Bronchogen

updated

Bronchogen is a synthetic tetrapeptide from the Khavinson group of Russian short-peptide bioregulators, sold for lung function support and less airway inflammation. No controlled human study exists: the record is cell cultures, rat tissue explants and one rat model of chemically induced lung injury, and no study in any species measured lung function. The group's own papers print two residue orders, Ala-Glu-Asp-Leu and Ala-Asp-Glu-Leu, so a vial labeled Bronchogen cannot be assumed to match the peptide in any given paper.

Synthetic tetrapeptide bioregulator

  • PubChem lists Bronchogen as CID 11690869, C18H30N4O9, molecular weight 446.5, CAS 857267-12-0, with a name that reads Ala-Glu-Asp-Leu.
  • The group's papers print two sequences: Ala-Asp-Glu-Leu in a 2014 paper in Lung and a 2011 paper, and Ala-Glu-Asp-Leu in three other papers, in PubChem and in the group's 2021 and 2022 tables.
  • In human embryonic bronchial cell cultures the peptide changed levels of Ki67, Mcl-1, p53, CD79 and NOS-3 and bound DNA in the major groove; the work measured gene and protein expression, not lung function or inflammation.
  • In rats exposed to nitrogen dioxide for 60 days to model COPD and given the peptide for 1 month, the abstract reports eliminated bronchial remodeling and a normalized lavage cytokine profile. It gives no dose, route or group size.
  • A PubMed search on 10 October 2026 for bronchogen restricted to clinical trial or randomized controlled trial publication types returned 0 records.
  • An openFDA Drugs@FDA query and a DailyMed search on 10 October 2026 found no FDA record for Bronchogen.

What is Bronchogen, and is it an approved drug?

Bronchogen is a synthetic tetrapeptide from the Khavinson group, listed in PubChem as Ala-Glu-Asp-Leu, though some of the group's papers print Ala-Asp-Glu-Leu. An openFDA Drugs@FDA query and a DailyMed search on 10 October 2026 found no FDA record for it, so it is not an FDA-approved drug or a labeled product.

PubChem lists Bronchogen as CID 11690869, C18H30N4O9, molecular weight 446.5, CAS 857267-12-0, with a systematic name that reads Ala-Glu-Asp-Leu (alanine, glutamic acid, aspartic acid, leucine). A PubChem name search for the hyphenated strings Ala-Glu-Asp-Leu and Ala-Asp-Glu-Leu returned no record, so the CID is reached through the trade name only.

The group's own papers print two residue orders. A 2014 paper in Lung by Khavinson and colleagues and a 2011 DNA-melting paper call the peptide Ala-Asp-Glu-Leu (ADEL). A 2012 differentiation paper, a 2011 DNA-binding paper and a 2017 tobacco-cell paper call it Ala-Glu-Asp-Leu (AEDL), which matches PubChem, and the group's 2021 systematic review and 2022 table of ultrashort peptides pair the name with AEDL. Glu and Asp swapped is a different peptide, so a vial labeled Bronchogen cannot be assumed to match the sequence behind any given paper. This page gives Ala-Glu-Asp-Leu, as PubChem does, and names the order a study used where its record states it.

On 10 October 2026 an openFDA Drugs@FDA query for bronchogen as a brand or generic name returned no matches, and a DailyMed search for the drug name bronchogen returned no label. No FDA record for Bronchogen was found in these two sources, so it is not an FDA-approved drug or a labeled product. That says nothing about other regulators.

PubChem: Bronchogen identity

Chemical identity record

National Library of Medicine. PubChem compound record CID 11690869.

PubChem lists Bronchogen as CID 11690869, C18H30N4O9, molecular weight 446.5, CAS 857267-12-0, with a systematic name that reads Ala-Glu-Asp-Leu (alanine, glutamic acid, aspartic acid, leucine). A PubChem name search for the hyphenated strings Ala-Glu-Asp-Leu and Ala-Asp-Glu-Leu returned no record, so the CID is reached through the trade name only.

Participants / model
Chemical identity, not a clinical population
Treatment
Defined synthetic peptide
Follow-up
Not applicable
Study design
NLM chemical record
Funding
not stated in the source

A defined tetrapeptide record. The group's own papers print a second residue order, so the record does not settle which sequence a given vial or paper used.

Read the original source
2014 Lung paper: bronchial cultures, DNA binding, sequence written ADEL

Cell study

Khavinson VKh et al. Lung. 2014;192(5):781-91. PMID 25015171.

In human embryonic bronchoepithelial cultures at passages 1, 7 and 14, the peptide (written Ala-Asp-Glu-Leu, ADEL, in this paper) changed levels of Ki67, Mcl-1, p53, CD79 and NOS-3, with the strongest proliferation effect in old late-passage cultures, and changed expression of NKX2-1, SCGB1A1, SCGB3A2, FOXA1, FOXA2, MUC4, MUC5AC and SFTPA1. By spectrophotometry, viscometry and circular dichroism it bound DNA in the major groove at guanine N7. The group's papers disagree on the residue order: this 2014 paper and a 2011 DNA-melting paper print Ala-Asp-Glu-Leu, while a 2012 differentiation paper, a 2011 DNA-binding paper and a 2017 tobacco-cell paper print Ala-Glu-Asp-Leu (AEDL), which matches PubChem. The group's 2021 systematic review lists AEDL, Bronchogen, and its 2022 table of ultrashort peptides lists Bronchogen (AEDL).

Participants / model
Human embryonic bronchoepithelial cell cultures at passages 1, 7 and 14
Treatment
Peptide in culture medium
Follow-up
not stated in the source
Study design
Cell-culture protein, gene expression and DNA-binding study
Funding
not stated in the source

Cultured embryonic cell work. It measures gene and protein expression, not lung function and not inflammation. Glu and Asp swapped is a different peptide, so a vendor vial cannot be assumed to match the sequence behind any given paper.

Read the original source
FDA records: no match for Bronchogen

Regulatory record

U.S. Food and Drug Administration, openFDA Drugs@FDA query for bronchogen as brand name, and DailyMed (U.S. National Library of Medicine) search for the drug name bronchogen, both run 10 October 2026.

