Bronchogen

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

Evidence: Preclinical

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Overview

Khavinson-series synthetic tetrapeptide (AEDL) for bronchial tissue; reported to restore bronchial epithelium in a rat NO2 model of COPD and to drive bronchial cell differentiation in vitro.

Bronchogen is a synthetic tetrapeptide (AEDL, Ala-Glu-Asp-Leu) from the St. Petersburg Institute of Bioregulation and Gerontology, listed by that group as a bronchoprotector (Khavinson 2022). In rats with COPD modelled by 60 days of intermittent NO2 exposure, a month of treatment reversed goblet cell hyperplasia and squamous metaplasia, restored ciliated cells and raised secretory IgA (Kuzubova 2015). In human embryonic bronchial cell cultures it raised Ki67, Mcl-1 and the differentiation genes NKX2-1, SCGB1A1 and FOXA1, most in late-passage cells (Khavinson 2014). Nearly all work comes from one group. No controlled human trial has been published; a 2020 review from the same group says oral use is effective in COPD but cites no clinical paper.

Benefits

Bronchial epithelium restoration in a rat COPD model (rodent), bronchial epithelial differentiation and proliferation markers (in vitro)

Dosing reference

Research dose: 200 to 1000 mcg daily: vendor/community range, no published human dose
Range: 200 to 1000 mcg, 1x daily

Sold as oral capsules and as lyophilized powder for injection. The rat COPD study gave a one-month course; its abstract does not state the dose (Kuzubova 2015). Community protocols run 10 to 20 day courses two or three times a year; no study compared schedules.

Mechanism

Proposed, from cell and biophysical work by the developing group. In bronchial epithelial cultures the peptide raised proliferation (Ki67, Mcl-1) and bronchial differentiation gene expression (NKX2-1, SCGB1A1, SCGB3A2, FOXA1, FOXA2, MUC4, MUC5AC, SFTPA1), and spectroscopy suggested binding in the DNA major groove (Khavinson 2014). Calorimetry showed it raises DNA melting temperature by 3.1 C, binding both strands without base specificity (Monaselidze 2011). Docking predicts uptake through PEPT1 and LAT transporters (Khavinson 2022). Gene regulation by direct DNA binding is the group's hypothesis and has not been tested independently.

Evidence

Preclinical: animal or in vitro data only

In rats with NO2-induced COPD, one month of treatment removed goblet cell hyperplasia, squamous metaplasia and emphysema, restored ciliated cells and raised secretory IgA (Kuzubova et al., 2015)
Expression of the differentiation factors CXCL12 and Hoxa3 rose in aged human bronchial epithelial cultures (Khavinson et al., 2012)
In human embryonic bronchial cell cultures it raised Ki67, Mcl-1, NKX2-1, SCGB1A1 and FOXA1, strongest in late passages (Khavinson et al., 2014)
Raised DNA melting temperature by 3.1 C in calorimetry, binding both strands (Monaselidze et al., 2011)
Human-trial status: no controlled human trial published; reviews from the developing group describe oral use in COPD and chronic bronchitis without citing a clinical paper

References

Side effects

No controlled safety study has been published in any species, and the animal and cell studies, almost all from the developing institute, were not designed to detect harm. Commonly reported (anecdotal): injection-site irritation with injectable forms; oral capsules draw few complaints.

Storage

Storage: Room temperature
Lyophilized: 24+ months

Pharmacology

Half-life: No published pharmacokinetic data in any species
Bioavailability: Not measured in any species. Docking predicts transport by PEPT1, LAT1 and LAT2 (Khavinson 2022)
Molecular weight: 446.45 Da
Sequence: AEDL (Ala-Glu-Asp-Leu)