What is not known about Bronchogen?

The residue order is not settled. Papers co-authored by the same senior author print both Ala-Asp-Glu-Leu and Ala-Glu-Asp-Leu, and because the two are anagrams no mass, formula or purity measurement can distinguish them. This entry prints ADEL because it appears in a paper title and in a second paper's methods, not because the conflict has been resolved. No human has been studied. There is no trial, no case series and no case report for this compound in the indexed literature, in any language. No pharmacokinetic data exists, so it is not known whether the intact tetrapeptide survives any route of administration or reaches airway tissue. The Lung paper states the peptide was effective in models of bacterial lung inflammation, fibrosis and toxic lung damage. Those studies were not located in the searches run here and could not be read or assessed. It is not established which extract, if an

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bioregulator

Bronchogen

Also known as: ADEL, AEDL, Ala-Asp-Glu-Leu, Ala-Glu-Asp-Leu

Animal draft

A synthetic tetrapeptide from the Khavinson cytogen series, assigned to bronchial epithelium and proposed as a geroprotector for the airway. Its literature is the smallest of any bioregulator in this codex — seven PubMed records mention it in title or abstract — and it carries an unresolved problem of identity: the same senior author's papers print the residue order two different ways, Ala-Asp-Glu-Leu and Ala-Glu-Asp-Leu. The two are anagrams, so they share a formula and a mass and no purity assay can tell them apart. There is no human data of any kind.

Sequence

ADEL

Ala-Asp-Glu-Leu · 4 residues · 446.46 Da (computed)

Contains no lysine.

single source C18H30N4O9 446.50 Da (published)

Sequence source: PMID 21240358 title: 'Effect of the peptide bronchogen (Ala-Asp-Glu-Leu) on DNA thermostability'; same order in PMID 25015171, which writes 'Tetrapeptide Ala-Asp-Glu-Leu (ADEL)'. PubChem CID 11690869 carries the name and the matching formula C18H30N4O9. CONFLICT: PMIDs 22808515 and 22117547 print Ala-Glu-Asp-Leu (AEDL). The gate cannot arbitrate — the orders are anagrams.

Khavinson lineage

Bioregulator context

Target tissue: bronchial epithelium (respiratory)

That a four-residue peptide corresponding to bronchial tissue can restore the differentiation and barrier function of ageing or damaged bronchial epithelium, and that it does so by binding DNA in the major groove and switching on the genes that control airway-cell identity.

Proposed to enter the nucleus and bind DNA at the N7 position of guanine in the major groove, thereby regulating the transcription factors NKX2-1, SCGB1A1, SCGB3A2, FOXA1 and FOXA2 that specify bronchial epithelial differentiation. The supporting work is spectrophotometry, viscometry and circular dichroism on isolated DNA, plus real-time PCR in embryonic bronchial cell cultures.

Claimed vs established

Mechanism

Claimed

Restores the structure and function of bronchial epithelium, protects against chronic obstructive lung pathology, and acts as a geroprotector for airway tissue by directly regulating gene expression.

Actually established

In cultured human embryonic bronchial epithelium the peptide changed levels of Ki67, Mcl-1, p53, CD79 and NOS-3 and altered expression of several differentiation genes, most strongly in late-passage cultures. Biophysical work shows it binds isolated DNA and raises its melting temperature. What is not established is that any of this happens in a living airway: the binding is described in the same papers as strong but occasional and not base-specific, which is closer to a general polyanion interaction than to targeted regulation.

Honest appraisal

How good is the evidence

Animal 0 human RCTs · 0 human trials · 1 animal

This is a sparse entry and it should be read as one. PubMed returned 12 records for the name on 2026-08-06 and only 7 mention it in title or abstract; the rest are unrelated papers about bronchogenic cysts. There is no human study, no trial of any kind, and no pharmacokinetic work. The single whole-organism result is a rat model of NO2-induced chronic obstructive lung disease in which a month of the tetrapeptide is reported to have reversed goblet-cell hyperplasia, squamous metaplasia and emphysematous change and raised secretory IgA. Everything else is cell culture and DNA biophysics. Three of the seven papers list the compound's developer as an author.

Where this evidence comes from

Khavinson is an author on the DNA calorimetry paper, the Lung gene-expression paper, the differentiation-factor paper and the nuclear-penetration paper. The rat COPD study comes from the Research Institute of Pulmonology at Pavlov First St Petersburg State Medical University with no Khavinson author, which makes it the only arguably independent work — though it is in the same city and the same journal as most of the rest, and material supply was not checked.

What is said vs what was shown

Claims, one at a time

Each claim carries its own evidence tier. A compound is never simply "well studied" — some of its claims may be, others not at all.

