Chonluten (EDG): Bronchial Bioregulator Claims Versus the Published Evidence

This is a short article because there is little to report. Chonluten is widely described as a bronchial bioregulator, but the published evidence leads somewhere else, and it is worth setting out exactly what exists.

What Chonluten is

Chonluten is the tripeptide H-Glu-Asp-Gly-OH, abbreviated EDG, with the formula C11H17N3O8 and a molecular weight of about 319.3. The name and sequence are matched in a 2022 cell study (Avolio et al., 2022) and in the group's 2022 review of peptide transport (Khavinson et al., 2022), and the sequence is claimed in a US patent filed by Khavinson and colleagues in 2007 and granted in 2011, which describes it as chemically synthesised.

The tissue association is less settled than its reputation. The bronchial label comes from the developers' tissue mapping, and the 2022 cell study describes Chonluten as derived from respiratory tissue. Yet the group's 2022 review lists the documented activities of EDG as gastroprotective and stress-protective, and gives the bronchoprotective label to a different peptide, Bronchogen (Ala-Glu-Asp-Leu).

The proposed mechanism

The class hypothesis applies: short peptides are proposed to enter cells and nuclei and regulate gene expression by interacting with DNA and histones. For EDG, the support is limited to computer docking, which ranks it among the strongest predicted binders of the amino acid transporter LAT1 and suggests a possible route into cells (Khavinson et al., 2022; Khavinson et al., 2023). The DNA and histone binding experiments behind the class mechanism, in the papers we reviewed, used other peptides.

What the studies show

• Rat gastric ulcer model. A 2012 report describes a peptide coded T-34 in male rats with chemically induced gastric ulcers. PubMed indexes the substance as glutamyl-aspartyl-glycine, and the group later cited the paper as its evidence for EDG. The peptide normalised the synthesis of antioxidant and anti-inflammatory proteins by regulating the corresponding genes (Khavinson et al., 2012). The abstract runs to three sentences; PubMed's indexing lists heat shock protein 70, nitric oxide synthases and the NF-κB subunit RelA among the targets.
• Monocyte and macrophage cell line. An Italian and Russian team, with Khavinson as co-author, tested Chonluten alongside four other Khavinson peptides in THP-1 cells, a human leukaemia monocyte line. All five increased phosphorylation of growth-signalling kinases. In macrophage-differentiated cells challenged with bacterial lipopolysaccharide, the peptides reduced release of TNF and IL-6, and the synthetic peptides reduced monocyte adhesion to activated endothelial cells. In undifferentiated monocytes, Chonluten alone produced a mild TNF release, which the authors read as a tolerance mechanism, and roughly doubled apoptosis compared with the other peptides (Avolio et al., 2022). These are immune cells, not airway epithelium.
• Patent data. The patent describes rats under restraint and osmotic stress, inhibition of enkephalin-degrading enzymes in human serum, and 80 healthy young men exposed to simulated high altitude, reporting better tolerance of low oxygen than in a placebo group. We could not find any of this published in a peer-reviewed journal.

Where the respiratory claims come from

A 2020 review by the group on peptides and COVID-19 calls EDG a bronchoprotector and states that it is effective in bronchopulmonary disease and improved the results of standard therapy in patients with chronic bronchitis (Khavinson et al., 2020). The only reference it gives for those statements is the 2012 rat gastric ulcer paper, whose abstract and indexing describe no respiratory or human data. The group's published bronchial epithelium work, on gene expression and DNA binding in human bronchial cell cultures, used Bronchogen rather than Chonluten (Khavinson et al., 2014).

How strong is the evidence?

Very thin. One rodent study with a three-sentence abstract, one cell line study in non-airway cells, computer modelling and patent data that never reached a journal. Khavinson is an author on all of it, and there is no independent replication. Most importantly for a compound labelled bronchial, we found no published experiment in airway cells, lung tissue or a respiratory disease model, and no registered trial. A researcher interested in the bioregulator hypothesis in bronchial epithelium will find the relevant published data under Bronchogen.

For background on the whole class, including where the tissue mapping comes from, see Bioregulator Peptides: What the Khavinson Research Actually Claims. The same approach is applied to Cardiogen and Cartalax.

References

1. Avolio F, et al. 2022. "Peptides Regulating Proliferative Activity and Inflammatory Pathways in the Monocyte/Macrophage THP-1 Cell Line." International Journal of Molecular Sciences 23(7):3607. PMID 35408963
2. Khavinson VKh, et al. 2012. "Peptidergic regulation of expression of genes encoding antioxidant and anti-inflammatory proteins." Bulletin of Experimental Biology and Medicine 152(5):615-618. PMID 22803148
3. Khavinson V, et al. 2022. "Transport of Biologically Active Ultrashort Peptides Using POT and LAT Carriers." International Journal of Molecular Sciences 23(14):7733. PMID 35887081
4. Khavinson VK, et al. 2023. "Feasibility of Transport of 26 Biologically Active Ultrashort Peptides via LAT and PEPT Family Transporters." Biomolecules 13(3):552. PMID 36979488
5. Khavinson V, et al. 2020. "Peptides: Prospects for Use in the Treatment of COVID-19." Molecules 25(19):4389. PMID 32987757
6. Khavinson VKh, et al. 2014. "Peptide regulation of gene expression and protein synthesis in bronchial epithelium." Lung 192(5):781-791. PMID 25015171
7. Khavinson VKh, et al. 2011. "Peptide substance revealing a stress protective effect, pharmaceutical composition on its base, and the method of its application." US Patent 8,071,556 B2.