Bronchogen and Chonluten are sold for the same organ and come from the same St. Petersburg bioregulator programme. They are not the same molecule, and neither has a published human trial.
Head-to-head
| Bronchogen | Chonluten | |
|---|---|---|
| Molecule | Synthetic tetrapeptide. A 2011 paper writes Ala-Glu-Asp-Leu; another paper that year titles it Ala-Asp-Glu-Leu. No US National Library of Medicine substance record settles it. | Tripeptide Glu-Asp-Gly (EDG), attributed to bronchial epithelium. |
| What has actually been tested | Rats given intermittent nitrogen dioxide for 60 days to produce COPD-like airway damage. Reported histology changes, not a human disease outcome. | One indexed experiment: human THP-1 monocytes at 100 ng/mL. An immune-cell readout, not airway tissue. |
| Human trials | None published. | None registered or published. A 2020 review by the originating group describes patient effects without a trial registration, participant count, or comparator. |
| Evidence tier | Minimal. Animal and cell-culture work from one research network. | Minimal. One experimental paper, co-authored by the concept's originator. |
| Regulatory status | No marketing authorisation. Not named on the WADA Prohibited List. | No marketing authorisation in the US, EU, UK, Canada, or Australia. Not named on the WADA Prohibited List. |
What Bronchogen's papers actually report
Bronchogen is a four-amino-acid peptide. Even the sequence is reported two ways: Ala-Glu-Asp-Leu in a DNA-binding study (Fedoreyeva et al., Biochemistry (Mosc) 2011) and Ala-Asp-Glu-Leu in the title of another paper from the same year (Monaselidze et al., Bull Exp Biol Med 2011). There is no receptor. The proposed mechanism is non-selective DNA binding.
The disease-model work gave rats intermittent nitrogen dioxide for 60 days and reported reversal of goblet-cell hyperplasia, restored ciliated epithelium, less neutrophilic infiltration, and higher secretory IgA and surfactant protein B (Kuzubova et al., Bull Exp Biol Med 2015). Those are rodent histology endpoints.
What Chonluten's paper actually reports
Chonluten is Glu-Asp-Gly. A PubMed search returns one experimental paper, co-authored by Vladimir Khavinson (Avolio et al., Int J Mol Sci 2022). It exposed human THP-1 monocytes to 100 ng/mL. Chonluten raised tyrosine phosphorylation of mitogen-activated kinases and, after a lipopolysaccharide challenge, suppressed TNF and IL-6 and reduced monocyte adhesion to endothelial cells. That says nothing about airway epithelium, mucociliary clearance, or gas exchange.
Claims that EDG improved standard therapy in chronic bronchitis, or raised a physical-performance index at low oxygen, appear in a review by the same group (Khavinson et al., Molecules 2020). The review supplies no trial registration, participant count, comparator, or outcome definition, and the underlying reports are not indexed in PubMed.
What the comparison does not support
Shelving the two names together is a catalog convention. No study has compared them, and no published human trial has tested either one. A vendor listing both for “lung support” is not evidence that they do the same thing, or that either does anything in people.
This page is educational. It describes what has been published and does not recommend using either compound.