On 10 October 2026 an openFDA Drugs@FDA query for bronchogen as brand or generic name returned no matches, and a DailyMed search for the drug name bronchogen returned no label. No FDA record for Bronchogen was found in these two sources, so it is not an FDA-approved drug or a labeled product.

Participants / model
Not a clinical population
Treatment
Not applicable
Follow-up
Queries run on 10 October 2026
Study design
Official FDA and NLM record searches
Funding
not stated in the source

These sources say nothing about other regulators.

Read the original source

What did the cell and rat studies find?

Bronchogen changed gene and protein expression in cultured human embryonic bronchial cells, stimulated growth of rat lung explants, and in rats with nitrogen dioxide lung injury was reported to reduce bronchial remodeling and normalize lavage cytokines. No study in any species measured lung function.

In human embryonic bronchoepithelial cultures at passages 1, 7 and 14, the 2014 Lung paper, which writes the peptide as ADEL, found changed levels of Ki67, Mcl-1, p53, CD79 and NOS-3, with the strongest proliferation effect in old late-passage cultures, and changed expression of NKX2-1, SCGB1A1, SCGB3A2, FOXA1, FOXA2, MUC4, MUC5AC and SFTPA1. By spectrophotometry, viscometry and circular dichroism it bound DNA in the major groove at guanine N7. This is cultured embryonic cell work. It measures gene and protein expression, not lung function and not inflammation.

A 2012 differentiation paper, which writes the peptide as Ala-Glu-Asp-Leu, found that expression of CXCL12 and Hoxa3 fell in late-passage (aging) cultures of human embryonic bronchial cells and that bronchogen raised expression of those markers in bronchial epithelial cells, more strongly in aged cultures. The same paper tested pancragen and vesugen in other cell types.

A 2006 Russian-language report used synthetic cardiogen, bronchogen, prostamax and pancragen on organotypic explants of heart, lung, prostate and pancreas from 3-week-old and 18-month-old rats. At 0.05 ng/ml each peptide stimulated growth in its matching tissue culture compared with control explants in all groups. The abstract reports no cell, cytokine or function endpoint beyond explant growth.

The only animal model of airway disease that names Bronchogen used rats exposed intermittently to nitrogen dioxide for 60 days to model chronic obstructive pulmonary disease. The rats were given the tetrapeptide for 1 month; the abstract does not say whether dosing began after the exposure or during it. It reports that the peptide eliminated bronchial epithelial remodeling (goblet cell hyperplasia, squamous metaplasia, lymphocytic infiltration, emphysema) and restored ciliated cells, raised secretory IgA in the lavage, and normalized cell composition and the proinflammatory cytokine profile in the bronchoalveolar space, which the authors read as reduced neutrophilic inflammation. A 2017 Russian-language paper from the same pulmonology institute used the same 60-day model and added a rise in surfactant protein B. The authors are at the pulmonology research institute of Pavlov First St. Petersburg State Medical University, and the abstracts give no dose, route, group size or statistics.

2014 Lung paper: bronchial cultures, DNA binding, sequence written ADEL

Cell study

Khavinson VKh et al. Lung. 2014;192(5):781-91. PMID 25015171.

In human embryonic bronchoepithelial cultures at passages 1, 7 and 14, the peptide (written Ala-Asp-Glu-Leu, ADEL, in this paper) changed levels of Ki67, Mcl-1, p53, CD79 and NOS-3, with the strongest proliferation effect in old late-passage cultures, and changed expression of NKX2-1, SCGB1A1, SCGB3A2, FOXA1, FOXA2, MUC4, MUC5AC and SFTPA1. By spectrophotometry, viscometry and circular dichroism it bound DNA in the major groove at guanine N7. The group's papers disagree on the residue order: this 2014 paper and a 2011 DNA-melting paper print Ala-Asp-Glu-Leu, while a 2012 differentiation paper, a 2011 DNA-binding paper and a 2017 tobacco-cell paper print Ala-Glu-Asp-Leu (AEDL), which matches PubChem. The group's 2021 systematic review lists AEDL, Bronchogen, and its 2022 table of ultrashort peptides lists Bronchogen (AEDL).

Participants / model
Human embryonic bronchoepithelial cell cultures at passages 1, 7 and 14
Treatment
Peptide in culture medium
Follow-up
not stated in the source
Study design
Cell-culture protein, gene expression and DNA-binding study
Funding
not stated in the source

Cultured embryonic cell work. It measures gene and protein expression, not lung function and not inflammation. Glu and Asp swapped is a different peptide, so a vendor vial cannot be assumed to match the sequence behind any given paper.

Read the original source
2012 differentiation paper: CXCL12 and Hoxa3 in bronchial cells

Cell study

Khavinson VKh et al. Bull Exp Biol Med. 2012;153(1):148-51. PMID 22808515.

In human embryonic bronchial cell cultures, expression of CXCL12 and Hoxa3 fell in late-passage (aging) cultures, and bronchogen (Ala-Glu-Asp-Leu) raised expression of those markers in bronchial epithelial cells, more strongly in aged cultures. The same paper tested pancragen and vesugen in other cell types.

Participants / model
Human embryonic bronchial epithelial cultures
Treatment
Peptide in culture medium
Follow-up
not stated in the source
Study design
Cell-culture gene expression study
Funding
not stated in the source

Measures CXCL12 and Hoxa3 expression in cultured cells, not lung function.

Read the original source
2006 explant study: lung explants from young and aged rats

Cell study

Zakutskiĭ AN et al. Adv Gerontol. 2006;19:93-6. PMID 17152728.

A 2006 Russian-language report used synthetic cardiogen, bronchogen, prostamax and pancragen on organotypic explants of heart, lung, prostate and pancreas from 3-week-old and 18-month-old rats. At 0.05 ng/ml each peptide stimulated growth in its matching tissue culture compared with control explants in all groups. The abstract reports no cell, cytokine or function endpoint beyond explant growth.

Participants / model
Explants from young (3-week) and aged (18-month) rats
Treatment
Peptide in culture medium at 0.05 ng/ml
Follow-up
not stated in the source
Study design
Organotypic explant culture, Russian-language report
Funding
not stated in the source

Explant growth is not a lung function endpoint.

