Bronchogen

Dosing from the Literature

Published for the airways: two 100 μg capsules twice a day for 30 days, given with standard treatment to 58 adults with chronic bronchitis with an asthmatic component in one Russian study without a placebo (Khavinson 2014, Molekulyarnaya Meditsina); the Russian supplement label gives one or two capsules once or twice a day for a month (Russian product labeling, 2012). Not published: a placebo-controlled or blinded trial.

One human study has published a dose; no placebo-controlled trial has. The rows below give that study's regimen, the Russian supplement label's directions and the developers' rat dose; no human dose by injection has been published. This is not FDA-approved prescribing.

What It Is

Bronchogen is a synthetic short peptide developed within the Khavinson peptide-bioregulator program at the St. Petersburg Institute of Bioregulation and Gerontology. The molecule is a tetrapeptide (a chain of 4 amino acids) with the sequence Ala-Glu-Asp-Leu (AEDL) and an approximate molecular weight of 446 daltons; some of the program's own papers write it Ala-Asp-Glu-Leu (ADEL) instead (Monaselidze 2011; Khavinson 2014, Lung, PMID 25015171). Structurally it is a close relative of several other Khavinson tissue-specific short peptides — it shares the N-terminal "Ala-Glu-Asp" acidic core with Epithalon (AEDG, pineal), Cortagen (AEDP, cortex), Cardiogen (AEDR, heart), and the cartilage peptide Cartalax, with a different C-terminal residue proposed to confer tissue specificity.

Bronchogen is presented as the short-peptide successor to an earlier polypeptide complex extracted from calf airway tissue; no record of a product named Broncholin, or of its clinical use, was found in PubMed or Europe PMC. The Khavinson program's central claim is that the bioregulatory activity of tissue extracts can be reproduced by defined short peptides (2–4 amino acids) designed from the amino-acid composition of those extracts (Khavinson 2002, PMID 12374906). Bronchogen (AEDL) is the short peptide the program assigns to the bronchial extract. Unlike Broncholin, Bronchogen is a chemically defined synthetic peptide; the developers' patent makes it by classical synthesis in solution and purifies it by HPLC to 98% peptide content (Khavinson 2005, RU patent 2255757).

Commercially, Bronchogen is distributed in two formats: as an oral capsule holding 100 μg of the peptide (Russian product labeling, 2012) and as a lyophilized research peptide in 20 mg vials, sold by research-chemical vendors. The oral-capsule presentation is sold as a dietary supplement (BAD — "biologically active additive") in Russia; the injectable lyophilized powder is research-only internationally.

In the Western optimization community, Bronchogen is used primarily by individuals seeking respiratory-tissue support in the context of a broader Khavinson bioregulator stack. It is not a bronchodilator, inhaled corticosteroid, leukotriene modifier, or biologic — and has no place in the evidence-based management of asthma, COPD, or any respiratory disease. Mainstream Western pulmonology has no awareness of, or use for, the compound.

Who Khavinson was, and what his record supports →

Mechanism of Action

The Khavinson group proposes that short bioregulator peptides act as sequence-specific DNA-binding molecules — short enough to enter cells and nuclei (the group's later papers model entry through LAT and PEPT transporters), and able to bind DNA in the major groove at the promoters of tissue-specific genes (Khavinson 2014, Lung, PMID 25015171; Khavinson 2021, PMID 34834147). Bronchogen's mechanism is described within this epigenetic-bioregulator framework. Importantly, this is a mechanism proposed by a single research group; no independent structural study of it was found. The group's later work models a carrier route instead: in a 2023 computer-docking study, AEDL was among the peptides the authors rank as the most effective ligands of the LAT1, LAT2 and PEPT1 transporters, which they say could carry such peptides into cells or be blocked by them; no uptake was measured (Khavinson 2023, PMID 36979488).

