Ovagen (EDL)
Ultra-short peptide bioregulator (Glu-Asp-Leu) studied for liver and gastrointestinal research, with documented sequence-specific bioactivity and cellular gene-expression modulation.
Sequence E-D-L MW ~375.4 Da PubChem 444128⚡ Executive Summary
Ovagen (EDL: Glu-Asp-Leu) is a research-grade ultra-short peptide associated with liver/GI bioregulation. Ultra-short peptides can penetrate cells and influence gene expression through chromatin/DNA interactions. EDL is structurally documented binding HIV-1 protease (Ki ≈ 50 µM), illustrating precise sequence-specific bioactivity. Research use only — not FDA approved.
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01 Overview 02 Properties 03 Mechanism 04 Evidence 05 Handling 06 Comparison 📋Overview
🧬 What is Ovagen?
Ovagen is the research-market name for the tripeptide Glu-Asp-Leu (EDL), a member of the “peptide bioregulator” family.
These very short peptides (2–7 amino acids) are studied for organ-directed gene-expression effects, with Ovagen positioned for liver and GI research.
🎯 Key Features
- 🔬 Ultra-short — only 3 amino acids
- 🫁 Liver/GI focus — tissue-biased effects
- 🧬 Gene regulatory — chromatin interactions
What is a bioregulator? A very short peptide shown to enter cells and influence gene expression with tissue-selective effects. They can translocate to nuclei, bind DNA/histones, and remodel chromatin — a regulatory action, not stimulant.
⚠️Naming note: “Ovagen” refers to the EDL tripeptide in research contexts. It is distinct from similarly named FSH-based fertility products in agriculture/medicine.
🔬Entity Properties
| Aliases | Ovagen, EDL, Glutamyl-aspartyl-leucine |
|---|---|
| Sequence | Glu-Asp-Leu (E-D-L) |
| Length | 3 amino acids (tripeptide) |
| Molecular Formula | C₁₅H₂₅N₃O₈ |
| Molecular Weight | ~375.4 Da |
| PubChem CID | 444128 |
| Family | Ultra-short peptide bioregulator; epigenetic/chromatin modulation |
| Diluent(s) | Sterile water for injection or bacteriostatic water |
| Concentration | 20 mg + 3 mL = ~6.7 mg/mL (example) |
| Storage (dry) | ≤ −20°C, cool, dry, light-protected; stable long-term |
| Storage (solution) | 2–8°C short-term; avoid freeze-thaw; aliquot if needed |
Mechanism of Action
🧠 How do bioregulator peptides work?
Ultra-short peptides work through a regulatory mechanism distinct from receptor agonism. They are transported into cells, reach the nucleus, and modulate chromatin/DNA interactions that change gene expression.
This action often shows greater impact in older systems where chromatin is more condensed — the “de-heterochromatinization” effect that restores transcriptional capacity.
🚪Cellular Entry
Uptake via peptide transporters (PEPT1/2, LAT family) to reach intracellular compartments including nucleus
🧬Chromatin Binding
Bind DNA/histones and remodel heterochromatin, opening compacted aging-associated regions
📈Gene Expression
Up- or down-regulate specific genes involved in cellular maintenance, stress response, differentiation
🔬EDL-specific evidence: The EDL tripeptide is crystallographically resolved binding HIV-1 protease active site (Ki ≈ 50 µM). While not an antiviral drug, this demonstrates sequence-specific bioactivity — a rare property for such a small peptide.
📊Research Evidence
📚 Evidence Landscape
Direct peer-reviewed data on “Ovagen-branded” interventions are limited. However, the evidence base includes:
- ✓ EDL structural data: Crystallographic resolution in HIV-1 protease active site; Ki ≈ 50 µM enzyme inhibition
- ✓ Class evidence: Ultra-short peptides shown to penetrate cells, bind chromatin, modulate gene expression
- ✓ Related peptides: Livagen (KEDA) shows liver-specific effects in hepatocyte and GI enzyme studies
🫁 Liver/GI Related Findings
- 📈 Livagen (KEDA): Increased protein synthesis in old rat hepatocytes
- 🔄 GI enzymes: Age-dependent modulation of digestive enzyme activity
- 👴 Age bias: Strongest effects in older animals/systems
🧬 Epigenetic Evidence
- 🔓 Chromatin remodeling: De-heterochromatinization in elderly human lymphocytes
- 📈 Gene restoration: Reactivation of silenced loci in aged cells
- 🧪 Multiple peptides: AEDG, KEDA, others show similar mechanisms
Limitations: EDL-specific clinical trials are lacking. The weight of evidence supports plausibility that an EDL-based agent can produce transcriptional normalization in liver/GI relevant pathways, with strongest signals in aging models.
