Liver-protecting peptide Livagen (KEDA): a Khavinson bioregulator supplement
A small synthetic peptide studied in animals for protecting the liver and restoring digestive function; sold as a supplement in Russia, experimental and not an approved drug.
- Class
- Synthetic bioregulator tetrapeptide (Khavinson series)
- Status
- Not approved as a medicine in any major regulatory jurisdiction; sold in Russia as an oral dietary supplement; available in Western markets as a research chemical only
- Best-supported effect
- Chromatin decondensation and ribosomal gene activation in aged human lymphocytes (ex vivo, Khavinson group only); hepatoprotective and digestive enzyme restoration effects in rodent models
- Main caveat
- No human clinical trials of any kind; all evidence originates exclusively from one Khavinson-affiliated research group in primarily Russian-language literature; no independent Western replication of any finding
A researcher, an agent, or an algorithm wrote down the sequence and picked a target to hit.
An AI model like OpenFold3 or AlphaFold built a 3D structure and scored how well it fits the binding site.
A second contributor repeated the computation on their own hardware and the scores matched.
A chemistry service or a researcher ordered the sequence, it was manufactured, and mass spectrometry confirmed the right molecule was produced.
A binding or activity measurement confirmed that it actually does what the computer predicted — or didn't.
Snapshot
Class: Synthetic bioregulator tetrapeptide (Khavinson series)
Evidence tier: Animal-only evidence
Status: Not approved as a medicine in any major regulatory jurisdiction; sold in Russia as an oral dietary supplement; available in Western markets as a research chemical only
Best-supported effect: Chromatin decondensation and ribosomal gene activation in aged human lymphocytes (ex vivo, single research group); hepatoprotective and digestive enzyme restoration effects in rodent models
Main caveat: No human clinical trials of any kind; all evidence originates exclusively from one Khavinson-affiliated research group in primarily Russian-language literature; no independent Western replication of any finding
What this is
Livagen is a synthetic tetrapeptide with the sequence Lys-Glu-Asp-Ala (KEDA), developed by Vladimir Khavinson at the Saint Petersburg Institute of Bioregulation and Gerontology as part of the Cytogen / Cytomax bioregulator series. It was proposed as the chemically defined synthetic counterpart to a bioactive fraction derived from porcine liver tissue extract. The Khavinson framework assigns it specificity for liver, gastrointestinal, and immune tissue.
Livagen shares its first three amino acids with Vesugen (Lys-Glu-Asp / KED), differing only at the C-terminal alanine. The originating research group claims distinct tissue tropism for each peptide — liver and immune cells for KEDA versus vascular endothelium for KED — but no molecular basis for this specificity has been established. Among Khavinson bioregulators, Livagen has some of the more developed mechanistic characterization due to ex vivo cytogenetic experiments in primary human lymphocytes, though the entire published evidence base originates from a single research network with no independent replication.
Evidence map
| Evidence layer | Grade | What it supports |
|---|---|---|
| Human clinical | None | No human clinical trials are identifieds available literature |
| Ex vivo (human tissue) | Moderate — single group | Chromatin decondensation and ribosomal gene activation in lymphocytes from elderly donors (ages 75–88); two published studies; both from the originating group only |
| Animal | Moderate — single group | Digestive enzyme restoration in aged rats; protein synthesis enhancement in aged hepatocyte cultures; hepatoprotective and immunomodulatory effects in rodent hepatitis models; tissue-specific effects confirmed in liver, GI, and immune tissue |
| In vitro / cell | Weak — single group | Protein synthesis effects in aged rat hepatocyte cultures; tissue culture work across liver, GI, and immune lines |
| Computational | None identified | No computational or structural prediction data identified in available literature |
| Mechanism | Plausible — not independently verified | Deheterochromatinization (heterochromatin to euchromatin conversion) proposed as primary mechanism; ex vivo cytogenetic observations provide concrete but unverified support; no binding target identified |
Evidence concentration caveat: Substantially all published evidence originates from one research network (Khavinson-affiliated investigators, Saint Petersburg Institute of Bioregulation and Gerontology), predominantly in Russian-language literature. Independent replication of the chromatin-decondensation finding by Western cytogenetics laboratories has not occurred. Confidence in claims derived from this evidence base reflects the absence of independent replication.