• Direct DNA interaction (proposed) — Fedoreyeva and colleagues (Fedoreyeva 2011, PMID 22117547) showed that fluorescently labeled epithalon, pinealon and testagen enter the nucleus of HeLa cells; AEDL was not among the labeled peptides. Monaselidze et al. (2011, Bulletin of Experimental Biology and Medicine 150:375-377) reported that AEDL alters the thermostability profile of DNA — interpreted by the authors as direct binding to DNA bases, with no preference for adenine-thymine or guanine-cytosine pairs. The group's computer-docking models place AEDL on the DNA sequence CTCC (Khavinson 2016, PMID 27909961), and its spectroscopy work points to binding in the major groove at guanine N7 (Khavinson 2014, Lung, PMID 25015171).
• Bronchial epithelial differentiation — Khavinson, Linkova and colleagues (Bull Exp Biol Med 2012, 153(1):148-151) described tissue-specific stimulation of cell differentiation by short peptides in aged cell cultures; AEDL is reported to promote differentiation markers in bronchial epithelial cell models.
• Mucins and ciliated cells — In human bronchial-epithelium cultures, AEDL is reported to activate the mucin genes MUC4 and MUC5AC and the surfactant gene SFTPA1 (Khavinson 2014, Lung, PMID 25015171), and in a rat COPD model a month of Bronchogen restored ciliated cells and removed goblet-cell hyperplasia (Kuzubova 2015, PMID 26468022). No study of AEDL and cilia structural proteins or tight-junction proteins (claudins, occludin, ZO-1) was found.
• Survival markers — In bronchial-epithelium cultures, AEDL is reported to change levels of the anti-apoptotic protein Mcl-1 and of p53, with the strongest rise in Ki67 and Mcl-1 in late-passage cultures (Khavinson 2014, Lung, PMID 25015171). No study of oxidative-stress markers or apoptosis in bronchial cells exposed to AEDL under oxidant challenge was found.
• Immune / cytokine modulation — Gumen, Kozinets, Shanin, Malinin, Rybakina (2006, Bull Exp Biol Med 142(3):360-362, PMID 17426849) described lymphocyte-activating-factor production by mouse macrophages under the influence of three short Khavinson peptides — Vilon, Epithalon and Cortagen; AEDL was not among them.
• Tissue specificity (claimed) — The group's tetrapeptides with the Ala-Glu-Asp core differ in their last residue, and the group assigns each to an organ: AEDG (Epithalon) to the pineal gland and retina (Khavinson 2002, PMID 12374906), AEDR (Cardiogen) to the cardiovascular system and AEDL to the lungs (Khavinson 2021, PMID 34834147). No study was found that tests whether the last residue sets the target tissue. In one Russian-language explant study from the same program, each of four peptides stimulated growth of its matching tissue from young (3-week) and old (18-month) rats at 0.05 ng/mL: bronchogen in lung, cardiogen in heart, prostamax in prostate and pancragen in pancreas explants (Zakutskii 2006, PMID 17152728).
• Systemic-epigenetic framing (Khavinson 2021 review) — Khavinson, Popovich, Linkova, Mironova, Ilina (Molecules 2021, 26(22):7053, PMID 34834147) published a systematic review of peptide regulation of gene expression, framing short-peptide bioregulators as epigenetic modulators acting on target genes' promoter methylation, histone status, and chromatin accessibility. For AEDL itself, the evidence behind each term is narrower. In aging human bronchial-epithelium cultures, promoter methylation of NKX2-1 and SCGB1A1 changed in step with their expression, which the authors suggest may underlie AEDL's effect on those genes, while the FOXA1, SCGB3A2 and SFTPA1 promoters were unaffected by age or AEDL even though their expression changed (Ashapkin 2015, PMID 25761685). The histone binding reported for AEDL comes from fluorescence tests in which it was one of six short peptides that bound wheat histones H1, H2B, H3 and H4 (Fedoreyeva 2013, PMID 23581987), and a Tbilisi DNA-melting study reports that the peptide unfolded nucleosome cores in rat-liver chromatin stripped of histone H1, releasing about 15% of the core DNA (Monaselidze 2011, Georgian Med News, PMID 21685526).

Limitation: the proposed mechanism remains primarily a hypothesis from one research program: every DNA- and gene-level study of AEDL cited above includes Khavinson or his co-authors. Structural biology validation (crystal structures, NMR binding footprints, independent ChIP-seq replication) at the level of what is available for well-characterized sequence-specific DNA binders is not available for Bronchogen.

What the Research Shows

The published Bronchogen literature is small and comes almost entirely from Russian and Georgian teams, most of it from Khavinson's group or its co-authors. One Russian study, without a placebo, added the capsules to standard treatment in 58 adults with chronic bronchitis (Khavinson 2014, Molekulyarnaya Meditsina); the rest is cell culture and animal work, and no placebo-controlled human trial of the synthetic tetrapeptide is indexed in PubMed or other Western databases.