🧪Research Handling
📘Research use only. The following is educational guidance for laboratory contexts — not medical advice. Ultra-short peptides often show cumulative effects tied to chromatin remodeling, not immediate stimulation.
1Plan Objectives
Define outcome variables (hepatocyte assays, inflammatory readouts). Decide exposure window (10–30 days).
2Reconstitute
20 mg + 3 mL sterile diluent = ~6.7 mg/mL. Add slowly, swirl gently. Label concentration/date.
3Store Properly
Lyophilized: ≤ −20°C, dry, dark. Solutions: 2–8°C short-term; aliquot to avoid freeze-thaw.
4Dosing Pattern
Front-loaded cycles (daily × 10–20 days) for transcriptional reset, then off-period for observation.
5Age Context
Expect larger deltas in older models — design statistical power accordingly.
6Document & Report
Capture pre/post baselines. Effects may be lagged as chromatin state equilibrates.
⚖️Comparison
Ovagen (EDL) sits among ultra-short bioregulator peptides. Choice depends on whether your research focus is liver/GI targeted (EDL/KEDA) or systemic aging/chromatin (AEDG).
Ovagen
EDL (Glu-Asp-Leu) 🫁 Liver/GI • Structural DataDocumented enzyme binding (HIV-1 protease, Ki ≈ 50 µM). Liver/GI positioning extrapolated from bioregulator class. Sequence-specific bioactivity proven.
Livagen
KEDA (Lys-Glu-Asp-Ala) 🫁 Liver • Most Preclinical DataLiver-centric data: Increased protein synthesis in old hepatocytes; age-modulated GI enzyme effects. Best-documented for hepatic outcomes.
Epitalon
AEDG (Ala-Glu-Asp-Gly) 🧬 Systemic • Most StudiedGlobal geroprotective: Gene-expression changes across tissues (pineal/brain/retina). Reference compound for ultra-short peptide epigenetics.
💡Key insight: All three share the same mechanistic class (transporter uptake, chromatin/DNA interaction, gene modulation) but differ in tissue emphasis and data availability.
❓FAQ
What is Ovagen? The research-market name for the ultra-short tripeptide Glu-Asp-Leu (EDL), grouped with “peptide bioregulators” studied for cellular entry, chromatin interactions, and gene-expression effects — positioned for liver/GI research. How does Ovagen work? Ultra-short peptides are transported into cells, reach the nucleus, and modulate chromatin/DNA interactions that change gene expression. This is a regulatory action (not stimulant) that often shows greater impact in older systems where chromatin is more condensed. Is there liver-specific evidence? Direct EDL/Ovagen liver trials are sparse. However, closely related short peptides show liver/GI effects — Livagen (KEDA) increased hepatocyte protein synthesis in old rats and modulated intestinal enzyme activity with age-dependence. Does EDL fight viruses? No clinical antiviral claim is supported. EDL inhibits HIV-1 protease in vitro (Ki ≈ 50 µM) and is crystallized in the protease active site — this shows sequence-specific bioactivity but does NOT translate to proven antiviral efficacy. How should it be stored? Lyophilized: ≤ −20°C, cool, dry, light-protected. After reconstitution: 2–8°C short-term; avoid repeated freeze-thaw; aliquot if the study extends beyond days. These are general peptide best practices. Is this medical advice? No. All information is educational and intended for research-use planning. Ovagen/EDL is not an FDA-approved drug for any indication; any human use should be evaluated by qualified professionals and within applicable laws. ✅Bottom line: Ultra-short peptides like EDL (Ovagen) are best understood as regulators — tools to nudge gene expression and tissue programs — rather than brute-force stimulants. Build your protocol to detect gradual, regulatory changes, particularly in models of aging or post-stress recovery. EDL’s crystallographic target engagement confirms sequence-specific bioactivity for this minimal tripeptide.