Read the original source
Rat nitrogen dioxide COPD model: 60-day exposure, 1 month of peptide

Animal study

Kuzubova NA et al. Bull Exp Biol Med. 2015;159(5):685-8. PMID 26468022.

Rats were exposed intermittently to nitrogen dioxide for 60 days to model chronic obstructive pulmonary disease and were given the tetrapeptide for 1 month; the abstract does not say whether dosing began after the exposure or during it. The abstract reports that it eliminated bronchial epithelial remodeling (goblet cell hyperplasia, squamous metaplasia, lymphocytic infiltration, emphysema) and restored ciliated cells, raised secretory IgA in the lavage, and normalized cell composition and the proinflammatory cytokine profile in the bronchoalveolar space, which the authors read as reduced neutrophilic inflammation. A 2017 Russian-language paper from the same pulmonology institute used the same 60-day model and added a rise in surfactant protein B. The authors are at the pulmonology research institute of Pavlov First St. Petersburg State Medical University.

Participants / model
Rats with nitrogen dioxide-induced COPD-like lung injury
Treatment
Tetrapeptide for 1 month; dose and route not stated in the abstract
Follow-up
60-day nitrogen dioxide exposure model; peptide for 1 month
Study design
Preclinical animal model of chemically induced lung injury
Funding
not stated in the source

The abstracts give no dose, route, group size or statistics. This is the evidence behind the less airway inflammation claim, and it is in rats with a chemically induced lung injury.

Read the original source

Has Bronchogen been tested in people?

No. A PubMed search on 10 October 2026 for bronchogen restricted to clinical trial or randomized controlled trial publication types returned 0 records. The searches found no human dose, no spirometry or other lung function measure in people, no human pharmacokinetics and no human safety data.

A PubMed search for bronchogen AND (patients OR children OR COPD OR asthma OR human) returned 9 records: 4 about the peptide (the rat COPD paper, its Russian-language companion, a HeLa and DNA-binding paper, and the differentiation-marker paper) and 5 older case reports of bronchogenic cysts or carcinoma that are unrelated to the peptide. A PubMed search for peptide bioregulator[tiab] AND (bronchial asthma OR bronchopulmonary OR COPD) AND patients[tiab] returned 0 records.

ClinicalTrials.gov returned 1 record for bronchogen, an airway gene expression test for lung cancer diagnosis that does not involve the peptide. Across these searches there is no human dose, no spirometry or any other lung function measure in people, no human pharmacokinetics and no human safety data for Bronchogen.

PubMed: no clinical trial, no human data

PubMed search record

PubMed searches run 10 October 2026: bronchogen restricted to clinical trial or randomized controlled trial publication types; bronchogen AND (patients OR children OR COPD OR asthma OR human); peptide bioregulator[tiab] AND (bronchial asthma OR bronchopulmonary OR COPD) AND patients[tiab]. ClinicalTrials.gov query for bronchogen, run the same day.

A PubMed search for bronchogen restricted to clinical trial or randomized controlled trial publication types returned 0 records. A search for bronchogen AND (patients OR children OR COPD OR asthma OR human) returned 9 records: 4 about the peptide (the rat COPD paper, its Russian-language companion, a HeLa and DNA-binding paper, and the differentiation-marker paper) and 5 older case reports of bronchogenic cysts or carcinoma unrelated to the peptide. A search for peptide bioregulator[tiab] AND (bronchial asthma OR bronchopulmonary OR COPD) AND patients[tiab] returned 0 records. ClinicalTrials.gov returned 1 record for bronchogen, an airway gene expression test for lung cancer diagnosis that does not involve the peptide. The searches found no human dose, no spirometry or other lung function measure in people, no human pharmacokinetics and no human safety data for Bronchogen.

Participants / model
Records reviewed, not a population
Treatment
Not applicable
Follow-up
Search run on 10 October 2026
Study design
Dated literature and registry search
Funding
not stated in the source

An absence finding as of 10 October 2026, not proof that no unpublished work exists.

Read the original source

Does Bronchogen support lung function or reduce airway inflammation?

Lung function support is untested, because no study measured lung function in any animal or person. Reduced airway inflammation is supported only as reduced neutrophilic inflammation and a normalized cytokine profile in the lungs of rats with nitrogen dioxide injury, in abstracts that give no dose or route.

Sellers promote Bronchogen for lung function support and less airway inflammation. The cell work shows changes in gene and protein expression in cultured human embryonic bronchial cells, which is not a functional benefit.

The inflammation claim traces to one rat model: nitrogen dioxide exposure for 60 days, then the peptide for 1 month, with reduced neutrophilic inflammation and a normalized lavage cytokine profile as the authors read it. It was run at one pulmonology institute, the abstracts give no dose, route, group size or statistics, and it is a chemically induced lung injury in rats, not a result in people.

Sellers also suggest using Chonluten with or instead of Bronchogen. No study of that combination or substitution was found.

Every Bronchogen result on this page is for the synthetic tetrapeptide. The developer's 2001 report uses cytogens for synthetic peptides and cytomedins for peptide complexes from tissue, and names Cortagen, Epithalon, Livagen and Vilon, not Bronchogen. No PubMed record describes a Cytomax or Cytogen lung product, so nothing on this page is cited to those product lines.

Rat nitrogen dioxide COPD model: 60-day exposure, 1 month of peptide

Animal study

Kuzubova NA et al. Bull Exp Biol Med. 2015;159(5):685-8. PMID 26468022.

Rats were exposed intermittently to nitrogen dioxide for 60 days to model chronic obstructive pulmonary disease and were given the tetrapeptide for 1 month; the abstract does not say whether dosing began after the exposure or during it. The abstract reports that it eliminated bronchial epithelial remodeling (goblet cell hyperplasia, squamous metaplasia, lymphocytic infiltration, emphysema) and restored ciliated cells, raised secretory IgA in the lavage, and normalized cell composition and the proinflammatory cytokine profile in the bronchoalveolar space, which the authors read as reduced neutrophilic inflammation. A 2017 Russian-language paper from the same pulmonology institute used the same 60-day model and added a rise in surfactant protein B. The authors are at the pulmonology research institute of Pavlov First St. Petersburg State Medical University.

