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Professor Peptides
Research compound

Bronchogen

Also known as Bronchogen · Ala-Glu-Asp-Leu · AEDL · AEDL peptide

Ala-Glu-Asp-Leu tetrapeptide; the one family member with a distinct DNA-binding preference

Last reviewed · Educational reference — not medical advice.

NCAEDL4 residuesN → C
  • Small / Pro
  • Hydrophobic
  • Polar
  • Acidic
  • Basic
Primary sequence, N → C, by residue class.
Formula
C18H30N4O9
Molecular weight
446.5 g/mol
Half-life
Not characterised in published pharmacokinetic studies
Route
Subcutaneous or intramuscular in the source literature
CAS
857267-12-0
PubChem
11690869 (opens in new tab)
Status
Research compound — short peptide bioregulator
Sequence
AEDL
Mechanism
Penetrates the cell nucleus and binds deoxyribooligonucleotides sequence-selectively with a preference for CTG-containing sequences — distinct from the CAG preference shown by epithalon, testagen and pinealon. Proposed to influence cytosine methylation status and gene activity. No receptor identified.
01

Overview

Bronchogen is the synthetic tetrapeptide Ala-Glu-Asp-Leu (AEDL). PubChem lists it under CID 11690869 with formula C18H30N4O9 and CAS 857267-12-0, matching the formula computed from AEDL, and the 2011 nuclear-penetration paper names it directly as "bronchogen (Ala-Glu-Asp-Leu)".

Bronchogen is the most interesting member of this family from a mechanism standpoint, because it is the one that behaves differently. In the fluorescence-quenching experiments, epithalon, testagen and pinealon all preferentially bound CAG-containing deoxyribooligonucleotide sequences — but bronchogen preferentially bound CTG-containing sequences instead. Since CNG sites are cytosine methylation targets in eukaryotes, this difference is the concrete evidence the Khavinson group offers that sequence identity determines which genes a given peptide can influence. Whatever one makes of the wider claims, this is a real, measured, peptide-specific difference rather than a general assertion.

Bronchogen is marketed as a lung and bronchial bioregulator. No indexed study measures pulmonary function, airway inflammation, or any respiratory endpoint after administration.

Research areasPeptide–DNA sequence-selective bindingCytosine methylation and CNG sitesEpigenetic regulation by ultrashort peptidesBronchial epithelial biology
02

What the evidence shows

Separated by study type
HumanClinical trials and human studies
No human studies of any kind in the indexed literature.
AnimalRodent and other animal models
No indexed animal outcome studies.
In vitroCell and tissue studies
Penetrated cytoplasm, nucleus and nucleolus of HeLa cells; bound deoxyribooligonucleotides sequence-selectively with a measured preference for CTG-containing sequences, distinguishing it from the CAG-preferring peptides in the same experiment.
03

Key studies & findings

1 study
  1. 1

    Bronchogen (Ala-Glu-Asp-Leu) bound preferentially to CTG-containing deoxyribooligonucleotides, whereas epithalon, testagen and pinealon in the same experiment preferred CAG-containing sequences — a measured, sequence-specific difference in DNA binding.

    In vitro2011Biochemistry (Moscow), 2011 (opens in new tab)

04

Benefits & effects

2 documented

  • Sequence-selective DNA binding at CTG-containing sites

    Verified

  • Nuclear and nucleolar penetration in cultured cells

    Verified
05

Side effects & safety

1 reported

Safety noteResearch compound for laboratory use only. No regulatory safety review, no established human safety database, and no controlled toxicology data in the public literature.

Recorded in the cited literature No controlled human safety data exist for this compound.

  • Marketed respiratory claims are unsupported by indexed research

    unknown
06

Limitations & open questions

Nearly all published work on this compound originates from a single research programme (the St Petersburg Institute of Bioregulation and Gerontology, Khavinson group) and its collaborators. Independent replication outside that network is sparse to non-existent, sample sizes are small, and much of the source literature is published in Russian-language journals with limited peer-review transparency. Effects reported in cell culture and in aged-donor lymphocytes have not been shown to produce clinical outcomes in controlled human trials. Specific to Bronchogen: the respiratory positioning derives from the tissue the original extract came from. No indexed study measures lung function, airway inflammation, or any respiratory endpoint.

07

Pharmacology

Bronchogen is the tetrapeptide Ala-Glu-Asp-Leu (C18H30N4O9, MW 446.5, CAS 857267-12-0, PubChem CID 11690869). The PubChem formula matches the formula computed from the sequence. No published human pharmacokinetic data exist.

08

Frequently asked questions

Why does Bronchogen's DNA-binding preference matter?

It is the cleanest piece of evidence for the family's core claim. Four peptides were tested in the same assay; three preferred CAG-containing sequences and bronchogen preferred CTG-containing ones. That is a peptide-specific, measured difference rather than a general assertion that 'short peptides regulate genes'.

Does Bronchogen help lung conditions?

No indexed study measures any respiratory endpoint. The lung positioning comes from the tissue source of the original extract, not from demonstrated pulmonary effects.

Is Bronchogen the same as Chonluten?

No. They are both marketed as lung bioregulators, but Bronchogen is the tetrapeptide Ala-Glu-Asp-Leu with a confirmed PubChem entry, while Chonluten is described in the literature as a bronchial-derived tripeptide whose sequence is not stated in any indexed source found here.

09

Citations

2 sources
  1. 1
  2. 2
    Peptide Regulation of Gene Expression: A Systematic Review (opens in new tab)Khavinson VKh, Popovich IG, Linkova NS, Mironova ES, Ilina AR (2021) · doi:10.3390/molecules26227053