Bronchogen Research, Specifications & Scientific Information

Introduction

Bronchogen is the bronchial member of the Khavinson bioregulator series — Ala-Glu-Asp-Leu, four residues, 446 daltons — and it is one of only two compounds in this batch whose proposed mechanism has been tested by a direct physical measurement rather than inferred from an expression profile.

That measurement is a DNA melting curve. In a differential scanning microcalorimeter the peptide raised the melting temperature of calf thymus DNA and mouse liver DNA by 3.1 °C, within a narrow band of peptide-to-base-pair ratios, without changing the melting enthalpy — and it was neither AT-specific nor GC-specific ^[3]. That is an instrument reporting on a purified sample, and it is a great deal more than a docking score.

The same compound also carries the batch's clearest bibliographic hazard. The title of that calorimetric paper spells the sequence Ala-Asp-Glu-Leu, transposing two residues relative to the PubChem register record and relative to a paper published the same year by an overlapping author group ^[4]. The two spellings have the same molecular formula and the same mass and describe different compounds. This page uses the register spelling and says so rather than silently correcting a published title.

The family's usual limitations apply and are stated once here: a single originating institute and its collaborators, several Russian-language publications, small or unstated group sizes, an emphasis on cell culture and excised tissue, no clinical report of any design, and no independent replication.

What Is Bronchogen?

A synthetic tetrapeptide with free termini, AEDL in single-letter code: L-alanyl-L-alpha-glutamyl-L-alpha-aspartyl-L-leucine.

Within the series it is assigned to lung tissue, designed from the amino acid composition of a pulmonary polypeptide complex. Two experiments support that assignment in a testable way. In organotypic culture, explants of heart, lung, prostate and pancreas from young and old rats each responded to their own matched peptide at 0.05 ng/ml ^[8]. And in late-passage cultures of three human cell types, this peptide raised the differentiation factors CXCL12 and Hoxa3 in bronchial cells while Pancragen acted on pancreatic cells and Vesugen on prostatic fibroblasts ^[6].

One experiment cuts hard the other way, and it is discussed below: the same peptide changes gene expression in tobacco.

Bronchogen has not been approved by the U.S. Food and Drug Administration for any indication. No marketing application is on record in the United States, and no study of it appears on ClinicalTrials.gov.

Bronchogen Specifications

PubChem carries the free tetrapeptide as compound identifier 11690869 with CAS registry number 857267-12-0, formula C18H30N4O9 and an average mass of 446.45 g/mol; the recorded structure is Ala-Glu-Asp-Leu. No unique ingredient identifier resolves in the FDA/NCATS Global Substance Registration System. One published discrepancy should be known to anyone reading this literature: a 2011 calorimetric paper gives the sequence in its own title as Ala-Asp-Glu-Leu, transposing the second and third residues relative to the register record and relative to every other paper located, including one published the same year by an overlapping author group. Ala-Glu-Asp-Leu and Ala-Asp-Glu-Leu have the same molecular formula and the same mass and are different compounds. This page uses the register spelling and flags the discrepancy rather than silently correcting it. Reagent material supplied as a salt will not match the free-peptide mass above.

Values that a public register does not carry are shown as not publicly characterised rather than estimated. Identifiers are reference values; the certificate of analysis supplied with a laboratory order is the record for a given lot.

How Does Bronchogen Work?

Not established. What exists is a nucleic-acid-binding hypothesis with more physical support than usual, and a body of cellular observations that the binding does not obviously explain.

The calorimetry. DNA melting was measured in the presence of the peptide across a range of molar ratios of peptide to base pair. Between ratios of 0.01 and 0.055 the melting temperature rose by 3.1 °C for DNA from both sources; beyond that range further peptide made no difference. The melting enthalpy stayed constant across a much wider ratio range, at 11.4 and 12.7 cal/g for thymus and liver DNA. The authors conclude that the peptide is a DNA-stabilising agent, that it is not base-composition-specific, and that binding is strong and occasional, involving both strands and mainly the nitrogen bases ^[3].

Three things follow. A saturating effect with a ceiling is what a real binding interaction looks like. A stabilising effect is the opposite direction from the chromatin-decondensation claims made for several sibling peptides, which is a tension inside the series that nobody has addressed. And "not base-composition-specific" sits awkwardly beside the sequence-selectivity reported for the same peptide in the fluorescence work below — the two methods disagree about how selective this molecule is.

The fluorescence work. Stern-Volmer quenching constants for labelled deoxyribooligonucleotides showed that different short peptides bind different sequences. Epitalon, Pinealon and this peptide all bound preferentially to oligonucleotides containing the CNG motif, a target for cytosine methylation; but within that, Epitalon, Testagen and Pinealon preferred CAG-containing sequences while this one preferred CTG ^[4]. A single-nucleotide preference separating one member of a series from three others is the most specific structure–activity observation in this batch.

Histones as well as DNA. A follow-up reported that this peptide and five siblings bind FITC-labelled wheat histones H1, H2B, H3 and H4, and that the binding depends on the histone, on the peptide's primary structure and on the oligonucleotide present ^[5].