Participants / model
Rats with nitrogen dioxide-induced COPD-like lung injury
Treatment
Tetrapeptide for 1 month; dose and route not stated in the abstract
Follow-up
60-day nitrogen dioxide exposure model; peptide for 1 month
Study design
Preclinical animal model of chemically induced lung injury
Funding
not stated in the source

The abstracts give no dose, route, group size or statistics. This is the evidence behind the less airway inflammation claim, and it is in rats with a chemically induced lung injury.

Read the original source
2014 Lung paper: bronchial cultures, DNA binding, sequence written ADEL

Cell study

Khavinson VKh et al. Lung. 2014;192(5):781-91. PMID 25015171.

In human embryonic bronchoepithelial cultures at passages 1, 7 and 14, the peptide (written Ala-Asp-Glu-Leu, ADEL, in this paper) changed levels of Ki67, Mcl-1, p53, CD79 and NOS-3, with the strongest proliferation effect in old late-passage cultures, and changed expression of NKX2-1, SCGB1A1, SCGB3A2, FOXA1, FOXA2, MUC4, MUC5AC and SFTPA1. By spectrophotometry, viscometry and circular dichroism it bound DNA in the major groove at guanine N7. The group's papers disagree on the residue order: this 2014 paper and a 2011 DNA-melting paper print Ala-Asp-Glu-Leu, while a 2012 differentiation paper, a 2011 DNA-binding paper and a 2017 tobacco-cell paper print Ala-Glu-Asp-Leu (AEDL), which matches PubChem. The group's 2021 systematic review lists AEDL, Bronchogen, and its 2022 table of ultrashort peptides lists Bronchogen (AEDL).

Participants / model
Human embryonic bronchoepithelial cell cultures at passages 1, 7 and 14
Treatment
Peptide in culture medium
Follow-up
not stated in the source
Study design
Cell-culture protein, gene expression and DNA-binding study
Funding
not stated in the source

Cultured embryonic cell work. It measures gene and protein expression, not lung function and not inflammation. Glu and Asp swapped is a different peptide, so a vendor vial cannot be assumed to match the sequence behind any given paper.

Read the original source
2001 report: synthetic peptides versus tissue peptide complexes

Cell study

Khavinson VK. Bull Exp Biol Med. 2001;132(2):807-8. PMID 11713572.

The developer's own 2001 report uses cytogens for synthetic peptides and cytomedins for peptide complexes from tissue, and says the synthetic peptides stimulated explants from the tissues whose cytomedins were used as the basis for chemical synthesis. It names Cortagen, Epithalon, Livagen and Vilon, not Bronchogen. A PubMed search for cytomax[tiab] OR cytomaxes[tiab] returned 2 records, a 1964 paper on a cytochrome C product and a 2007 sports-drink paper. A search for cytogen[tiab] OR cytogens[tiab] returned 37 records, of which 3 are Khavinson-group cytogens papers and 34 are unrelated by title, mostly radiolabeled antibody imaging reports using a company's Cytogen product names.

Participants / model
Rat tissue explants
Treatment
Synthetic peptides in organotypic culture
Follow-up
not stated in the source
Study design
Original preclinical report
Funding
not stated in the source

Every Bronchogen result on this page is for the synthetic tetrapeptide. None tests a tissue extract or a Cytomax or Cytogen retail product.

Read the original source
PubMed: no clinical trial, no human data

PubMed search record

PubMed searches run 10 October 2026: bronchogen restricted to clinical trial or randomized controlled trial publication types; bronchogen AND (patients OR children OR COPD OR asthma OR human); peptide bioregulator[tiab] AND (bronchial asthma OR bronchopulmonary OR COPD) AND patients[tiab]. ClinicalTrials.gov query for bronchogen, run the same day.

A PubMed search for bronchogen restricted to clinical trial or randomized controlled trial publication types returned 0 records. A search for bronchogen AND (patients OR children OR COPD OR asthma OR human) returned 9 records: 4 about the peptide (the rat COPD paper, its Russian-language companion, a HeLa and DNA-binding paper, and the differentiation-marker paper) and 5 older case reports of bronchogenic cysts or carcinoma unrelated to the peptide. A search for peptide bioregulator[tiab] AND (bronchial asthma OR bronchopulmonary OR COPD) AND patients[tiab] returned 0 records. ClinicalTrials.gov returned 1 record for bronchogen, an airway gene expression test for lung cancer diagnosis that does not involve the peptide. The searches found no human dose, no spirometry or other lung function measure in people, no human pharmacokinetics and no human safety data for Bronchogen.

Participants / model
Records reviewed, not a population
Treatment
Not applicable
Follow-up
Search run on 10 October 2026
Study design
Dated literature and registry search
Funding
not stated in the source

An absence finding as of 10 October 2026, not proof that no unpublished work exists.

Read the original source

How is Bronchogen thought to work?

In test-tube work the peptide bound DNA in the major groove at guanine N7, and in cultured human embryonic bronchial cells it changed expression of lung differentiation and mucin genes. How it would act in a living lung is not established, and no pharmacokinetic data exist.

The group's cell work describes a DNA-binding, gene-expression mechanism. By spectrophotometry, viscometry and circular dichroism the peptide bound DNA in the major groove at guanine N7. In human embryonic bronchial cultures it changed expression of NKX2-1, SCGB1A1, SCGB3A2, FOXA1, FOXA2, MUC4, MUC5AC and SFTPA1, and it raised CXCL12 and Hoxa3 expression, more strongly in aged cultures.

Whether any of this happens in a living airway is not shown. The rat lung injury study reports tissue structure, lavage cells, cytokines, secretory IgA and surfactant protein B, not mechanism. No human pharmacokinetics were found, and the rat abstracts give no dose or route, so exposure in any species is not described.

2014 Lung paper: bronchial cultures, DNA binding, sequence written ADEL

Cell study

Khavinson VKh et al. Lung. 2014;192(5):781-91. PMID 25015171.