Claim	Verdict	Evidence	Basis
Reverses the airway damage of chronic obstructive pulmonary disease	mixed	Animal	In rats exposed to nitrogen dioxide for 60 days, a month of the tetrapeptide is reported to have eliminated goblet-cell hyperplasia, squamous metaplasia, lymphocytic infiltration and emphysema, restored ciliated cells, and raised secretory IgA. The abstract gives no animal counts, no control-group description, no effect sizes and no statistics — the entire result is stated qualitatively. An NO2 exposure model reproduces some features of human COPD and not the smoking-driven pathology that defines it, and nobody has repeated the experiment.
Regulates the genes that control bronchial epithelial differentiation	mixed	In vitro	In human embryonic bronchoepithelial cultures the peptide altered NKX2-1, SCGB1A1, SCGB3A2, FOXA1 and FOXA2 expression and raised Ki67 and Mcl-1 most strongly in late-passage cultures; a separate paper reports the same direction for CXCL12 and Hoxa3. Both are developer-authored, both are embryonic cell lines rather than adult airway, neither reports statistics in its abstract, and the second paper prints the residue order the other way round — so it is not certain the two studies tested the same molecule.
Binds DNA directly and regulates transcription from the major groove	mixed	In vitro	Differential scanning microcalorimetry shows the peptide raises the melting temperature of calf-thymus and mouse-liver DNA by 3.1 degrees within a narrow molar-ratio window, and fluorescence quenching suggests preference for CTG-containing sequences. But the calorimetry paper concludes the binding is neither AT- nor GC-specific and describes it as 'strong and occasional' with both strands, which is not the profile of a sequence-specific regulator. No experiment links a binding event to a measured transcriptional change.

Primary sources

The studies themselves

Study	Design	Subjects	Quality
Modulating Effect of Peptide Therapy on the Morphofunctional State of Bronchial Epithelium in Rats with Obstructive Lung Pathology Kuzubova NA, Lebedeva ES, Dvorakovskaya IV, Surkova EA, Platonova IS, Titova ON · Bulletin of experimental biology and medicine · 2015 PMID 26468022	animal_uncontrolled / rat	— Rats with chronic obstructive pulmonary disease modelled by 60-day intermittent nitrogen-dioxide exposure, then given the tetrapeptide for one month	Animal risk of bias: high
Peptide regulation of gene expression and protein synthesis in bronchial epithelium Khavinson VKh, Tendler SM, Vanyushin BF, Kasyanenko NA, Kvetnoy IM, Linkova NS, Ashapkin VV, Polyakova VO, Basharina VS, Bernadotte A · Lung · 2014 PMID 25015171	in_vitro / cell_culture	— Human embryonic bronchoepithelial cell cultures at passages 1, 7 and 14; plus spectrophotometry, viscometry and circular dichroism of the peptide with isolated DNA	In vitro risk of bias: high authored by the developer
Peptides tissue-specifically stimulate cell differentiation during their aging Khavinson VKh, Linkova NS, Polyakova VO, Kheifets OV, Tarnovskaya SI, Kvetnoy IM · Bulletin of experimental biology and medicine · 2012 PMID 22808515	in_vitro / cell_culture	— Human embryonic pancreatic and bronchial cell cultures and human prostatic fibroblasts, early and late passage, exposed to pancragen, bronchogen or vesugen	In vitro risk of bias: high authored by the developer
Effect of the peptide bronchogen (Ala-Asp-Glu-Leu) on DNA thermostability Monaselidze JR, Khavinson VKh, Gorgoshidze MZ, Khachidze DG, Lomidze EM, Jokhadze TA, Lezhava TA · Bulletin of experimental biology and medicine · 2011 PMID 21240358	in_vitro / mixed	— Purified DNA from calf thymus and mouse liver, melted on a differential scanning microcalorimeter across a range of peptide-to-base-pair molar ratios	Mechanistic risk of bias: high authored by the developer
Penetration of short fluorescence-labeled peptides into the nucleus in HeLa cells and in vitro specific interaction of the peptides with deoxyribooligonucleotides and DNA Fedoreyeva LI, Kireev II, Khavinson VKh, Vanyushin BF · Biochemistry. Biokhimiia · 2011 PMID 22117547	in_vitro / cell_culture	— HeLa cells incubated with FITC-labelled short peptides, plus fluorescence-quenching assays of unlabelled peptides against labelled deoxyribooligonucleotides and DNA	In vitro risk of bias: high authored by the developer

What we do not know

The residue order is not settled. Papers co-authored by the same senior author print both Ala-Asp-Glu-Leu and Ala-Glu-Asp-Leu, and because the two are anagrams no mass, formula or purity measurement can distinguish them. This entry prints ADEL because it appears in a paper title and in a second paper's methods, not because the conflict has been resolved.
No human has been studied. There is no trial, no case series and no case report for this compound in the indexed literature, in any language.
No pharmacokinetic data exists, so it is not known whether the intact tetrapeptide survives any route of administration or reaches airway tissue.
The Lung paper states the peptide was effective in models of bacterial lung inflammation, fibrosis and toxic lung damage. Those studies were not located in the searches run here and could not be read or assessed.
It is not established which extract, if any, this peptide is the synthetic counterpart of; a second peptide, Chonluten, is also assigned to bronchial epithelium in the same body of work.
The single animal study describes no comparison group, no animal counts and no statistics, so its effect size is unknown even in direction-of-magnitude terms.
No dose is recorded on any study on this page, because no full text has been read.

Discussion, not evidence

What people actually report

Read this differently from everything above. Public posts from Reddit and X. Nothing here has been verified beyond confirming the post exists, and community reports are the weakest tier this site recognises. Doses discussed in these threads are deliberately not reproduced.

comparison with Chonluten
interest related to pulmonary fibrosis

What people keep asking

How does Bronchogen compare with Chonluten?
Has anyone with pulmonary fibrosis tried Bronchogen?