Bronchogen
A Khavinson tetrapeptide from bronchial tissue — proposed to support respiratory epithelium function in chronic obstructive airway disease; evidence is preliminary and Russian-language.
One of the Khavinson short-chain bioregulators (Ala-Glu-Asp-Leu), derived from bronchial mucosal extract and proposed to support epithelial regeneration and ciliary function in aging lung tissue and in chronic obstructive pulmonary disease models.
Mechanism of action
Proposed to act on bronchial epithelial cells via promoter binding to upregulate expression of genes supporting ciliary function and epithelial repair. Khavinson-group animal studies report reduced inflammation and improved mucociliary clearance in experimental COPD models.
Primary uses
- Investigational adjunct in chronic obstructive pulmonary disease (Russian literature)
- Research into respiratory aging
Typical dosing
Russian supplement protocols typically use 10 mg oral capsules once daily for 10–20 days.
Educational information, not medical advice. The doses on this page come from approved labels, published studies and, where no study exists, amounts reported by users. None is a recommendation for you. An unapproved compound has no established safe or effective human dose, and products sold for “research use only” are not made or tested for people. Talk to a doctor before acting on anything on this site, including before you start, stop or change any medicine or dose. Full medical disclaimer.
Regulatory status
Not FDA-approved. Marketed in Russia as a bioregulator supplement.
Status as of this entry's last review, October 4, 2026. Approvals, compounding rules and sport rules change; the regulatory tracker is checked more often.
What the studies show
Bronchogen is the tetrapeptide Ala-Glu-Asp-Leu (AEDL) from the Russian short-peptide programme. Its published work is one DNA-binding study and a series of plant studies in tobacco; none has tested it in people.
In Vitro · 2011
Binding to DNA
Microcalorimetry showed bronchogen raising the thermal stability of DNA and binding both strands, mainly at the bases, without preferring A-T or G-C pairs. The paper writes the sequence as Ala-Asp-Glu-Leu.
Plant · 2022
Tobacco roots under salt stress
AEDL lengthened tobacco roots under salinity through a mechanism involving expansin genes, which loosen the cell wall in the elongation zone.
Plant · 2024
With glutathione
AEDL and glutathione stimulated root development in tobacco, and the authors propose a scheme for how the two regulate redox balance in the root's stem-cell niche.
Plant · 2025
Metabolism and autophagy
At 10^-7 M, AEDL stimulated tobacco shoot and root development, which the authors attribute to activated metabolism and autophagy in root cells.
References
- [review] Khavinson VK, Malinin VV. "Gerontological aspects of genome peptide regulation." Karger AG, Basel, 2005.
- [pubmed] Khavinson VKh, et al. "[Peptide bioregulators: the new class of geroprotectors. Communication 1. Results of experimental studies]." Adv Gerontol, 2012;25(4):696-708. PMID: 23734519.
- [pubmed] Monaselidze JR, et al. "Effect of the peptide bronchogen (Ala-Asp-Glu-Leu) on DNA thermostability." Bull Exp Biol Med, 2011;150(3):375-7. PMID: 21240358.
- [pubmed] Fedoreyeva LI, et al. "Elongating Effect of the Peptide AEDL on the Root of Nicotiana tabacum under Salinity." Plants (Basel), 2022;11(10). PMID: 35631778.
- [pubmed] Kononenko NV, et al. "Peptide AEDL and Glutathione Stimulates Root Development Nicotiana tabacum." Int J Mol Sci, 2024;26(1). PMID: 39796141.
- [pubmed] Lazareva EM, et al. "Peptide AEDL Activates Metabolism and Autophagy in Root Cells of Nicotiana tabacum." Int J Mol Sci, 2025;26(22). PMID: 41303518.
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Guides & tools
This entry is for educational purposes only and does not constitute medical advice. Dosing information reflects published regulatory or research data and is not a recommendation. Many compounds described here are not approved for human use in the United States. Consult a licensed medical professional before considering any peptide therapy.