In human embryonic bronchoepithelial cultures at passages 1, 7 and 14, the peptide (written Ala-Asp-Glu-Leu, ADEL, in this paper) changed levels of Ki67, Mcl-1, p53, CD79 and NOS-3, with the strongest proliferation effect in old late-passage cultures, and changed expression of NKX2-1, SCGB1A1, SCGB3A2, FOXA1, FOXA2, MUC4, MUC5AC and SFTPA1. By spectrophotometry, viscometry and circular dichroism it bound DNA in the major groove at guanine N7. The group's papers disagree on the residue order: this 2014 paper and a 2011 DNA-melting paper print Ala-Asp-Glu-Leu, while a 2012 differentiation paper, a 2011 DNA-binding paper and a 2017 tobacco-cell paper print Ala-Glu-Asp-Leu (AEDL), which matches PubChem. The group's 2021 systematic review lists AEDL, Bronchogen, and its 2022 table of ultrashort peptides lists Bronchogen (AEDL).

Participants / model
Human embryonic bronchoepithelial cell cultures at passages 1, 7 and 14
Treatment
Peptide in culture medium
Follow-up
not stated in the source
Study design
Cell-culture protein, gene expression and DNA-binding study
Funding
not stated in the source

Cultured embryonic cell work. It measures gene and protein expression, not lung function and not inflammation. Glu and Asp swapped is a different peptide, so a vendor vial cannot be assumed to match the sequence behind any given paper.

Read the original source
2012 differentiation paper: CXCL12 and Hoxa3 in bronchial cells

Cell study

Khavinson VKh et al. Bull Exp Biol Med. 2012;153(1):148-51. PMID 22808515.

In human embryonic bronchial cell cultures, expression of CXCL12 and Hoxa3 fell in late-passage (aging) cultures, and bronchogen (Ala-Glu-Asp-Leu) raised expression of those markers in bronchial epithelial cells, more strongly in aged cultures. The same paper tested pancragen and vesugen in other cell types.

Participants / model
Human embryonic bronchial epithelial cultures
Treatment
Peptide in culture medium
Follow-up
not stated in the source
Study design
Cell-culture gene expression study
Funding
not stated in the source

Measures CXCL12 and Hoxa3 expression in cultured cells, not lung function.

Read the original source
Rat nitrogen dioxide COPD model: 60-day exposure, 1 month of peptide

Animal study

Kuzubova NA et al. Bull Exp Biol Med. 2015;159(5):685-8. PMID 26468022.

Rats were exposed intermittently to nitrogen dioxide for 60 days to model chronic obstructive pulmonary disease and were given the tetrapeptide for 1 month; the abstract does not say whether dosing began after the exposure or during it. The abstract reports that it eliminated bronchial epithelial remodeling (goblet cell hyperplasia, squamous metaplasia, lymphocytic infiltration, emphysema) and restored ciliated cells, raised secretory IgA in the lavage, and normalized cell composition and the proinflammatory cytokine profile in the bronchoalveolar space, which the authors read as reduced neutrophilic inflammation. A 2017 Russian-language paper from the same pulmonology institute used the same 60-day model and added a rise in surfactant protein B. The authors are at the pulmonology research institute of Pavlov First St. Petersburg State Medical University.

Participants / model
Rats with nitrogen dioxide-induced COPD-like lung injury
Treatment
Tetrapeptide for 1 month; dose and route not stated in the abstract
Follow-up
60-day nitrogen dioxide exposure model; peptide for 1 month
Study design
Preclinical animal model of chemically induced lung injury
Funding
not stated in the source

The abstracts give no dose, route, group size or statistics. This is the evidence behind the less airway inflammation claim, and it is in rats with a chemically induced lung injury.

Read the original source

What is known about the safety of Bronchogen?

No human safety data exist for Bronchogen: the searches found no human dose, pharmacokinetics or safety outcome. The rat abstracts give no dose, route or group size, so animal safety is not described either, and the two printed sequences mean a vial may not match any studied peptide.

A PubMed search on 10 October 2026 found no human study of Bronchogen of any design, so there is no human dose, no human pharmacokinetics and no human safety outcome. The rat lung injury abstracts report tissue and lavage outcomes and give no dose, route, group size or statistics.

The group prints the sequence in two orders, Ala-Glu-Asp-Leu and Ala-Asp-Glu-Leu. Glu and Asp swapped is a different peptide, so a vial labeled Bronchogen cannot be assumed to match the sequence behind any given paper, and results for one order cannot be assumed to apply to the other.

PubMed: no clinical trial, no human data

PubMed search record

PubMed searches run 10 October 2026: bronchogen restricted to clinical trial or randomized controlled trial publication types; bronchogen AND (patients OR children OR COPD OR asthma OR human); peptide bioregulator[tiab] AND (bronchial asthma OR bronchopulmonary OR COPD) AND patients[tiab]. ClinicalTrials.gov query for bronchogen, run the same day.

A PubMed search for bronchogen restricted to clinical trial or randomized controlled trial publication types returned 0 records. A search for bronchogen AND (patients OR children OR COPD OR asthma OR human) returned 9 records: 4 about the peptide (the rat COPD paper, its Russian-language companion, a HeLa and DNA-binding paper, and the differentiation-marker paper) and 5 older case reports of bronchogenic cysts or carcinoma unrelated to the peptide. A search for peptide bioregulator[tiab] AND (bronchial asthma OR bronchopulmonary OR COPD) AND patients[tiab] returned 0 records. ClinicalTrials.gov returned 1 record for bronchogen, an airway gene expression test for lung cancer diagnosis that does not involve the peptide. The searches found no human dose, no spirometry or other lung function measure in people, no human pharmacokinetics and no human safety data for Bronchogen.

Participants / model
Records reviewed, not a population
Treatment
Not applicable
Follow-up
Search run on 10 October 2026
Study design
Dated literature and registry search
Funding
not stated in the source

An absence finding as of 10 October 2026, not proof that no unpublished work exists.

