Bronchogen — EU research guide.
Bronchogen is a synthetic tetrapeptide (Ala-Glu-Asp-Leu) from the Khavinson short peptide bioregulator series — the same research family as Epitalon, Vilon, Thymalin, Cortagen and Crystagen, which PeptideCompare already tracks. It is proposed to act on bronchopulmonary tissue, theoretically by influencing gene expression patterns specific to lung epithelial cells.
What is Bronchogen?
Bronchogen is a synthetic tetrapeptide (Ala-Glu-Asp-Leu) from the Khavinson short peptide bioregulator series — the same research family as Epitalon, Vilon, Thymalin, Cortagen and Crystagen, which PeptideCompare already tracks. It is proposed to act on bronchopulmonary tissue, theoretically by influencing gene expression patterns specific to lung epithelial cells.
What does the research show?
Published research comes almost entirely from Russian and Eastern European laboratories associated with the original Khavinson research group, reporting reduced airway inflammation and improved airway tissue parameters in a rat model of obstructive lung disease, and altered gene expression in cultured human bronchial epithelial cells; no human study of Bronchogen itself could be verified. No large-scale, independently replicated randomized controlled trials have been published in mainstream Western journals as of mid-2026.
EU legal status
Not approved as a medicine anywhere in the EU. A small number of specialist research vendors sell it as a peptide bioregulator for laboratory research only.
Molecular information
Pharmacokinetics
Potency retained over time
Each line is one storage condition: it starts at 100% and declines as potency is lost. Above the dotted 80% line the material is considered reliable — hover the chart for exact values.
⚠ Estimates modelled per component from molecular properties (chain length, cyclisation, oxidation- and deamidation-sensitive residues, light sensitivity). Indicative only — not lab-measured per batch.
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References
- Rat COPD model (NO2 exposure) with one month of tetrapeptide treatment; reports reversal of airway tissue remodelling. Animal data from a Russian group, no human component, and no independent replication was found. Kuzubova NA, Lebedeva ES, Dvorakovskaya IV, Surkova EA, Platonova IS, Titova ON. Modulating effect of peptide therapy on the morphofunctional state of bronchial epithelium in rats with obstructive lung pathology. Bull Exp Biol Med. 2015;159(5):685-688. DOIPubMed 26468022
- Human bronchial epithelial cell cultures treated with the tetrapeptide, with gene-expression and DNA-binding measurements. Khavinson, originator of the peptide series, is a co-author; in vitro only, and the sequence is written Ala-Asp-Glu-Leu here. Khavinson VKh, Tendler SM, Vanyushin BF, Kasyanenko NA, Kvetnoy IM, Linkova NS, Ashapkin VV, Polyakova VO, Basharina VS, Bernadotte A. Peptide regulation of gene expression and protein synthesis in bronchial epithelium. Lung. 2014;192(5):781-791. DOI
- Cell-free calorimetry showing a 3.1 degrees C rise in DNA melting temperature. Supports the idea that the peptide binds DNA, but says nothing about effects in living tissue or people. Monaselidze JR, Khavinson VKh, Gorgoshidze MZ, Khachidze DG, Lomidze EM, Jokhadze TA, Lezhava TA. Effect of the peptide bronchogen (Ala-Asp-Glu-Leu) on DNA thermostability. Bull Exp Biol Med. 2011;150(3):375-377. DOIPubMed 21240358