Livagen peptide: what the Khavinson liver tetrapeptide is, what the studies show and what is unknown

Livagen is the trade name for the tetrapeptide Lys-Glu-Asp-Ala: lysine, glutamic acid, aspartic acid and alanine in that order, written KEDA in single-letter code, so the KEDA peptide and livagen are the same molecule. An early paper transliterates the name as lyvagen ^[1]. It was obtained, in the words of that paper, by directed chemical synthesis on the basis of amino acid analysis of liver polypeptide preparations ^[1], following the method Vladimir Khavinson’s group used for its whole series: analyse an organ extract, then synthesise a very short peptide meant to reproduce that organ’s tissue-specific activity ^[13]. The extract in question is the liver preparation the group calls Hepalin or, in later work, Ventvil ^{[3] [12]}.

Livagen shares its first three residues, Lys-Glu-Asp, with vesugen (KED), pancragen (KEDW), testagen (KEDG) and prostamax (KEDP). The developers assign each of these to a different organ on the strength of the fourth residue, or its absence; in livagen’s case alanine and the liver. Sellers list it as the livagen bioregulator or livagen liver peptide.

As with the rest of the family, nearly every paper on livagen has Khavinson or a close collaborator among the authors, and the chromatin work was done with a group in Tbilisi that has published mainly in Georgian Medical News. The English-language papers appeared in the Bulletin of Experimental Biology and Medicine, a translated Russian journal indexed in PubMed, and one in the Annals of the New York Academy of Sciences. No laboratory independent of this network has, to our knowledge, published on KEDA.

The developers’ explanation for all their short peptides is that they enter the nucleus and change gene activity, and livagen is the peptide on which the chromatin version of that claim was first worked out. In 2002, Khavinson, Lezhava and colleagues treated cultured lymphocytes from old people with livagen and reported activation of ribosomal genes, decondensation of pericentromeric structural heterochromatin and release of genes that had been silenced by age-related condensation of euchromatic regions, which they called de-heterochromatinisation ^[5]. A 2004 comparison of five short peptides (vilon, epitalon, livagen, prostamax and cortagen) in leukocytes from people aged 75 to 88 found that all five activated ribosomal genes and loosened condensed chromatin, and that epitalon, livagen and prostamax also decondensed chromosome 1 pericentromeric heterochromatin, with epitalon and livagen affecting chromosome 9 as well ^[7].

A 2006 paper from the Tbilisi group restated these findings for epitalon, livagen and vilon in lymphocytes from people aged 75 to 88 ^[9], and a 2007 paper in the Annals of the New York Academy of Sciences reported that livagen reactivated heterochromatin in lymphocytes from 80- to 91-year-olds, reduced the chromosomal aberrations induced by cobalt chloride from 4.2% to 3.4%, and shifted sister chromatid exchanges from pericentromeric to telomeric heterochromatin when combined with cobalt ^[10]. The same group reported that livagen corrected the radiation adaptive response of lymphocytes from 72- to 86-year-old donors ^[11].

These are laboratory treatments of cells in a dish, not of the people who donated them. Whether chromatin decondensation in cultured lymphocytes is good, bad or meaningless for an old person is not known; loosened heterochromatin is also a feature of some cancers and of cellular ageing itself. No study has shown that livagen reaches the nucleus of liver cells in a living animal at the concentrations used, and no receptor has been identified.

Liver cells: the first livagen paper, in 2001, measured the roughly hourly rhythm of protein synthesis in cultured hepatocytes from rats aged one to 24 months. Livagen increased the level of protein synthesis at every age, most strongly in cells from old animals, and increased the amplitude of the rhythm in old rats; epitalon, tested alongside, did nothing to hepatocytes ^[1]. In organ culture of rat liver, livagen was reported to stabilise the structure of cell populations and strengthen cellular and intracellular regeneration ^[4]. Across tissues, livagen stimulated the growth of liver explants but not brain or thymus explants, which the developers present as tissue specificity ^{[2] [3]}.

Digestion: a 2005 study found that livagen is barely broken down by small-intestine peptidases, that in the test tube it halved the activity of glycyl-leucine dipeptidase, and that two weeks of oral livagen reduced digestive enzyme activity in young rats but increased it in old rats, bringing old animals close to young control levels ^[8]. This is one of the few oral-dosing results in the Khavinson series and is the main basis for the claim that livagen is orally active.

Opioid system: a 2003 study found that livagen inhibited enkephalin-degrading enzymes in human serum with an IC50 of 20 µM, 25 times more potent than epitalon and, the authors said, more effective than the standard inhibitors puromycin and leupeptin. Neither peptide bound mu- or delta-opioid receptors in rat brain membranes ^[6]. This is an in-vitro enzyme result and its relevance at the concentrations any dose would produce is unknown.

Liver disease: a 2020 review by Kuznik and colleagues states that the liver extract Ventvil and the KEDA tetrapeptide showed high efficacy in animal models of liver fibrosis and acute and chronic hepatitis, normalising immune and antioxidant status and restoring liver function, with the largest effect in old animals ^[12]. The primary studies behind that claim are not indexed in PubMed and we have not been able to read them, so the fibrosis and hepatitis claims rest on the review’s summary alone. There is no study of livagen in human liver disease, fatty liver, alcohol-related damage or liver enzymes.