Read the original source
2014 Lung paper: bronchial cultures, DNA binding, sequence written ADEL

Cell study

Khavinson VKh et al. Lung. 2014;192(5):781-91. PMID 25015171.

In human embryonic bronchoepithelial cultures at passages 1, 7 and 14, the peptide (written Ala-Asp-Glu-Leu, ADEL, in this paper) changed levels of Ki67, Mcl-1, p53, CD79 and NOS-3, with the strongest proliferation effect in old late-passage cultures, and changed expression of NKX2-1, SCGB1A1, SCGB3A2, FOXA1, FOXA2, MUC4, MUC5AC and SFTPA1. By spectrophotometry, viscometry and circular dichroism it bound DNA in the major groove at guanine N7. The group's papers disagree on the residue order: this 2014 paper and a 2011 DNA-melting paper print Ala-Asp-Glu-Leu, while a 2012 differentiation paper, a 2011 DNA-binding paper and a 2017 tobacco-cell paper print Ala-Glu-Asp-Leu (AEDL), which matches PubChem. The group's 2021 systematic review lists AEDL, Bronchogen, and its 2022 table of ultrashort peptides lists Bronchogen (AEDL).

Participants / model
Human embryonic bronchoepithelial cell cultures at passages 1, 7 and 14
Treatment
Peptide in culture medium
Follow-up
not stated in the source
Study design
Cell-culture protein, gene expression and DNA-binding study
Funding
not stated in the source

Cultured embryonic cell work. It measures gene and protein expression, not lung function and not inflammation. Glu and Asp swapped is a different peptide, so a vendor vial cannot be assumed to match the sequence behind any given paper.

Read the original source
Rat nitrogen dioxide COPD model: 60-day exposure, 1 month of peptide

Animal study

Kuzubova NA et al. Bull Exp Biol Med. 2015;159(5):685-8. PMID 26468022.

Rats were exposed intermittently to nitrogen dioxide for 60 days to model chronic obstructive pulmonary disease and were given the tetrapeptide for 1 month; the abstract does not say whether dosing began after the exposure or during it. The abstract reports that it eliminated bronchial epithelial remodeling (goblet cell hyperplasia, squamous metaplasia, lymphocytic infiltration, emphysema) and restored ciliated cells, raised secretory IgA in the lavage, and normalized cell composition and the proinflammatory cytokine profile in the bronchoalveolar space, which the authors read as reduced neutrophilic inflammation. A 2017 Russian-language paper from the same pulmonology institute used the same 60-day model and added a rise in surfactant protein B. The authors are at the pulmonology research institute of Pavlov First St. Petersburg State Medical University.

Participants / model
Rats with nitrogen dioxide-induced COPD-like lung injury
Treatment
Tetrapeptide for 1 month; dose and route not stated in the abstract
Follow-up
60-day nitrogen dioxide exposure model; peptide for 1 month
Study design
Preclinical animal model of chemically induced lung injury
Funding
not stated in the source

The abstracts give no dose, route, group size or statistics. This is the evidence behind the less airway inflammation claim, and it is in rats with a chemically induced lung injury.

Read the original source

Why does Bronchogen sit in C tier?

A defined peptide with cell studies in human bronchial cultures and one rat lung injury model forms a coherent but thin laboratory record. There is no human study, no lung function endpoint in any species, and the group prints its sequence in two orders.

Bronchogen has a PubChem record, cell work in human bronchial cultures, rat explant growth, and one rat model of chemically induced COPD-like injury run at a pulmonology institute. That is a coherent but thin laboratory profile.

No record measures lung function in any animal or person. The airway inflammation result is from rats with nitrogen dioxide injury, the abstracts give no dose, route or group size, and a PubMed search on 10 October 2026 found no clinical trial and no human data.

PubChem: Bronchogen identity

Chemical identity record

National Library of Medicine. PubChem compound record CID 11690869.

PubChem lists Bronchogen as CID 11690869, C18H30N4O9, molecular weight 446.5, CAS 857267-12-0, with a systematic name that reads Ala-Glu-Asp-Leu (alanine, glutamic acid, aspartic acid, leucine). A PubChem name search for the hyphenated strings Ala-Glu-Asp-Leu and Ala-Asp-Glu-Leu returned no record, so the CID is reached through the trade name only.

Participants / model
Chemical identity, not a clinical population
Treatment
Defined synthetic peptide
Follow-up
Not applicable
Study design
NLM chemical record
Funding
not stated in the source

A defined tetrapeptide record. The group's own papers print a second residue order, so the record does not settle which sequence a given vial or paper used.

Read the original source
2014 Lung paper: bronchial cultures, DNA binding, sequence written ADEL

Cell study

Khavinson VKh et al. Lung. 2014;192(5):781-91. PMID 25015171.

In human embryonic bronchoepithelial cultures at passages 1, 7 and 14, the peptide (written Ala-Asp-Glu-Leu, ADEL, in this paper) changed levels of Ki67, Mcl-1, p53, CD79 and NOS-3, with the strongest proliferation effect in old late-passage cultures, and changed expression of NKX2-1, SCGB1A1, SCGB3A2, FOXA1, FOXA2, MUC4, MUC5AC and SFTPA1. By spectrophotometry, viscometry and circular dichroism it bound DNA in the major groove at guanine N7. The group's papers disagree on the residue order: this 2014 paper and a 2011 DNA-melting paper print Ala-Asp-Glu-Leu, while a 2012 differentiation paper, a 2011 DNA-binding paper and a 2017 tobacco-cell paper print Ala-Glu-Asp-Leu (AEDL), which matches PubChem. The group's 2021 systematic review lists AEDL, Bronchogen, and its 2022 table of ultrashort peptides lists Bronchogen (AEDL).

Participants / model
Human embryonic bronchoepithelial cell cultures at passages 1, 7 and 14
Treatment
Peptide in culture medium
Follow-up
not stated in the source
Study design
Cell-culture protein, gene expression and DNA-binding study
Funding
not stated in the source

Cultured embryonic cell work. It measures gene and protein expression, not lung function and not inflammation. Glu and Asp swapped is a different peptide, so a vendor vial cannot be assumed to match the sequence behind any given paper.