What is still missing. No receptor. No demonstration that the peptide reaches a nucleus in the lung cells where the biological effects were measured. No pharmacokinetic data of any kind. And no account connecting a 3.1 °C shift in DNA melting temperature to the reversal of bronchial epithelial remodelling in a rat.

Preclinical Research on Bronchogen

Animal research

Obstructive lung pathology in rats

Chronic obstructive pulmonary disease was modelled in rats by 60 days of intermittent exposure to nitrogen dioxide. One month of the tetrapeptide was then administered ^[1].

Reported structural results. The features of remodelling characteristic of the model were eliminated: goblet cell hyperplasia, squamous metaplasia, lymphocytic infiltration and emphysema, with restoration of ciliated cells.

Reported functional results. Secretory IgA — a marker of local immunity — rose, which the authors read as normalisation of bronchial epithelial function. Cell composition and the profile of pro-inflammatory cytokines in the bronchoalveolar space normalised, reflecting reduced neutrophilic inflammation ^[1].

The companion report from the same group examined bronchoalveolar lavage fluid in the same model and added surfactant protein B to the measured set, alongside cell composition, a cytokine and enzyme profile, and secretory IgA ^[2].

How much weight this carries. The model is a recognised one and the endpoints are a mixture of histological and biochemical, which is a reasonable design. Against that: neither indexed abstract states group sizes, randomisation, blinding of the histological assessment, route or amount administered, or any statistical test. Histological grading of epithelial remodelling is subjective, and an unblinded assessment of it by the group testing the compound is the weakest link in the chain. "Eliminates symptoms of remodelling" is also a very strong summary phrase for a result reported without a measure of variance.

Findings in this section were obtained in rats. Nothing in them establishes anything about humans.

Bronchogen Mechanism of Action

In vitro research

Bronchial cell differentiation. In late-passage cultures of human bronchial cells, expression of the differentiation markers CXCL12 and Hoxa3 was reduced relative to early passages, and this tetrapeptide raised it — more strongly in the aged cultures than the young ones. Two sibling peptides acted on pancreatic cells and on prostatic fibroblasts instead ^[6].

The tobacco experiment. The finding that most complicates everything else on this page. Callus cultures of Nicotiana tabacum were exposed to this peptide, Epitalon and Vilon at 10⁻⁷ to 10⁻⁹ M. Epitalon and this peptide both increased callus growth and stimulated formation and growth of leaves in plant regenerants. All three modulated expression of CLE family genes, which encode endogenous plant regulatory peptides, and of the KNOX1 transcription-factor genes and GRF genes encoding DNA-binding proteins ^[7].

The authors present this as support for an epigenetic, signalling-type mode of action analogous to a phytohormone. Read alongside the rest of this page it has a second implication. A peptide named for bronchial tissue, designed from a lung extract, and reported to act tissue-specifically in mammalian culture also regulates development genes in tobacco — an organism with no lungs, no immune system and no bronchial epithelium. Either the tissue-specificity premise is weaker than the series' own experiments suggest, or two quite different mechanisms are in play. The literature does not choose.

Organotypic lung explants. Growth stimulated at 0.05 ng/ml, matched to the tissue the compound was designed from, alongside three sibling peptides in their own tissues ^[8].

Everything in this section was observed in cultured cells, excised tissue, plant callus or purified nucleic acids. None of it establishes anything about an intact animal, and none of it about a person.

What Is Bronchogen Being Researched For?

• Experimental obstructive lung pathology — bronchial epithelial structure, secretory IgA, surfactant protein B and bronchoalveolar inflammation in rats ^{[1, 2]}.
• Peptide–DNA interaction — melting thermodynamics and sequence-selective binding ^{[3, 4]}.
• Peptide–histone interaction — binding to four wheat histone classes and their oligonucleotide complexes ^[5].
• Bronchial cell differentiation in ageing culture — CXCL12 and Hoxa3 ^[6].
• Plant development genes — CLE, KNOX1 and GRF expression in tobacco callus ^[7].

None of that is research into, or evidence about, research-grade material supplied for laboratory use.

Current Research Status

Status as of September 22, 2026. This block is rendered from maintained fields, not from prose, so it cannot go stale in one place and stay current in another.

Bronchogen vs Related Compounds

Chonluten :: The other lung-assigned peptide of the series, the tripeptide Glu-Asp-Gly. Two compounds from one programme assigned to the same tissue is unusual and the literature does not explain the division of labour between them. Epitalon, Pinealon and Testagen :: The three peptides tested beside this one in the DNA-binding work, where all bound CNG-containing sequences but this one alone preferred CTG over CAG ^[4]. That is the cleanest sequence-level separation in this batch. Pancragen and Vesugen :: Tested beside this one in the three-tissue differentiation comparison, each acting on its own cell type ^[6]. Vilon :: The third peptide in the tobacco experiment, where it modulated plant gene expression but, unlike this one and Epitalon, did not increase callus growth ^[7].

Evidentiary position

Not approved by the U.S. Food and Drug Administration, no registered trial, no clinical report of any design, and a signature animal result published without group sizes or statistics.

No comparison of effect between these compounds is made on this page.

