Livagen Research

Livagen is a synthetic tetrapeptide. Its sequence is lysine, glutamic acid, aspartic acid, alanine, written Lys-Glu-Asp-Ala or KEDA ^[1]. It belongs to a group of short peptides developed in Russia and sold as peptide bioregulators. Very little has been published about Livagen. This page states what that literature contains and what it does not.

Identity

The molecule is well defined, even though its biology is not. The US National Library of Medicine indexes Livagen under the entry terms lysyl-glutamyl-aspartylalanine and Lys-Glu-Asp-Ala. PubChem holds it as CID 87919683, molecular formula C18H31N5O9. The CAS number 433257-50-2 re-resolves to that same record ^[1].

What has been reported

Every compound-specific biological result for Livagen comes from human cells in culture. No study has given Livagen to a living animal or a living person.

Lymphocytes from donors aged 75 to 88 were treated with Livagen alongside three other peptides in the family. The authors reported selective effects, with each peptide acting on different chromosome regions. They also stated that pericentromeric structural heterochromatin was not decondensed ^[1]. This is in vitro work on human cells.

In lymphocyte cultures from patients with ductal breast cancer, Livagen was reported to have a protective effect on DNA single-strand breaks, chromosomal abnormalities and sister chromatid exchange ^[2]. Sister chromatid exchange is a DNA-damage marker, and protective is the authors' reading of it. Two further culture studies applied it to cells from breast cancer patients and from patients with hypertrophic cardiomyopathy, in both cases alongside epithalon ^[3][4]. The cardiomyopathy paper concluded that epithalon, not Livagen, was the most protective agent tested ^[4]. The same laboratory published at least three further Livagen papers, in 2006, 2007 and 2014 ^[5].

Cells taken from a patient are not the patient, and that is the most common misreading of this literature. These endpoints are cytogenetic markers with no established clinical meaning, and none of this work shows an effect in a person.

One result in this line of work contradicts another. An earlier, near-identical 2004 study reported pericentromeric decondensation of chromosome 1 by Livagen and two other peptides ^[6]. The 2023 paper reports the opposite for that same compartment ^[1].

Who produced this work

All of the above comes from one laboratory, the genetics group at Tbilisi State University in Georgia, publishing mainly in Georgian Medical News. Most of those papers are Russian-language with English abstracts only. A plain PubMed search for livagen returned 19 records in August 2026 ^[7]. The compound-specific studies number eight, all of them cited here ^{[1][2][3][4][5][6]}.

This group should not be called independent. Its lead author published with Khavinson as second author in Biogerontology in 2004 ^[8], and the earlier version of its main Livagen study carries Khavinson as an author ^[6]. Vladimir Khavinson and the St Petersburg Institute of Bioregulation and Gerontology discovered these peptides, hold patents covering them, and sell them.

What has not been studied

No animal study of Livagen was identified, and no lifespan or survival data of any kind exists for it ^[7].

There is no human clinical study of Livagen, and no trial of it is registered on ClinicalTrials.gov ^[9].

No pharmacokinetic data has been published for Livagen in any species ^[10]. Nothing is known about how much reaches the bloodstream, how long it persists, or where it goes.

Livagen is a tetrapeptide. The intestinal transporter that carries small peptides intact across the gut wall, PepT1, handles di- and tripeptides ^[11][12]. No carrier-mediated intestinal route is known for a tetrapeptide of this kind. That is a mechanistic constraint rather than an experiment, and other routes have not been ruled out.

These absences are scoped to the indexed literature, since Russian-language work outside MEDLINE could not be searched.

How Livagen relates to its siblings

These compounds are nested sub-sequences of one another. Vesugen (KED) is Livagen's N-terminal tripeptide, and vilon (KE) is its N-terminal dipeptide. Testagen (KEDG) and prostamax (KEDP) differ from Livagen only in the final residue ^[13].

There is no published basis on which to tell a reader what functionally distinguishes Livagen from any of them. The literature is silent on that question.

Lifespan and mortality figures that circulate for "Khavinson peptides" belong to other substances, including crude bovine extracts. None of that is Livagen data.

Livagen is a research compound and is not for human consumption.

