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Livagen peptide (KEDA) is a Khavinson tetrapeptide bioregulator targeting hepatic tissue. This research-grade compound modulates gene expression and chromatin structure in hepatocytes for preclinical liver aging, hepatic repair, and epigenetic rejuvenation research. 20mg lyophilized powder, =98% purity, COA included.
Livagen peptide is a synthetic tetrapeptide bioregulator with the amino acid sequence Lys-Glu-Asp-Ala (KEDA), developed by Professor Vladimir Khavinson at the St. Petersburg Institute of Bioregulation and Gerontology. Livagen targets hepatic tissue, functioning as a liver bioregulator that modulates gene expression in hepatocytes, hepatic stellate cells, and supporting liver parenchyma. It belongs to the Khavinson bioregulator peptides class — short regulatory peptides that exhibit tissue-specific gene expression modulation at physiological concentrations — and has been studied in preclinical models of liver aging, hepatic repair, chromatin remodeling, and age-related hepatic functional decline.
The liver is uniquely positioned as both the body’s primary metabolic organ and one of the few tissues with significant regenerative capacity. Despite this regenerative potential, age-related epigenetic changes progressively impair hepatocyte function, compromise detoxification pathways, and reduce the liver’s capacity for self-renewal. Livagen addresses this research gap by operating at the chromatin level, modulating the transcriptional programs that govern hepatocyte function and renewal. Among the Khavinson bioregulators, livagen is distinguished by its documented effects on chromatin condensation and decondensation in hepatic tissue, offering a direct window into the epigenetic mechanisms of liver aging. PrymaLab Livagen 20mg is manufactured to high purity standards and supplied exclusively for qualified preclinical research.
| Specification | Detail |
|---|---|
| Compound | Livagen (tetrapeptide bioregulator) |
| Sequence | Lys-Glu-Asp-Ala (KEDA) |
| Quantity | 20mg |
| Target Tissue | Liver (hepatocytes, hepatic stellate cells, liver parenchyma) |
| Class | Khavinson bioregulator peptide (short regulatory peptide) |
| Purity | ≥98% (HPLC-verified per batch) |
| Testing | HPLC, mass spectrometry, identity verification |
| Form | Lyophilized powder |
| Storage | Store at −20°C desiccated; protect from light |
| Intended Use | Preclinical research only — not for human or veterinary therapeutic use |
Livagen is one of the most mechanistically characterized peptides in the Khavinson bioregulator system due to its documented effects on chromatin structure. The KEDA sequence has been shown to induce decondensation of heterochromatin in hepatocyte nuclei, effectively “opening” previously silenced regions of the genome and restoring access to genes that become epigenetically suppressed during aging. This chromatin remodeling mechanism provides a direct molecular explanation for how a short peptide can reactivate age-suppressed gene expression programs in liver tissue.
Through its chromatin-modifying activity, livagen modulates the expression of genes governing hepatocyte metabolic function, detoxification enzyme systems, protein synthesis, and cellular renewal. Preclinical studies have demonstrated that livagen treatment in aged hepatocyte cultures restores expression levels of genes that decline during liver aging, including cytochrome P450 enzymes, albumin synthesis genes, and mitochondrial biogenesis factors. This broad transcriptional restoration distinguishes livagen from compounds that target single metabolic pathways.
The tissue specificity of livagen derives from the selective affinity of the KEDA sequence for regulatory DNA motifs enriched in hepatocyte gene promoters. While livagen’s chromatin effects have been most extensively documented in liver tissue, the specificity of its gene expression modulation to hepatic programs confirms its classification as a dedicated liver bioregulator within the Khavinson system.
Published studies on livagen peptide benefits report multiple hepatic-specific effects relevant to liver aging and repair research. All findings described below are from preclinical animal and cell culture models.
The most distinctive livagen peptide benefit documented in the literature is its capacity to reverse age-related heterochromatin accumulation in hepatocyte nuclei. Aging liver cells progressively silence genes through chromatin condensation, reducing functional gene expression capacity. Livagen has been shown to specifically decondense these silenced chromatin regions, effectively reversing one of the fundamental epigenetic hallmarks of cellular aging. This finding has significance beyond hepatology, providing experimental evidence for the reversibility of age-related epigenetic changes.
Age-related liver functional decline involves reduced drug metabolism, impaired protein synthesis, and diminished bile production. Livagen research reports restoration of cytochrome P450 enzyme expression, improved albumin and transferrin gene expression, and enhanced hepatic metabolic capacity in aged animal models. These metabolic restoration effects correlate with the observed chromatin remodeling, suggesting a causal relationship between epigenetic rejuvenation and functional recovery.
Hepatic fibrosis (progressive scarring) impairs liver architecture and function during aging and in chronic liver disease models. Among the reported livagen benefits, modulation of hepatic stellate cell activation and reduced collagen deposition have been documented. These anti-fibrotic findings position livagen as a research tool for studying whether epigenetic interventions can prevent or reverse the fibrotic cascade in aging liver tissue.
The liver’s regenerative potential declines with age as hepatocytes lose proliferative capacity. Livagen research has demonstrated enhanced hepatocyte proliferation markers and improved liver regeneration kinetics in aged models following partial hepatectomy. These findings suggest that chromatin remodeling may help restore the regenerative programs that become epigenetically silenced during liver aging.