Chemical & Molecular Characteristics

Leucine makes this the most hydrophobic tetrapeptide in the batch. Its isobutyl side chain is the largest purely aliphatic group in the standard set, and it is the only substantial hydrophobic surface anywhere in this molecule. Two practical consequences follow: reversed-phase retention on C18 is meaningfully better than for the polar tripeptides of this family, so a purity figure by HPLC carries more information; and the molecule has at least a small hydrophobic face that could contact a groove or a protein surface, which the wholly polar members of the series do not.

Net charge is still acidic. With no basic side chain — alanine, leucine and the two acidic residues supply none — only the N-terminal amine offsets the glutamate side chain, the aspartate side chain and the C-terminal carboxyl. The molecule is net negative at physiological pH, which is worth holding against a proposed mechanism of binding to DNA, itself a polyanion. The calorimetric paper's description of the binding as strong but occasional, and involving nitrogen bases rather than the phosphate backbone, is at least consistent with that electrostatic problem.

No aromatic residue, so no absorbance at 280 nm. Quantification relies on peptide-bond absorbance near 214 nm, where buffers and solvents also absorb.

The sequence discrepancy is a mass-spectrometry blind spot. Ala-Glu-Asp-Leu and the Ala-Asp-Glu-Leu of the 2011 title have the same molecular formula, C18H30N4O9, and the same mass. No mass measurement distinguishes them. Only a sequencing method — Edman degradation or tandem mass spectrometry with fragment assignment — does, and a certificate of analysis reporting a single expected molecular ion has not established which of the two is in the vial.

Aspartate and glutamate bring further isomers of identical mass. Both residues undergo alpha/beta and alpha/gamma rearrangement under thermal and acidic stress, giving species indistinguishable by mass from the intended compound. For a peptide whose published sequence is already in dispute, connectivity is the analytical question that matters.

One register field is empty. CAS registry number 857267-12-0 and PubChem compound identifier 11690869 both resolve; no FDA/NCATS unique ingredient identifier does. That field is shown as unknown above rather than filled from a neighbouring substance.

Frequently Asked Questions

Scientific References

1. Kuzubova NA, Lebedeva ES, Dvorakovskaya IV, et al.. Modulating Effect of Peptide Therapy on the Morphofunctional State of Bronchial Epithelium in Rats with Obstructive Lung Pathology Bulletin of experimental biology and medicine; 2015. PMID 26468022 doi:10.1007/s10517-015-3047-x
2. Titova ON, Kuzubova NA, Lebedeva ES, et al.. [ANTIINFLAMMATORY AND REGENERATIVE EFFECT OF PEPTIDE THERAPY IN THE MODEL OF OBSTRUCTIVE LUNG PATHOLOGY] Rossiiskii fiziologicheskii zhurnal imeni I.M. Sechenova; 2017. PMID 30199201
3. Monaselidze JR, Khavinson VKh, Gorgoshidze MZ, et al.. Effect of the peptide bronchogen (Ala-Asp-Glu-Leu) on DNA thermostability Bulletin of experimental biology and medicine; 2011. PMID 21240358 doi:10.1007/s10517-011-1146-x
4. Fedoreyeva LI, Kireev II, Khavinson VKh, et al.. Penetration of short fluorescence-labeled peptides into the nucleus in HeLa cells and in vitro specific interaction of the peptides with deoxyribooligonucleotides and DNA Biochemistry. Biokhimiia; 2011. PMID 22117547 doi:10.1134/S0006297911110022
5. Fedoreyeva LI, Smirnova TA, Kolomijtseva GY, et al.. Interaction of short peptides with FITC-labeled wheat histones and their complexes with deoxyribooligonucleotides Biochemistry. Biokhimiia; 2013. PMID 23581987 doi:10.1134/S0006297913020053
6. Khavinson VKh, Linkova NS, Polyakova VO, et al.. Peptides tissue-specifically stimulate cell differentiation during their aging Bulletin of experimental biology and medicine; 2012. PMID 22808515 doi:10.1007/s10517-012-1664-1
7. Fedoreyeva LI, Dilovarova TA, Ashapkin VV, et al.. Short Exogenous Peptides Regulate Expression of CLE, KNOX1, and GRF Family Genes in Nicotiana tabacum Biochemistry. Biokhimiia; 2017. PMID 28371610 doi:10.1134/S0006297917040149
8. Zakutskiĭ AN, Chalisova NI, Ryzhak GA, et al.. [The tissue-specific effect of synthetic peptides-biologic regulators in organotypic tissues culture in young and old rats] Advances in gerontology = Uspekhi gerontologii; 2006. PMID 17152728

Every identifier above is resolved against PubMed, Crossref or ClinicalTrials.gov at build time, and the title returned by the register is compared with the title stored here. A page does not publish if a reference fails to resolve.

Research-Use Information

For in vitro research use only. This material is a laboratory reagent. It is not a drug, food, dietary supplement, or cosmetic and is not for human or veterinary use, including ingestion, injection, or any other administration. No information on this page describes or implies any effect in humans or animals. Sold only to researchers under our Terms of Sale.