Claim check
| Claim | Verdict | Evidence layer | Confidence |
|---|---|---|---|
| Chromatin decondensation and ribosomal gene reactivation in aged human lymphocytes ex vivo | Supported (ex vivo, single group) | In vitro / ex vivo (primary human cells) | Medium — single research group; no independent Western replication |
| Digestive enzyme restoration in aged animals | Supported (animal) | Animal (aged rat model) | Medium — rodent model only; no human translation established |
| Hepatoprotective effects | Supported (animal — rodent hepatitis model) | Animal | Low — rodent models and a single-group 2020 review; no human clinical evidence |
| Immune cell reactivation in elderly | Partially supported (ex vivo / animal) | In vitro / ex vivo + animal | Low — ex vivo lymphocyte data and rodent tissue work; no clinical immune-endpoint trial |
| Treatment for hepatitis or diagnosed liver disease in humans | Not established | None | High confidence in verdict — no human clinical trials in any hepatic indication |
| Anti-aging or longevity benefit in humans | Not established | None | High confidence in verdict — no human clinical endpoint data of any kind |
Experimental exposure
This section reports exposure used in animal experiments and ex vivo assays described in the available literature. It does not establish human dosing.
| Context | System | Experimental exposure / condition | Duration | Endpoint | Limitation |
|---|---|---|---|---|---|
| Animal experiment | Aged rats (oral administration) | Oral Livagen; exact dose not individually extracted from source | Multi-day to multi-week; not individually extracted | Digestive enzyme activity (dipeptidases) in GI tissue vs. young-animal baseline | Rodent only; no human equivalent; dose regimen not extractable from source |
| Ex vivo assay | Lymphocytes from elderly human donors (ages 75–88) | Livagen applied to isolated lymphocyte cultures; exact concentration not individually extracted | Assay duration not individually extracted | Heterochromatin decondensation; ribosomal gene activation on chromosomes 1 and 9 | Ex vivo, not a clinical intervention; single research group only; no independent replication |
| In vitro assay | Hepatocyte cultures from aged rats | Livagen applied to hepatocyte culture medium; exact concentration not individually extracted | Culture duration not individually extracted | Protein synthesis rhythm and intensity vs. young-cell controls | In vitro; no human hepatocyte or clinical data |
| Animal experiment | Rodent hepatitis model | Source describes hepatoprotective effects; exact model, dose, and regimen not individually extracted | Not individually extracted | Antioxidant markers, liver function indicators | Rodent model; exact experimental parameters not extractable from review; no human clinical equivalence |
Community and commercial dosing conventions described in available literature (Khavinson oral capsule schedules, injectable research-chemical conventions) are not rendered in this section. These involve routes and patterns not represented in the published experimental evidence.
Preclinical safety signals
| Signal | System | Notes |
|---|---|---|
| No adverse effects reported in published studies | Animal models and ex vivo tissue | Published reports describe the peptide as well-tolerated; formal toxicology studies are absent; surveillance quality is limited |
| Theoretical: unintended gene activation concern | Mechanistic concern — not observed in published studies | The proposed mechanism (chromatin reactivation and ribosomal gene activation in aged cells) operates in the same biology where unintended growth-promoting effects would be a concern; no formal genotoxicity or carcinogenicity study is present in available literature |
| Theoretical: lymphocyte hyperactivity concern | Mechanistic concern | Claimed immune-cell reactivation is mechanistically a concern in conditions driven by lymphocyte hyperactivity (autoimmune disease context); no controlled safety study in this population |
| One Khavinson-program multi-peptide study found no chromatin condensation abnormalities in elderly subjects | Human tissue / multi-peptide study | Per available sources, this as a safety-relevant observation; it is not a dedicated Livagen safety trial |
| Long-term safety | Not established in any system | No chronic exposure data across repeated courses; effects on oncogene-suppressor balance over multi-year use are unknown |
Source-noted cautions without clinical safety data: Research active or recent malignancy, active autoimmune disease, pregnancy, breastfeeding, and pediatric use as populations for which no data exist and for which the proposed mechanism raises theoretical concerns. No reproductive toxicology, developmental, or pediatric safety studies are identified. These are source-noted precautions, not label exclusions from a clinical trial or approved label.
Theoretical interaction context from source: Research theoretical mechanistic concerns about concurrent use with anticancer chemotherapy and radiation (due to claimed transcriptional reactivation working against treatment intent) and with immunosuppressive regimens (due to claimed lymphocyte reactivation). No controlled drug-interaction data are present; these are mechanistic concerns only, not clinical pharmacovigilance findings.
No human pharmacovigilance data are present in available literature.
Regulatory status
| Region / body | Status | Notes |
|---|---|---|
| US (FDA) | Not approved | Per available sources, not FDA-approved for any indication; not recognized as a dietary supplement ingredient; not on the FDA compounding-eligible peptide list; available in Western markets as a research chemical — not an authorized clinical channel |
| EU (EMA / MHRA) | Not authorized | Per available sources, no EMA or MHRA authorization; not independently verified in this card |
| Canada (Health Canada) | Not authorized | Per available sources, no Health Canada authorization; not independently verified in this card |
| Russia | Sold as dietary supplement / functional food | Per available sources, availability under the Peptides.ru / Khavinson Peptides brand as an oral peptide bioregulator capsule; positioned as a dietary supplement, not a registered prescription medicine; this does not constitute regulatory approval by a major stringent regulatory authority |
| WADA | Probable S0 coverage — per available sources | Source states Livagen is not specifically named on the WADA Prohibited List but may fall under the S0 catch-all for substances not currently approved by any governmental regulatory health authority for human therapeutic use; per available sources only; current list status not independently verified in this card |
No approved therapeutic status identified in major regulatory jurisdictions. This card describes a research and commercially sold peptide, not an approved medicine.