We found no study in which livagen was given to a person. The human material in the literature consists of blood cells and serum taken from donors and treated in the laboratory: lymphocytes from people aged 72 to 91 in the chromatin studies ^{[5] [7] [9] [10] [11]} and pooled human serum in the enkephalinase study ^[6]. The developers’ 2013 review of clinical results for their peptides lists thymalin, thymogen, vilon, epithalamin, prostatilen, cortexin and retinalamin, and does not claim clinical trials of livagen ^[14]. There is no livagen entry on ClinicalTrials.gov as of September 2026.

This places livagen with testagen and prostamax at the bottom of the series for human evidence. Its position is slightly better in that its cell work was done on human cells, but that does not change the fundamental point: nothing is known about what livagen does when a person takes it.

There is no human time-course. In rats, two weeks of oral livagen changed digestive enzyme activity ^[8]; in hepatocyte culture, protein synthesis was measured over hours ^[1]; in lymphocyte culture, chromatin changes were assessed after the cells had been cultured with the peptide for the usual two to three days ^[5]. None of this predicts onset or duration of any effect in people.

The figures below describe what published studies used. They are not recommendations, and no human dose has been established. In rats, livagen was given by mouth for two weeks at a dose not stated in the abstract ^[8]. In lymphocyte culture, the developers’ standard concentration for these peptides is in the low nanogram-per-millilitre range, and the enkephalinase IC50 of 20 µM corresponds to about 9 µg/mL, many thousand times higher ^[6]. No animal study reports a dose per kilogram in its abstract, and no human dose exists.

Research suppliers sell livagen as a lyophilised powder, usually in 10 to 20 mg vials, and Russian supplement versions are sold as capsules; neither amount derives from a dose-finding study. For converting vial contents to a concentration for a laboratory protocol, use the peptide calculator or the livagen calculator page.

Livagen has been given to rats by mouth ^[8], and its resistance to intestinal peptidases in that study is the most direct evidence in the series that one of these tetrapeptides could survive digestion. The developers have also modelled absorption of short peptides through the intestinal transporters LAT1, LAT2 and PEPT1 ^[15]. Even so, no study has measured livagen in the blood or liver of any animal or person after any route, so bioavailability, half-life and whether it reaches the liver at all remain unknown. Research suppliers sell the powder for reconstitution; there is no injected-dose data in any species.

At about 461.5 g/mol, livagen sits between testagen (about 447) and prostamax (about 488) in mass, and all three share the Lys-Glu-Asp start. A certificate of analysis should therefore report the exact measured mass, since HPLC purity alone cannot tell these related sequences apart.

No safety study of livagen has been published in any species and there is no human data of any kind. The questions people ask, whether it affects liver enzymes, interacts with alcohol or medicines metabolised by the liver, or is safe long term, cannot be answered.

Two concerns follow from the published mechanism. First, livagen’s defining laboratory effect is to loosen condensed chromatin and reactivate silenced genes in old cells ^{[5] [7] [10]}. The developers frame this as reversing an ageing change; but heterochromatin also silences repetitive elements and some oncogenes, and no study has asked what genes are switched on or whether the change is safe. Second, livagen inhibits enkephalin-degrading enzymes in human serum at micromolar concentrations ^[6], which, if it occurred in a person, would prolong the action of endogenous opioid peptides; nothing is known about whether any dose reaches that concentration. Livagen is not on the FDA’s compounding list of substances that may present significant safety risks ^[16], which reflects only that nobody nominated it.

Livagen is not an approved medicine in the UK, US, EU, Canada or Australia. A product marketed for human use with claims about the liver, detoxification or ageing would be treated as a medicine in the UK regardless of a research-use label, and the MHRA has licensed no such product. In the US it is not an FDA-approved drug and has not appeared on the compounding category 2 list ^[16]. In Russia it is sold as a dietary supplement rather than a registered medicine, which confers no status elsewhere. We have not confirmed its standing under the WADA Prohibited List.

For the rules on buying and holding research peptides in your country, see the legal status overview, the UK page, the US page and the Europe page.

Livagen is supplied as a freeze-dried powder. It contains no cysteine, methionine or tryptophan and should be reasonably stable, but the general rules apply: keep the sealed vial cold, dry and away from light, refrigerate any reconstituted solution and use it within a limited period. See how to store peptides and the bacteriostatic water guide.

A four-amino-acid peptide costs little to make, so price per milligram says nothing about quality. Compare livagen prices across the stores we track, including UK listings and US listings. Read how to read a peptide COA first and check that the measured mass is about 461.5 g/mol. Our third-party tested suppliers list shows which stores publish independent tests, and the third-party testing guide explains what those tests do and do not prove.

Sellers often group livagen with glutathione and NAD+ as liver or detox products, or with the other Khavinson peptides such as thymalin and pinealon. Glutathione has a large independent literature; livagen does not, and the two should not be assumed to be comparable. For a general orientation, see what research peptides are and how to spot a fake peptide supplier.