• DNA thermostability (Monaselidze 2011) — Reported a 3.1 °C rise in the melting temperature of calf-thymus and mouse-liver DNA with AEDL, within a narrow band of peptide-to-base-pair ratios (0.01–0.055) and no further change above it. Biophysical foundation for the direct-DNA-binding hypothesis.
• Nuclear penetration (Fedoreyeva 2011, PMID 22117547) — Fluorescein-labeled epithalon, pinealon and testagen were tracked into the nuclei of HeLa cells; AEDL itself was not labeled or tracked. In the same paper's fluorescence-quenching tests, unlabeled bronchogen bound preferentially to DNA oligonucleotides containing CTG, one of the CNG sites where cytosine methylation occurs.
• Tissue-specific differentiation (Khavinson/Linkova 2012, Bull Exp Biol Med 153:148-151) — Described differentiation-promoting effects of short peptides in aged tissue cultures; AEDL-class peptides promoted bronchial-specific differentiation markers.
• Bronchial-epithelium gene expression (Khavinson 2014, Lung, PMID 25015171) — In human embryonic bronchial-epithelium cultures at passages 1, 7 and 14, the group reports that the peptide (written in this paper as Ala-Asp-Glu-Leu, "ADEL") raised the proliferation markers Ki67 and Mcl-1 most in the late-passage "old" cultures, changed the expression of the differentiation genes NKX2-1, SCGB1A1, SCGB3A2, FOXA1 and FOXA2, and activated MUC4, MUC5AC and SFTPA1, genes whose low expression the authors link to lung disease.
• Rat COPD model (Kuzubova 2015; Titova 2017) — In rats given 60 days of intermittent nitrogen dioxide to model chronic obstructive pulmonary disease, a team at the Research Institute of Pulmonology of Pavlov First St. Petersburg State Medical University, with no Khavinson co-author, reported that a month of Bronchogen removed signs of airway remodeling (goblet-cell hyperplasia, squamous metaplasia, lymphocytic infiltration and emphysema), restored ciliated cells, raised secretory IgA and normalized the inflammatory cells and cytokines in lung lavage fluid (Kuzubova 2015, PMID 26468022). A Russian-language follow-up from the same team also reports a rise in surfactant protein B (Titova 2017, PMID 30199201). Neither abstract gives the dose or the route.
• Cytokine modulation (Gumen 2006, PMID 17426849) — Vilon, Epithalon and Cortagen had opposite effects on lymphocyte-activating-factor production by macrophages from young and old mice; AEDL was not among the peptides tested.
• Peptide gene-regulation review (Khavinson 2021, PMID 34834147) — Systematic review of Khavinson-program peptide bioregulator literature, including AEDL, within the broader epigenetic-modulator framework. Comprehensive reference for the program's claims and evidence base.
• Parent-extract era — The indexed papers on airway-tissue peptide extracts are early-1990s animal studies from Khavinson's group: peptides isolated from tracheal mucosa reduced bleomycin-induced lung fibrosis in rats (Khavinson 1994, PMID 7700699) and were protective in acute oxygen-induced lung injury in mice and rats (Khavinson 1992, PMID 1480431). No clinical report on such an extract was found in PubMed or Europe PMC, and none of this work tests AEDL.
• Plant-biology corollary (Kononenko & Fedoreyeva) — AEDL has been reported to stimulate root and shoot growth in tobacco (Nicotiana tabacum), a plant result the Khavinson group sets beside its view that short peptides were among the earliest signaling molecules (Khavinson 2021, PMID 34834147). In the 2024 study by Kononenko and Fedoreyeva, tobacco seedlings grown with AEDL at 10⁻⁷ M had 3.24 times more glutathione in their roots than controls and better-developed root systems; glutathione itself was not added to the growth medium (Kononenko 2024, PMID 39796141).
• Clinical bronchial disease — one small study — One Russian study without a placebo reports rises in lung volumes from before treatment after 30 days of capsules beside standard treatment in 58 adults with chronic bronchitis with an asthmatic component (Khavinson 2014, Molekulyarnaya Meditsina; see Human Data). No published randomized, placebo-controlled trials of synthetic AEDL (Bronchogen) for asthma, COPD, bronchiectasis, post-infectious recovery, or respiratory long-COVID exist in English-indexed peer-reviewed journals.

