Chonluten

A synthetic tripeptide (Glu-Asp-Gly) from the Khavinson bioregulator family, marketed as a bronchial peptide but studied by its developers mainly in gastric-ulcer rats, stress models, and a monocyte cell line.

Also referenced as: Honluten, Khonluten, Glu-Asp-Gly, Glutamyl-aspartyl-glycine, H-Glu-Asp-Gly-OH

Also appears in: Longevity

What is Chonluten?

Chonluten is a synthetic tripeptide with the sequence Glu-Asp-Gly (EDG; glutamyl-aspartyl-glycine, molecular weight about 319 Da), one of the short “cytogen” peptides developed at the Saint Petersburg Institute of Bioregulation and Gerontology under Vladimir Khavinson. In the developers’ own 2014 review table of their peptides it is listed as “Honluten (EDG), regulation of the functions of the respiratory system,” and the same three residues form the C-terminal end of Epitalon (Ala-Glu-Asp-Gly). It appears in the research-peptide market as the “bronchial” or “lung” member of the Khavinson family, usually sold alongside Bronchogen (Ala-Glu-Asp-Leu), even though the published experiments on the tripeptide itself are in gastric, stress, and immune-cell models rather than airway tissue.

How it works

The proposed mechanism is the general Khavinson model: a di- to tetrapeptide small enough to enter cells and the nucleus, where it is said to bind DNA or histones and shift transcription of a tissue-relevant gene set. For EDG specifically, the published mechanistic data are limited to the following.

• Antioxidant and anti-inflammatory gene expression in gastric ulcer (rat) — the developers reported that “peptide T-34” normalized synthesis of antioxidant and anti-inflammatory proteins in a gastric ulcer model by regulating the corresponding genes; Khavinson’s 2014 review identifies this peptide as EDG and states that it lowered mRNA for SOD, TNF-α, and COX-2 in an induced gastric ulcer model in rats, citing the 2012 report as its source (Khavinson et al., Bulletin of Experimental Biology and Medicine, 2012, 152(5):615–618; Khavinson, Advances in Gerontology, 2014, 27(2):257–264, English translation 4(4):337–345)
• Immune-cell signaling and cytokine release (human THP-1 line) — at 100 ng/mL, Chonluten increased THP-1 growth, activated STAT1 phosphorylation without inducing interferon-alpha, reduced TNF-α, IL-6, and IL-17 release from LPS-stimulated macrophage-differentiated cells, and lowered monocyte adhesion to LPS-activated endothelial cells; it was also the only peptide of five that raised the apoptotic fraction, roughly doubling it relative to the others. The paper itself describes Chonluten as “derived from bronchial epithelial cells” but tests no airway cells (Avolio et al., International Journal of Molecular Sciences, 2022, 23(7):3607)
• Stress-protective and c-Fos effects (rat, patent data) — the US patent on the tripeptide describes raised noradrenaline, dopamine, and serotonin in rat cortex with lowered dopamine, serotonin, and histamine in serum, dose-dependent changes in c-Fos-positive hypothalamic neurons after restraint stress, c-Fos induction in pinealocytes under osmotic stress, and in vitro inhibition of serum enkephalinase; the developers’ later reviews summarize this as regulation of c-Fos, HSP70, SOD, COX-2, and TNF-α (US Patent 8,071,556; Khavinson et al., Molecules, 2020, 25(19):4389)
• Cell entry via amino-acid and peptide transporters (in silico) — in the developers’ 2022 LAT1 docking table EDG has the second-highest predicted binding score of 27 ultrashort peptides, and a 2023 follow-up extends this to LAT2 and PEPT1, naming EDG among the most effective predicted ligands; the authors propose these carriers as the route into cells. In the 2022 table EDG is labeled a “gastroprotector” and “stress protector,” citing the 2012 ulcer report and the stress patent, not a respiratory peptide (Khavinson et al., International Journal of Molecular Sciences, 2022, 23(14):7733; Khavinson et al., Biomolecules, 2023, 13(3):552)

Research status

The evidence base is thin, almost entirely from the originating group, and does not include airway tissue.