Frequently Asked Questions

Has Livagen been tested in humans? No. There is no human clinical study of Livagen and no registered trial of it ^[9]. What exists is work on human cells in culture, taken from elderly donors and from patients with breast cancer or cardiomyopathy ^[1][2][3][4]. Treating cells in a dish is not the same as treating a person.

Has any independent group studied Livagen? No. The compound-specific work comes from one Tbilisi laboratory that has co-authored with Khavinson ^[8], and the earlier version of its main Livagen study lists him as an author ^[6]. Khavinson's institute discovered, patents and sells these peptides. The word independent does not apply to this literature.

What makes Livagen different from vesugen or testagen? Nothing published answers that. Vesugen is Livagen's N-terminal tripeptide, and testagen differs from Livagen by one residue ^[13]. No study has compared them in a way that would show a functional difference, so any claim of one is unsupported.

References

1. 1

   Lezhava T, et al. Georgian Medical News. 2023;(335):79-83. PMID 37042594. (Livagen = Lys-Glu-Asp-Ala; differential scanning calorimetry and cytogenetics on lymphocytes from donors aged 75 to 88; selective effects by chromosome region; pericentromeric structural heterochromatin not decondensed. Database records verified in the same pass: NLM C473185; PubChem CID 87919683, C18H31N5O9; CAS 433257-50-2 re-resolved to the same CID.)
2. 2

   Jokhadze T, et al. Georgian Medical News. 2017;(265):120-125. PMID 28574395. (Russian. Livagen in lymphocyte cultures from ductal breast cancer patients; DNA single-strand breaks, chromosomal abnormalities, sister chromatid exchange.)
3. 3

   Dzhokhadze TA, et al. Georgian Medical News. 2008;(162):11-14. PMID 18830022. (Russian. Fragile-site expression in cultures from breast cancer patients and age groups, with epithalon.)
4. 4

   Dzhokhadze TA, et al. Georgian Medical News. 2013;(225):94-97. PMID 24423684. (Russian. Cultures from hypertrophic cardiomyopathy patients and first-degree relatives, with epithalon and vilon; epithalon reported the most protective agent.)
5. 5

   Lezhava T, Jokhadze T. Annals of the New York Academy of Sciences. 2007. PMID 17460203. With two further Livagen records from the same Tbilisi group: Georgian Medical News. 2006, PMID 16705247. (English; Epitalon, Livagen and Vilon); Georgian Medical News. 2014, PMID 25541832. (Russian; Livagen). (No Khavinson author on the 2007 record. All three cited for existence only; their content was not established in verification, so no result is attributed to them.)
6. 6

   Khavinson VKh, Lezhava TA, Malinin VV. Bulletin of Experimental Biology and Medicine. 2004;137(1):78-81. PMID 15085253. (Earlier, near-identical study; reported pericentromeric decondensation of chromosome 1 by epithalon, livagen and prostamax.)
7. 7

   PubMed E-utilities record counts and absence searches, run 27 August 2026. (livagen bare-term count 19, reproduced exactly; no lifespan or survival record located for livagen.)
8. 8

   Lezhava T, Khavinson V. Biogerontology. 2004. PMID 15105581. (Tbilisi first author with Khavinson as second author, indexed under the misspelling "Khavison V".)
9. 9

   ClinicalTrials.gov API v2 registry query, run 27 August 2026. (Zero registered trials returned for livagen.)
10. 10

    PubMed E-utilities pharmacokinetic absence searches, run 27 August 2026. (No pharmacokinetic study located for livagen in humans or animals.)
11. 11

    Spanier B, Rohm F. Comprehensive Physiology. 2018;8:843-869. PMID 29687907. (PepT1/SLC15A1 substrate specificity.)
12. 12

    Terada T. Current Topics in Membranes. 2012. PMID 23177989. (Peptide transporter substrate specificity.)
13. 13

    Khavinson V, et al. International Journal of Molecular Sciences. 2022. PMID 35887081. (Family sequence table; nested KED- series: vilon KE, vesugen KED, livagen KEDA, testagen KEDG, prostamax KEDP. Note the paper's Table 2 spells prostamax as Prostomax, so a text search of it for the usual spelling returns nothing.)