Human Data

The synthetic tetrapeptide Bronchogen (AEDL) has been tested in people in one published study, in Russian, by Khavinson's group: 58 adults aged 34–65 with chronic bronchitis with an asthmatic component, in remission, took two 100 μg capsules twice a day for 30 days beside standard treatment, and 20 had standard treatment alone, the groups split by what the authors call stratified randomization, with no placebo. The authors report that vital capacity, total lung capacity and forced vital capacity rose from their pre-treatment values with the capsules, but only forced vital capacity on standard treatment alone, and that no side effects were seen (Khavinson 2014, Molekulyarnaya Meditsina). The other accessible human-use information consists of:

• Broncholin historical clinical experience (not AEDL) — The polypeptide parent extract was used observationally in Soviet-era pulmonology. Case-series and single-arm reports described symptomatic improvements in chronic bronchitis and post-infectious respiratory recovery. These reports predate modern randomized-trial methodology, are largely untranslated from Russian, and apply to the crude extract, not the defined AEDL tetrapeptide.
• Khavinson supplement-line post-market observations — The Khavinson bioregulator product line has been marketed in Russia as a dietary supplement since the early 2000s; observational and clinician-reported experience exists but does not meet the evidentiary standard of a controlled human trial. A 2020 review by Khavinson's group states that Bronchogen and Chonluten taken by mouth are effective in chronic obstructive pulmonary disease and in chronic bronchitis with an asthmatic component, but that passage cites no human study (Khavinson 2020, Molecules, PMID 32987757).
• Community self-experimentation — Longevity-focused users have self-reported taking Bronchogen in short oral or injected courses for "respiratory tissue support" alongside other bioregulators. These are anecdotal; selection bias, concurrent-use confounding, and placebo effects dominate.
• No WADA-relevant ergogenic data — There is no published evidence that Bronchogen affects exercise performance, VO₂ max, FEV1 in athletes, or anti-doping-relevant endpoints.
• No pharmacokinetics in humans — No human PK/ADME data for AEDL are published. The general Khavinson assumption — that short peptides are absorbed orally and reach tissues at low nanomolar concentrations — rests on animal studies, not on validated human exposure-response data.

In the context of Western evidence-based medicine, Bronchogen would be described as an experimental compound with no established human efficacy for any indication.

Position Within Evidence-Based Respiratory Medicine

Asthma, COPD, bronchiectasis, and allergic airway disease each have mature evidence-based management pathways. Asthma treatment is structured around inhaled corticosteroid + long-acting β2 agonist combinations, leukotriene modifiers, long-acting muscarinic antagonists in more severe disease, and biologics (omalizumab, mepolizumab, reslizumab, benralizumab, dupilumab, tezepelumab) for type 2 and allergic phenotypes. COPD management centers on smoking cessation, inhaled therapy (LAMA, LAMA+LABA, triple therapy in appropriate patients), pulmonary rehabilitation, oxygen where indicated, and surgical or bronchoscopic intervention in selected cases. Bronchiectasis care involves airway clearance, targeted antimicrobial therapy, and management of exacerbations. Each of these pathways has extensive RCT support and outcome data.

Bronchogen sits outside all of this. It has no respiratory-guideline recognition, no biomarker-validated effect, and no human exacerbation / FEV1 / quality-of-life data. No study has tested Bronchogen in place of evidence-based care for asthma, COPD or bronchiectasis; the one clinical study added it to standard treatment (Khavinson 2014, Molekulyarnaya Meditsina). Adding a research-grade peptide on top of standard care may be a research-chemical choice, but it is not a respiratory therapeutic in any defensible sense.

The developers recommend it by mouth for chronic respiratory disease and for keeping respiratory function in older age groups (Khavinson 2014, Molekulyarnaya Meditsina), and in longevity circles it is taken in courses for "respiratory tissue support" alongside other Khavinson peptides. No study has tested it in healthy older people.

Reconstitution & Storage

Research sellers list Bronchogen in 20 mg vials of lyophilized powder. The oral supplement capsule is pre-formulated and does not require reconstitution.

• Reconstitution — Online reconstitution guides describe adding bacteriostatic water slowly down the vial wall at a 45° angle, then swirling gently until fully dissolved rather than shaking.
• Storage (powder) — One research seller lists a 36-month shelf life for the 20 mg vial; it gives no storage temperature.
• Oral-capsule product — The Russian label lists storage in a dry place, away from light, at 2–25°C, and a 5-year shelf life (Russian product labeling, 2012).