• Peer-reviewed experimental work: one indexed experimental paper tests the tripeptide directly, the 2022 THP-1 cell-line study co-authored by Khavinson with an Italian group (Avolio et al., International Journal of Molecular Sciences, 2022). Its abstract says Chonluten “inhibited” LPS-driven TNF production, while its results section describes “a slight release” of TNF from monocytes interpreted as a tolerance-like state; the paper does not resolve this and reports no gene-expression data. The 2012 gastric ulcer paper (Khavinson et al., Bulletin of Experimental Biology and Medicine, 2012) is a short report on “peptide T-34” whose sequence is given only in the developers’ later reviews.
• The bronchial-epithelium literature belongs to a different peptide: the frequently cited Lung study of human bronchial epithelial cultures (Ki-67, Mcl-1, p53, NKX2-1, SCGB1A1, FOXA1/2, MUC4, MUC5AC, SFTPA1) and its promoter-methylation follow-up tested the tetrapeptide Ala-Asp-Glu-Leu/Ala-Glu-Asp-Leu, i.e., Bronchogen, not EDG (Khavinson et al., Lung, 2014, 192(5):781–791; Ashapkin et al., Biochemistry (Moscow), 2015, 80(3):310–322). The respiratory patent in the same family (US 7,625,870) also covers Ala-Glu-Asp-Leu. No peer-reviewed study of Glu-Asp-Gly in bronchial or lung tissue is indexed on PubMed as of October 2026.
• Human data: the developers’ 2020 review states that oral EDG is “effective” in COPD and chronic bronchitis with an asthmatic component and improves physical performance under low oxygen partial pressure, but the only reference attached to that paragraph is the group’s own 2012 rat gastric-ulcer report; no trial, registration, sample size, or outcome definition is given (Khavinson et al., Molecules, 2020). The only described human experiment is in the stress-protection patent: 80 healthy men aged 20–22 given peptide by intranasal or intramuscular route at three dose levels, or water for injection as placebo, before a 60-minute simulated 5,000 m hypoxia exposure, with reported improvements in tolerance, heart-rate response, and PWC170; blinding, randomization, and statistics are not described, and the study has not appeared as a peer-reviewed paper.
• Patents and regional status: EP 2667887 B1 (Garmonia Ltd, granted December 2015) claims Glu-Asp-Gly for Helicobacter pylori-associated gastroduodenal disease on the basis of mitochondrial-apoptosis assays in gastric epithelial cells and a cysteamine rat ulcer model; US 8,071,556 (granted December 2011) claims the stress-protective and anti-hypoxic use. In Russia, Honluten is registered as a dietary supplement (an “additional source of peptides”), not as a drug, and its registration card states no indication.
• Registry status: no study of Chonluten, Honluten, or Glu-Asp-Gly is registered on ClinicalTrials.gov, and there is no FDA submission, approval, warning letter, or compounding pathway. No independent laboratory outside the Khavinson network has replicated any EDG finding.

Common dosage forms

Research vendors sell Chonluten as lyophilized powder in vials, most commonly labeled 20 mg per vial and marked for research use only. In Russia and neighboring markets the same peptide is sold under the Honluten name as a dietary supplement in 0.2 g capsules and 0.16 g or 0.3 g tablets, and a separate “Honluten Lingual” sublingual drop product is registered there as well. No pharmaceutical formulation is approved anywhere.

Key considerations

• Regulatory status: no US approval, no clinical development aimed at approval, and no FDA compounding pathway; the Russian dietary-supplement registration and the two patents do not amount to a drug approval. The Research Market status reflects regional supplement registration with no US approval or development program.
• The respiratory attribution rests on the developers’ labeling, not on airway data: The bronchial-epithelium data often attached to this peptide belong to Bronchogen (Ala-Glu-Asp-Leu). For EDG the developers’ own experiments are gastric (ulcer rats, H. pylori assays) and stress/hypoxia related, their 2022 transport review labels it a gastroprotector, and the only indexed experimental paper is a study of immune-cell signaling.
• Evidence gaps: a single cell-line paper with an internal contradiction on TNF, a short 2012 rat report, patent examples that were never peer reviewed, and review claims about COPD and chronic bronchitis that rest on a rat ulcer citation; no pharmacokinetics, no controlled human safety data.
• Safety signals: the only reported adverse-direction finding is the roughly doubled apoptotic fraction in THP-1 cells treated with Chonluten versus other Khavinson peptides; patent toxicity studies in 66 mice, 64 rats (90 days), and 92 guinea pigs (6 months) reported no major toxicity beyond a transient leukocyte rise, but these are unpublished sponsor data.
• Naming confusions: “Chonluten,” “Honluten,” and “Khonluten” are transliterations of the same Russian trade name; the developers’ older papers call the peptide “T-34”; the abbreviation EDG is also the historical name of the endothelial differentiation gene (S1P/LPA) receptor family and should not be used alone in literature searches; some retail guides assign the EDG sequence to Crystagen/Kristagen or to a gastrointestinal product, whereas the developers list Kristagen as Glu-Asp-Pro; and Chonluten should not be conflated with Bronchogen (Ala-Glu-Asp-Leu), the peptide actually studied in bronchial epithelium.