Read the original source
Rat nitrogen dioxide COPD model: 60-day exposure, 1 month of peptide

Animal study

Kuzubova NA et al. Bull Exp Biol Med. 2015;159(5):685-8. PMID 26468022.

Rats were exposed intermittently to nitrogen dioxide for 60 days to model chronic obstructive pulmonary disease and were given the tetrapeptide for 1 month; the abstract does not say whether dosing began after the exposure or during it. The abstract reports that it eliminated bronchial epithelial remodeling (goblet cell hyperplasia, squamous metaplasia, lymphocytic infiltration, emphysema) and restored ciliated cells, raised secretory IgA in the lavage, and normalized cell composition and the proinflammatory cytokine profile in the bronchoalveolar space, which the authors read as reduced neutrophilic inflammation. A 2017 Russian-language paper from the same pulmonology institute used the same 60-day model and added a rise in surfactant protein B. The authors are at the pulmonology research institute of Pavlov First St. Petersburg State Medical University.

Participants / model
Rats with nitrogen dioxide-induced COPD-like lung injury
Treatment
Tetrapeptide for 1 month; dose and route not stated in the abstract
Follow-up
60-day nitrogen dioxide exposure model; peptide for 1 month
Study design
Preclinical animal model of chemically induced lung injury
Funding
not stated in the source

The abstracts give no dose, route, group size or statistics. This is the evidence behind the less airway inflammation claim, and it is in rats with a chemically induced lung injury.

Read the original source
PubMed: no clinical trial, no human data

PubMed search record

PubMed searches run 10 October 2026: bronchogen restricted to clinical trial or randomized controlled trial publication types; bronchogen AND (patients OR children OR COPD OR asthma OR human); peptide bioregulator[tiab] AND (bronchial asthma OR bronchopulmonary OR COPD) AND patients[tiab]. ClinicalTrials.gov query for bronchogen, run the same day.

A PubMed search for bronchogen restricted to clinical trial or randomized controlled trial publication types returned 0 records. A search for bronchogen AND (patients OR children OR COPD OR asthma OR human) returned 9 records: 4 about the peptide (the rat COPD paper, its Russian-language companion, a HeLa and DNA-binding paper, and the differentiation-marker paper) and 5 older case reports of bronchogenic cysts or carcinoma unrelated to the peptide. A search for peptide bioregulator[tiab] AND (bronchial asthma OR bronchopulmonary OR COPD) AND patients[tiab] returned 0 records. ClinicalTrials.gov returned 1 record for bronchogen, an airway gene expression test for lung cancer diagnosis that does not involve the peptide. The searches found no human dose, no spirometry or other lung function measure in people, no human pharmacokinetics and no human safety data for Bronchogen.

Participants / model
Records reviewed, not a population
Treatment
Not applicable
Follow-up
Search run on 10 October 2026
Study design
Dated literature and registry search
Funding
not stated in the source

An absence finding as of 10 October 2026, not proof that no unpublished work exists.

Read the original source

Studies and sources

PubChem: Bronchogen identity

Chemical identity record

National Library of Medicine. PubChem compound record CID 11690869.

PubChem lists Bronchogen as CID 11690869, C18H30N4O9, molecular weight 446.5, CAS 857267-12-0, with a systematic name that reads Ala-Glu-Asp-Leu (alanine, glutamic acid, aspartic acid, leucine). A PubChem name search for the hyphenated strings Ala-Glu-Asp-Leu and Ala-Asp-Glu-Leu returned no record, so the CID is reached through the trade name only.

Participants / model
Chemical identity, not a clinical population
Treatment
Defined synthetic peptide
Follow-up
Not applicable
Study design
NLM chemical record
Funding
not stated in the source

A defined tetrapeptide record. The group's own papers print a second residue order, so the record does not settle which sequence a given vial or paper used.

Read the original source
2014 Lung paper: bronchial cultures, DNA binding, sequence written ADEL

Cell study

Khavinson VKh et al. Lung. 2014;192(5):781-91. PMID 25015171.

In human embryonic bronchoepithelial cultures at passages 1, 7 and 14, the peptide (written Ala-Asp-Glu-Leu, ADEL, in this paper) changed levels of Ki67, Mcl-1, p53, CD79 and NOS-3, with the strongest proliferation effect in old late-passage cultures, and changed expression of NKX2-1, SCGB1A1, SCGB3A2, FOXA1, FOXA2, MUC4, MUC5AC and SFTPA1. By spectrophotometry, viscometry and circular dichroism it bound DNA in the major groove at guanine N7. The group's papers disagree on the residue order: this 2014 paper and a 2011 DNA-melting paper print Ala-Asp-Glu-Leu, while a 2012 differentiation paper, a 2011 DNA-binding paper and a 2017 tobacco-cell paper print Ala-Glu-Asp-Leu (AEDL), which matches PubChem. The group's 2021 systematic review lists AEDL, Bronchogen, and its 2022 table of ultrashort peptides lists Bronchogen (AEDL).

Participants / model
Human embryonic bronchoepithelial cell cultures at passages 1, 7 and 14
Treatment
Peptide in culture medium
Follow-up
not stated in the source
Study design
Cell-culture protein, gene expression and DNA-binding study
Funding
not stated in the source

Cultured embryonic cell work. It measures gene and protein expression, not lung function and not inflammation. Glu and Asp swapped is a different peptide, so a vendor vial cannot be assumed to match the sequence behind any given paper.

Read the original source
2001 report: synthetic peptides versus tissue peptide complexes

Cell study

Khavinson VK. Bull Exp Biol Med. 2001;132(2):807-8. PMID 11713572.

The developer's own 2001 report uses cytogens for synthetic peptides and cytomedins for peptide complexes from tissue, and says the synthetic peptides stimulated explants from the tissues whose cytomedins were used as the basis for chemical synthesis. It names Cortagen, Epithalon, Livagen and Vilon, not Bronchogen. A PubMed search for cytomax[tiab] OR cytomaxes[tiab] returned 2 records, a 1964 paper on a cytochrome C product and a 2007 sports-drink paper. A search for cytogen[tiab] OR cytogens[tiab] returned 37 records, of which 3 are Khavinson-group cytogens papers and 34 are unrelated by title, mostly radiolabeled antibody imaging reports using a company's Cytogen product names.