→ Calculator — vial-to-syringe math

Side Effects & Risks

• Reported tolerability — In the one clinical study, no side effects were seen in 58 adults who took two 100 μg capsules twice a day for 30 days (Khavinson 2014, Molekulyarnaya Meditsina), and the Russian label lists none (Russian product labeling, 2012). No larger or longer human safety study has been published.
• Toxicology — The developers' patent describes injected toxicity tests: single doses up to 5 mg/kg in mice, and 1 μg/kg to 1 mg/kg daily for 90 days in rats and for 6 months in guinea pigs, with no toxic effects reported apart from a rise in white blood cells in guinea pigs given 1 μg/kg for 6 months (Khavinson 2005, RU patent 2255757). No reproductive or genotoxicity study, and no human toxicology, has been published.
• Not a bronchodilator — No human study has tested Bronchogen for quick relief of airway narrowing, or in place of inhaled β2 agonists, corticosteroids, leukotriene modifiers or biologics in asthma or COPD; the one clinical study added it to standard treatment (Khavinson 2014, Molekulyarnaya Meditsina).
• Allergy / hypersensitivity — The Russian label lists intolerance of the capsule's ingredients as a contraindication (Russian product labeling, 2012); no published study reports an allergic reaction to Bronchogen.
• Purity / source concerns — The 20 mg vials are sold as research chemicals, labeled for research use only, so no regulator vouches for their identity, purity or dose.
• Pregnancy / lactation — No human safety data; the Russian label contraindicates the capsules in pregnancy and breastfeeding (Russian product labeling, 2012).
• Pediatric use — No safety data in children: the one clinical study enrolled adults aged 34–65 (Khavinson 2014, Molekulyarnaya Meditsina), and the Russian label's directions are for adults (Russian product labeling, 2012).
• Drug interactions — No interaction study, and no pharmacokinetic study, has been published.
• WADA status — Bronchogen is not specifically named on the 2026 WADA Prohibited List. Short-peptide bioregulators generally are not classified in current S2 categories; the List’s S0 clause covers substances no other section names and no government has approved for human therapeutic use (WADA Prohibited List 2026).
• Theoretical epigenetic concerns — If AEDL acts on DNA and gene promoters, as the Khavinson group proposes (Khavinson 2021, PMID 34834147), effects on unintended genes are a theoretical risk. Whether Bronchogen reaches target tissue at concentrations sufficient to act on DNA in humans is unknown.

Bloodwork & Monitoring

No trial, label or guideline sets monitoring for Bronchogen. The one human study followed symptoms, sputum under the microscope and lung function (vital capacity, total lung capacity, forced vital capacity) over 30 days (Khavinson 2014, Molekulyarnaya Meditsina). The rat studies measured cells, cytokines, secretory IgA and surfactant protein B in lung-lavage fluid (Kuzubova 2015, PMID 26468022; Titova 2017, PMID 30199201), and the developers' toxicity tests measured blood counts and blood chemistry, finding a rise in white blood cells in guinea pigs after 6 months of daily injections (Khavinson 2005, RU patent 2255757).

