021-05192-6. PMID 34173097.

17. 17

    Linkova NS, Khavinson VKh, Chalisova NI, Katanugina AS, Koncevaya EA. Peptidegic stimulation of differentiation of pineal immune cells. Bull Exp Biol Med. 2011;152(1):124-7. doi:10.1007/s10517-011-1470-1. PMID 22803057.

18. 18

    Kozina LS. [Investigation of antihypoxic properties of short peptides]. Adv Gerontol. 2008;21(1):61-7. Russian, English abstract only, no DOI. PMID 18546825.

19. 19

    Kozina LS, Arutiunian AV, Stvolinskii SL, Khavinson VKh. [Biological activity of regulatory peptides in model experiments in vitro]. Adv Gerontol. 2008;21(1):68-73. Russian, English abstract only, no DOI. PMID 18546826.

20. 20

    Rytomaa T, Grip-Rytomaa K. Spontaneous death of rat chloroleukaemia cells induced by an endogenous growth inhibitor. Cell Prolif. 2018;51(1):e12421. Retained as evidence of query contamination: the molecule studied is the pentapeptide pyroGlu-Glu-Asp-Cys-Lys, not Lys-Glu-Asp. doi:10.1111/cpr.12421. PMID 29226462.

21. 21

    Jing J. Synthesis and activity of a cyclo-heptapeptide containing Lys-Gly-Asp-sequence as a novel anti-platelet agent. Bioorg Khim. 2013;39(5):547-51. Retained as evidence of query contamination: the sequence carries glycine in the middle position, not glutamic acid. No DOI in the record. PMID 25702411.

22. 22

    U.S. Food and Drug Administration, openFDA drug application, label, adverse-event and enforcement endpoints, queried 4 August 2026 for the trade name and for Lys-Glu-Asp. Every endpoint returned an HTTP 404 carrying the body NOT_FOUND, while the positive control search for semaglutide on the same drug-application endpoint returned six records. api.fda.gov, drug application query.

23. 23

    ClinicalTrials.gov API version 2, queried 4 August 2026. Total study count zero for the trade name and zero for the developing laboratory's surname, against 757 for the positive control semaglutide run the same minute. clinicaltrials.gov, study count query.

Related pages

Four pages next door, on the questions this one hands off: what a document can prove about a molecule, and what a vial cannot.

• How to read a COA: which line on the certificate is an identity result and which line is only a percentage.
• What HPLC purity does not settle: a chromatogram counts how much of one thing is there, without saying which thing it is.
• What a lyophilized peptide is: freeze-drying, the cake it leaves behind, and why the weight of the solid and the weight of the peptide are two different numbers.
• Cardarine, classified: what the compound sold as a SARM turns out to be, and what its own trial record contains.

Where the rest of this series lands: each compound audit in this run goes out to the mailing list as it is finished.