Participants / model
Rat tissue explants
Treatment
Synthetic peptides in organotypic culture
Follow-up
not stated in the source
Study design
Original preclinical report
Funding
not stated in the source

Every Bronchogen result on this page is for the synthetic tetrapeptide. None tests a tissue extract or a Cytomax or Cytogen retail product.

Read the original source
2012 differentiation paper: CXCL12 and Hoxa3 in bronchial cells

Cell study

Khavinson VKh et al. Bull Exp Biol Med. 2012;153(1):148-51. PMID 22808515.

In human embryonic bronchial cell cultures, expression of CXCL12 and Hoxa3 fell in late-passage (aging) cultures, and bronchogen (Ala-Glu-Asp-Leu) raised expression of those markers in bronchial epithelial cells, more strongly in aged cultures. The same paper tested pancragen and vesugen in other cell types.

Participants / model
Human embryonic bronchial epithelial cultures
Treatment
Peptide in culture medium
Follow-up
not stated in the source
Study design
Cell-culture gene expression study
Funding
not stated in the source

Measures CXCL12 and Hoxa3 expression in cultured cells, not lung function.

Read the original source
2006 explant study: lung explants from young and aged rats

Cell study

Zakutskiĭ AN et al. Adv Gerontol. 2006;19:93-6. PMID 17152728.

A 2006 Russian-language report used synthetic cardiogen, bronchogen, prostamax and pancragen on organotypic explants of heart, lung, prostate and pancreas from 3-week-old and 18-month-old rats. At 0.05 ng/ml each peptide stimulated growth in its matching tissue culture compared with control explants in all groups. The abstract reports no cell, cytokine or function endpoint beyond explant growth.

Participants / model
Explants from young (3-week) and aged (18-month) rats
Treatment
Peptide in culture medium at 0.05 ng/ml
Follow-up
not stated in the source
Study design
Organotypic explant culture, Russian-language report
Funding
not stated in the source

Explant growth is not a lung function endpoint.

Read the original source
Rat nitrogen dioxide COPD model: 60-day exposure, 1 month of peptide

Animal study

Kuzubova NA et al. Bull Exp Biol Med. 2015;159(5):685-8. PMID 26468022.

Rats were exposed intermittently to nitrogen dioxide for 60 days to model chronic obstructive pulmonary disease and were given the tetrapeptide for 1 month; the abstract does not say whether dosing began after the exposure or during it. The abstract reports that it eliminated bronchial epithelial remodeling (goblet cell hyperplasia, squamous metaplasia, lymphocytic infiltration, emphysema) and restored ciliated cells, raised secretory IgA in the lavage, and normalized cell composition and the proinflammatory cytokine profile in the bronchoalveolar space, which the authors read as reduced neutrophilic inflammation. A 2017 Russian-language paper from the same pulmonology institute used the same 60-day model and added a rise in surfactant protein B. The authors are at the pulmonology research institute of Pavlov First St. Petersburg State Medical University.

Participants / model
Rats with nitrogen dioxide-induced COPD-like lung injury
Treatment
Tetrapeptide for 1 month; dose and route not stated in the abstract
Follow-up
60-day nitrogen dioxide exposure model; peptide for 1 month
Study design
Preclinical animal model of chemically induced lung injury
Funding
not stated in the source

The abstracts give no dose, route, group size or statistics. This is the evidence behind the less airway inflammation claim, and it is in rats with a chemically induced lung injury.

Read the original source
FDA records: no match for Bronchogen

Regulatory record

U.S. Food and Drug Administration, openFDA Drugs@FDA query for bronchogen as brand name, and DailyMed (U.S. National Library of Medicine) search for the drug name bronchogen, both run 10 October 2026.

On 10 October 2026 an openFDA Drugs@FDA query for bronchogen as brand or generic name returned no matches, and a DailyMed search for the drug name bronchogen returned no label. No FDA record for Bronchogen was found in these two sources, so it is not an FDA-approved drug or a labeled product.

Participants / model
Not a clinical population
Treatment
Not applicable
Follow-up
Queries run on 10 October 2026
Study design
Official FDA and NLM record searches
Funding
not stated in the source

These sources say nothing about other regulators.

Read the original source
PubMed: no clinical trial, no human data

PubMed search record

PubMed searches run 10 October 2026: bronchogen restricted to clinical trial or randomized controlled trial publication types; bronchogen AND (patients OR children OR COPD OR asthma OR human); peptide bioregulator[tiab] AND (bronchial asthma OR bronchopulmonary OR COPD) AND patients[tiab]. ClinicalTrials.gov query for bronchogen, run the same day.

A PubMed search for bronchogen restricted to clinical trial or randomized controlled trial publication types returned 0 records. A search for bronchogen AND (patients OR children OR COPD OR asthma OR human) returned 9 records: 4 about the peptide (the rat COPD paper, its Russian-language companion, a HeLa and DNA-binding paper, and the differentiation-marker paper) and 5 older case reports of bronchogenic cysts or carcinoma unrelated to the peptide. A search for peptide bioregulator[tiab] AND (bronchial asthma OR bronchopulmonary OR COPD) AND patients[tiab] returned 0 records. ClinicalTrials.gov returned 1 record for bronchogen, an airway gene expression test for lung cancer diagnosis that does not involve the peptide. The searches found no human dose, no spirometry or other lung function measure in people, no human pharmacokinetics and no human safety data for Bronchogen.

Participants / model
Records reviewed, not a population
Treatment
Not applicable
Follow-up
Search run on 10 October 2026
Study design
Dated literature and registry search
Funding
not stated in the source

An absence finding as of 10 October 2026, not proof that no unpublished work exists.

Read the original source

Why is Bronchogen in C tier?

C fits a defined peptide with several cell and rat studies that add up to a coherent but thin laboratory record. It has no human study of any design and no lung function measurement in any species, and the group prints its sequence in two orders. The airway inflammation result comes from rats with chemically induced lung injury, in abstracts that give no dose or route.