F tier · safety concern
There is no registered clinical trial and no identifiable published human study of AEDL; the evidence is a small set of cell-culture papers from Khavinson's St Petersburg group plus one rat COPD study from a separate Russian pulmonology institute, and the originating group's own 2014 review of clinical results does not list Bronchogen at all.
Bronchogen
Bronchogen is a synthetic tetrapeptide (AEDL) developed by Vladimir Khavinson's St Petersburg Institute of Bioregulation and Gerontology and marketed as a bronchopulmonary 'bioregulator'. Published work is limited to DNA-binding assays, organotypic culture, and a rat model of NO2-induced obstructive lung disease. Notably the rat study comes from a separate St Petersburg pulmonology institute with no Khavinson co-authors, but no human data of any kind was located.
// we supply this one
available as a research reagent
≥ 98% HPLC · lyophilised powder · batch certificate published. Grade F above is our own and is not adjusted because we stock it.
the explanation
Bronchogen is a four-amino-acid peptide from a Russian research institute that markets organ-specific 'bioregulator' peptides. The only studies are in rats and in cells in dishes. One rat study was run by a different Russian lung institute, which is a point in its favour, but nobody has tested it in people and no clinical trial has ever been registered.
regulatory status
No medicinal approval anywhere; research reagent
Bronchogen holds no marketing authorisation as a medicine in the UK, EU, or US, and no MHRA, EMA, or FDA assessment exists. A ClinicalTrials.gov query covering Bronchogen and its sibling bioregulators returns zero registered studies of the peptide. In Russia the material reaches consumers through the 'Cytogens' consumer peptide product line associated with Khavinson's institute rather than as a registered pharmaceutical; we could not verify any Russian medicines-register entry for AEDL itself, and the originating group's own 2014 summary of clinical results covers Thymalin, Thymogen, Vilon, Epithalamin, Prostatilen, Cortexin, and Retinalamin — not Bronchogen. It is supplied in the UK strictly as a research reagent, not for human use.
how it works · proposed mechanism
The proposed mechanism is not receptor pharmacology but direct gene regulation: ultrashort peptides are said to enter cells and nuclei and interact with DNA and histones to switch tissue-specific genes on or off. This framework is applied uniformly across the whole Khavinson family, with the C-terminal residue supposedly conferring organ specificity. It is a hypothesis generated and tested almost exclusively inside one institute.
Direct DNA interaction
The group reports that AEDL alters the thermal denaturation profile of DNA, which they interpret as sequence-selective binding to specific promoter regions. This is a physicochemical observation in cell-free systems, not a demonstrated transcriptional mechanism in intact tissue.
Nuclear penetration
Fluorescently labelled short peptides including AEDL have been shown entering the nucleus of HeLa cells in the group's imaging work. Nuclear localisation is a prerequisite for the proposed epigenetic mechanism but does not itself establish that gene expression is regulated in a therapeutically meaningful way.
Claimed bronchial tissue specificity
In organotypic culture and in rats, AEDL is reported to selectively affect bronchial epithelium — restoring ciliated cells and reversing goblet-cell hyperplasia and squamous metaplasia — while other family members act on other organs. The specificity claim itself rests on within-group comparisons rather than on independent testing.
Reversal of NO2-induced lung pathology in rats
In rats given 60 days of intermittent NO2 exposure, a month of Bronchogen was reported to eliminate goblet-cell hyperplasia, squamous metaplasia, lymphocytic infiltration and emphysema. This study came from the Research Institute of Pulmonology at Pavlov First St Petersburg State Medical University, with no Khavinson co-authors — the only animal work in this family not authored by the originating group.
what’s reported
evidence shape
6 sourcesThe composition of the cited literature by study type. This describes the shape of the evidence, not its quality — and it does not by itself set the grade.
⚠ the catch
There is no registered trial, no published human study and no human pharmacokinetic data for Bronchogen, so the 'lung bioregulator' framing rests entirely on rat histology and cell-free DNA assays. The best datapoint — reversal of NO2-induced bronchial pathology in rats — does come from a group with no Khavinson co-authors, but it is a separate institute in the same city, animal-only, published in a Russian translated journal, and has not been replicated outside Russia in the decade since. Compounding this, the sequence designation is inconsistent in the primary literature: the group's reviews give AEDL (Ala-Glu-Asp-Leu) while its own 2011 paper is titled with Ala-Asp-Glu-Leu, a same-formula isomer, so material sold under this name cannot be assumed to match the compound in any given paper. Treat it as a preclinical research chemical with an unresolved identity question.
key published findings
- ClinicalTrials.gov contains no registered study of Bronchogen or AEDL (verified by registry query; the term-matched hits are unrelated studies).