Preclinical livagen studies report upregulation of endogenous antioxidant defense genes in hepatic tissue, including superoxide dismutase (SOD), catalase, and glutathione-related enzymes. Enhanced antioxidant gene expression in the liver has systemic significance given the organ’s central role in detoxification and oxidative stress management throughout the body.
Published research provides context for livagen peptide dosage parameters across different experimental paradigms. The following represents reported dosage ranges from preclinical literature and is intended solely to inform research protocol design.
| Research Application | Reported Dosage Range | Protocol Context |
|---|---|---|
| Cell Culture (Hepatocytes) | 10–200 nM | Chromatin remodeling and gene expression studies |
| Liver Aging Models | 1–10 µg/kg | Chronic administration in aged rodent hepatic studies |
| Hepatic Fibrosis Models | 5–20 µg/kg | Anti-fibrotic protocols in chronic liver injury paradigms |
| Liver Regeneration Models | 1–10 µg/kg | Post-hepatectomy regeneration and recovery studies |
Important: These are reported research dosages from published preclinical literature. Optimal dosing depends on experimental design, animal model, route of administration, and research objectives. This product is not intended for therapeutic use.
Researchers studying hepatic aging often compare livagen and ovagen because both target the liver within the Khavinson bioregulator system. Understanding their distinct mechanisms and overlapping applications is essential for selecting the appropriate hepatic bioregulator peptide for specific research protocols.
| Feature | Livagen | Ovagen |
|---|---|---|
| Classification | Liver bioregulator (hepatic tissue) | Liver and GI bioregulator (hepatic + gastrointestinal) |
| Sequence | Lys-Glu-Asp-Ala (KEDA) | Glu-Asp-Leu (EDL) |
| Primary Target | Hepatocytes, hepatic stellate cells | Hepatocytes, GI mucosal epithelium |
| Unique Mechanism | Chromatin decondensation and epigenetic remodeling | Dual-organ gene expression modulation (liver + gut) |
| Research Emphasis | Epigenetic liver aging, chromatin biology, hepatic repair | Liver-gut axis, GI barrier function, dual-organ aging |
| Anti-Fibrotic Data | Direct hepatic stellate cell modulation | Indirect via hepatocyte support and GI integrity |
| Best For | Pure hepatic research: chromatin, regeneration, fibrosis | Liver-gut interaction research: barrier, microbiome, dual-organ |
| Combined Use | Complementary: epigenetic hepatic + gut-liver axis support | Complementary: gut-liver axis + epigenetic hepatic support |
The livagen-ovagen combination represents the most thorough hepatic bioregulator research approach in the Khavinson system, with livagen providing deep epigenetic modulation of hepatocyte gene expression and ovagen addressing the gut-liver axis and dual-organ interactions that influence overall hepatic health during aging.
PrymaLab supplies Livagen 20mg as a high-purity research-grade liver bioregulator peptide verified at ≥98% purity by reverse-phase HPLC and identity-confirmed by mass spectrometry. Each batch ships with a unique lot number and Certificate of Analysis. Independent third-party testing ensures unbiased quality verification and full traceability for GLP-compliant hepatic and aging research.
Livagen is a synthetic tetrapeptide bioregulator (Lys-Glu-Asp-Ala, KEDA) developed by Professor Khavinson targeting hepatic tissue. It modulates gene expression in hepatocytes and hepatic stellate cells through chromatin remodeling. Research applications include liver aging, hepatic repair, fibrosis, and epigenetic rejuvenation in preclinical models.
Published preclinical research reports livagen peptide benefits including chromatin decondensation in aged hepatocyte nuclei (reversing epigenetic silencing), restored expression of metabolic enzymes (cytochrome P450, albumin synthesis), anti-fibrotic effects through hepatic stellate cell modulation, enhanced hepatocyte proliferative capacity, and upregulated antioxidant defense gene expression. All benefits are from preclinical research.
Livagen operates through chromatin remodeling and epigenetic gene expression modulation rather than receptor agonism, enzyme supplementation, or direct antioxidant activity. It targets the transcriptional programs governing liver function rather than supplementing individual metabolic pathways. Among Khavinson bioregulators, livagen provides direct hepatic epigenetic effects complementary to ovagen’s dual liver-GI bioregulation.
Published livagen dosage ranges include 10–200 nM for cell culture studies and 1–10 µg/kg for in vivo liver aging models. Dosing depends on experimental design, model system, and research objectives. This product is for preclinical research only and is not intended for therapeutic dosing.
Store lyophilized livagen at −20°C, desiccated and protected from light, for 24+ months stability. After reconstitution, store at 2–8°C and use within 2–4 weeks. Aliquot to avoid freeze-thaw cycles.
For Research Use Only. PrymaLab Livagen 20mg is intended exclusively for qualified preclinical research use. This product is not intended for human consumption, therapeutic use, veterinary treatment, or any application outside controlled research environments. Livagen has not been approved by the FDA or any equivalent regulatory authority for therapeutic use. All research applications described are from published preclinical and gerontological literature. Researchers are responsible for regulatory compliance.
| Weight | N/A |
|---|---|
| Dimensions | N/A |
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