Mechanism
Livagen (Lys-Glu-Asp-Ala) is proposed to act through chromatin remodeling: specifically, inducing deheterochromatinization — the conversion of condensed, transcriptionally silent heterochromatin back to open, transcriptionally active euchromatin. In aging cells, portions of the genome are progressively silenced by chromatin compaction; the Khavinson group's core claim is that the KEDA tetrapeptide reverses this process, reactivating ribosomal genes and other age-silenced programs.
Published cytogenetic evidence from the originating group (PMIDs 12533768, 15085253) shows direct ex vivo visualization of heterochromatin decondensation in lymphocytes from elderly donors (ages 75–88), including decondensation of pericentromeric structural heterochromatin on chromosomes 1 and 9 and activation of ribosomal RNA genes. In aged rat hepatocyte cultures, Livagen was reported to enhance protein synthesis rhythm and intensity with larger effects in older cells. Oral administration in aged rats was reported to restore dipeptidase activity in GI tissue toward young-animal levels. A 2020 review from the same research group describes hepatoprotective and immunomodulatory effects in rodent hepatitis models, including normalization of antioxidant markers.
The proposed oral activity is attributed by published research to resistance of the KEDA tetrapeptide to degradation by small intestinal peptidases; human pharmacokinetic characterization does not exist.
Mechanism limitations: No molecular binding target or receptor has been identified. Mechanism is inferred from ex vivo cytogenetic end-states only. The entire mechanistic evidence base originates from a single research group with no independent replication. The tissue tropism of KEDA for liver and immune tissue — as distinct from the related KED (Vesugen) for vascular endothelium — has no established molecular explanation. Ex vivo chromatin effects in isolated lymphocytes may not translate to in vivo or clinical outcomes.
Chemistry
| Field | Value |
|---|---|
| Amino-acid sequence | Lys-Glu-Asp-Ala (KEDA) |
| Length | 4 amino acids |
| Topology | Linear |
| Modifications | None described in source |
| Molecular weight | Not individually extracted from source |
| Formula | Not individually extracted from source |
| CAS | Not individually extracted from source |
| Salt form | Not individually extracted from source |
| Sequence confidence | Consistent throughout the available literature |
Relation to Vesugen: Livagen (Lys-Glu-Asp-Ala) shares its first three residues with Vesugen (Lys-Glu-Asp / KED). The originating research group claims distinct tissue tropism; they are not interchangeable based on published research literature, though the molecular basis for this distinction has not been independently validated.
Open questions
- Independent replication of the chromatin-decondensation finding: The defining mechanistic claim — heterochromatin decondensation and ribosomal gene activation in aged human lymphocytes — has not been replicated by any laboratory outside the originating Khavinson group. This is the foundational gap before any clinical translation argument can be made.
- Human pharmacokinetics: Oral and parenteral bioavailability of the KEDA tetrapeptide in humans is uncharacterized. The oral capsule is the dominant commercial form, claimed to exploit peptidase resistance, but no human absorption, distribution, metabolism, or excretion data are identifieds source.
- Tissue-specificity mechanism: The molecular basis for why Lys-Glu-Asp-Ala preferentially affects liver and immune tissue while the near-identical Lys-Glu-Asp (Vesugen) is claimed to target vascular endothelium has no established explanation. Without this, the tissue-tropism claim cannot be independently assessed.
- Blinded randomized controlled trials in any indication: No controlled clinical trial in any liver, immune, or aging indication is identified in available literature. Evidence remains dominated by ex vivo human-tissue work and rodent models. The step from preclinical to any human clinical endpoint has not been taken.
- Long-term safety of repeated chromatin-reactivation cycles: The proposed mechanism operates in biology adjacent to oncogene and tumor-suppressor regulation. Formal genotoxicity, carcinogenicity, and chronic-exposure studies do not exist in available literature. The theoretical concern about unintended gene activation in aged cells has not been evaluated.
- Comparative efficacy versus established interventions: No head-to-head data comparing Livagen to established hepatoprotective agents or standard interventions exists. The clinical magnitude and relevance of animal-model effects is uncharacterized.
Research directions for this peptide, selected from the current sources — hypotheses you can explore and model. None of it is proven yet; tap any one to see the full thinking.
Could KEDA organise itself into microscopic beads or gels that act as natural packaging for delivering drugs that are normally too fragile to survive digestion?
Short therapeutic peptides are almost always destroyed before they can be absorbed. If KEDA forms its own stable nano-carriers, it could solve this delivery problem cheaply and safely, benefiting the development of many peptide drugs, not just Livagen itself.
▸3-letter notation
▸citationbibtex
@peptide{pep10941,
sequence = {KEDA},
target = {},
author = {peptidemodel},
year = {2026},
status = {designed}
}