- No published human study of AEDL was located in PubMed, Europe PMC, or the originating group's own literature.
- The originating group's 2014 review of clinical results for its peptide bioregulators lists Thymalin, Thymogen, Vilon, Epithalamin, Prostatilen, Cortexin, and Retinalamin — Bronchogen is absent.
- The strongest finding is a 2015 rat study (60-day intermittent NO2 exposure) reporting reversal of goblet-cell hyperplasia, squamous metaplasia, lymphocytic infiltration and emphysema after a month of Bronchogen.
- That rat study was authored by Kuzubova and colleagues at the Research Institute of Pulmonology, Pavlov First St Petersburg State Medical University, with no Khavinson co-authors — partial independence of authorship, though same city and research ecosystem, and animal-only.
- Chemistry is verifiable: PubChem CID 11690869 gives C18H30N4O9, 446.5 g/mol, CAS 857267-12-0.
- Sequence designation conflicts between the group's own publications (AEDL in reviews vs Ala-Asp-Glu-Leu in a 2011 primary title).
limitations of the evidence
- No human evidence of any kind — no trial, no clinical report, no pharmacokinetics or bioavailability data.
- Mechanistic and cell-culture work is almost entirely authored by Khavinson and colleagues at the St Petersburg Institute of Bioregulation and Gerontology and the Pavlov Institute of Physiology.
- The one non-Khavinson-authored study is still Russian, still St Petersburg-based, animal-only, single model, and unreplicated in the decade since publication.
- Primary evidence appears in Russian-language or Russian-translated, low-indexing journals — Bulletin of Experimental Biology and Medicine, Rossiiskii Fiziologicheskii Zhurnal.
- Sequence ambiguity (AEDL vs ADEL) is unresolved in the primary literature.
- Sources are deliberately shared with the other Khavinson bioregulators in this index, because these compounds are described in a single common body of literature; the shared reviews should not be read as independent support for each compound.
- Absence of retrieved human data is not proof none exists — Russian-language clinical reports outside PubMed/Europe PMC indexing may not have been captured.
documented safety signals
- No documented safety signals — but also no published human safety data, no toxicology available to us, and no adverse-event reporting system covering the compound.
- Absence of reported harm reflects absence of monitored human exposure, not demonstrated safety.
- Unapproved research material carries unquantified impurity and endotoxin risk; there is no regulator-audited manufacturing standard for it.
identity
| full name | Bronchogen (Ala-Glu-Asp-Leu, AEDL) |
| category | Other |
| modality | peptide |
| formula | C18H30N4O9 |
| molar mass | 446.5 g/mol |
| cas | 857267-12-0 |
| sequence | Ala-Glu-Asp-Leu (AEDL) |
laboratory handling
| storage | Lyophilised powder is stored desiccated at -20 °C and protected from light. Once reconstituted, laboratory practice is refrigeration at 2-8 °C for short-term use, or aliquoting and freezing to avoid repeated freeze-thaw cycles. Handling information only; this compound has no approved human use. |
| solubility | Short hydrophilic peptide, readily soluble in sterile or bacteriostatic water and in dilute aqueous buffer. Lot-specific solubility is stated on the certificate of analysis. |
Handling information describes laboratory practice for a research reagent. It is not a preparation guide for use in humans.
the receipts
6 citedPubChem, US National Library of Medicine · 2026 · official
ClinicalTrials.gov, US National Library of Medicine · 2026 · official
Bulletin of Experimental Biology and Medicine (Russian translated journal) · 2011 · preclinical
Bulletin of Experimental Biology and Medicine (Russian translated journal) · 2015 · preclinical
Rossiiskii Fiziologicheskii Zhurnal im. I.M. Sechenova (Russian-language, low-indexing) · 2017 · preclinical
Molecules · 2021 · systematic review
others in Other