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References

1. Monaselidze JR, Khavinson VKh, Gorgoshidze MZ, Khachidze DG, Lomidze EM, Jokhadze TA, Lezhava TA. Effect of the peptide Bronchogen (Ala-Asp-Glu-Leu) on DNA thermostability. Bulletin of Experimental Biology and Medicine. 2011;150(3):375-377. PMID: 21240358. DOI: 10.1007/s10517-011-1146-x.
2. Fedoreyeva LI, Kireev II, Khavinson VKh, Vanyushin BF. Penetration of short fluorescence-labeled peptides into the nucleus in HeLa cells and in vitro specific interaction of the peptides with deoxyribooligonucleotides and DNA. Biochemistry (Moscow). 2011;76(11):1210-1219. PMID: 22117547.
3. Khavinson VKh, Linkova NS, Polyakova VO, Kheifets OV, Tarnovskaya SI, Kvetnoy IM. Peptides tissue-specifically stimulate cell differentiation during their aging. Bulletin of Experimental Biology and Medicine. 2012;153(1):148-151. PMID: 22808515.
4. Gumen AV, Kozinets IA, Shanin SN, Malinin VV, Rybakina EG. Production of lymphocyte-activating factors by mouse macrophages during aging and under the effect of short peptides. Bulletin of Experimental Biology and Medicine. 2006;142(3):360-362. PMID: 17426849.
5. Khavinson VKh, Popovich IG, Linkova NS, Mironova ES, Ilina AR. Peptide Regulation of Gene Expression: A Systematic Review. Molecules. 2021;26(22):7053. PMID: 34834147. DOI: 10.3390/molecules26227053.
6. Khavinson VKh. Peptides and ageing. Neuroendocrinology Letters. 2002;23(Suppl 3):11-144. PMID: 12374906. (Program-level review of the Khavinson short-peptide bioregulator framework.)
7. Morozov VG, Khavinson VKh. Natural and synthetic thymic peptides as therapeutics for immune dysfunction. International Journal of Immunopharmacology. 1997;19(9-10):501-505. PMID: 9637345. (Foundational Khavinson-program peptide therapy context.)
8. FDA. Bulk Drug Substances Nominated for Use in Compounding Under Section 503A of the FD&C Act (503A categories list), versions updated April 15, April 22 and May 14, 2026. fda.gov/media/94155/download. Read October 3, 2026. (Notice that 12 peptides would leave Category 2 because their nominations were withdrawn; their removal; GHK-Cu, except injectable, back in Category 1.)
9. Khavinson VK, Linkova NS, Rudskoy AI, Petukhov MG. Feasibility of Transport of 26 Biologically Active Ultrashort Peptides via LAT and PEPT Family Transporters. Biomolecules. 2023;13(3):552. PMID: 36979488.
10. Khavinson VK, Lin'kova NS, Tarnovskaya SI. Short Peptides Regulate Gene Expression. Bulletin of Experimental Biology and Medicine. 2016;162(2):288-292. PMID: 27909961.
11. Khavinson VKh, Tendler SM, Vanyushin BF, Kasyanenko NA, Kvetnoy IM, Linkova NS, Ashapkin VV, Polyakova VO, Basharina VS, Bernadotte A. Peptide regulation of gene expression and protein synthesis in bronchial epithelium. Lung. 2014;192(5):781-791. PMID: 25015171.
12. Zakutskiĭ AN, Chalisova NI, Ryzhak GA, Aniskina AI, Filippov SV, Zeziulin PN. The tissue-specific effect of synthetic peptides-biologic regulators in organotypic tissues culture in young and old rats. Advances in Gerontology. 2006;19:93-96. PMID: 17152728. (In Russian.)
13. Ashapkin VV, Linkova NS, Khavinson VKh, Vanyushin BF. Epigenetic mechanisms of peptidergic regulation of gene expression during aging of human cells. Biochemistry (Moscow). 2015;80(3):310-322. PMID: 25761685.
14. Fedoreyeva LI, Smirnova TA, Kolomijtseva GY, Khavinson VKh, Vanyushin BF. Interaction of short peptides with FITC-labeled wheat histones and their complexes with deoxyribooligonucleotides. Biochemistry (Moscow). 2013;78(2):166-175. PMID: 23581987.
15. Monaselidze J, Gorgoshidze M, Jokhadze T, Gaiozishvili M, Lezhava T. Influence of tetrapeptide on chromatin thermostability. Georgian Medical News. 2011;(194):64-66. PMID: 21685526.
16. Kuzubova NA, Lebedeva ES, Dvorakovskaya IV, Surkova EA, Platonova IS, Titova ON. Modulating Effect of Peptide Therapy on the Morphofunctional State of Bronchial Epithelium in Rats with Obstructive Lung Pathology. Bulletin of Experimental Biology and Medicine. 2015;159(5):685-688. PMID: 26468022.
17. Titova ON, Kuzubova NA, Lebedeva ES, Preobrazhenskaya TN, Surkova EA, Dvorakovskaya IV. Antiinflammatory and regenerative effect of peptide therapy in the model of obstructive lung pathology. Rossiiskii Fiziologicheskii Zhurnal imeni I.M. Sechenova. 2017;103(2):201-208. PMID: 30199201. (In Russian.)
18. Kononenko NV, Fedoreyeva LI. Peptide AEDL and Glutathione Stimulates Root Development Nicotiana tabacum. International Journal of Molecular Sciences. 2024;26(1):289. PMID: 39796141.
19. Khavinson V, Linkova N, Dyatlova A, Kuznik B, Umnov R. Peptides: Prospects for Use in the Treatment of COVID-19. Molecules. 2020;25(19):4389. PMID: 32987757.
20. Khavinson VKh, Ryzhak GA, Linkova NS, Ashapkin VV, Drobintseva AO, Basharina VS, Vanyushin BF. Prospects of tetrapeptide application in treatment of chronic bronchitis: molecular mechanisms. Molekulyarnaya Meditsina. 2014;(6):14-20. cyberleninka.ru/article/n/perspektivy-primeneniya-tetrapeptida-v-lechenii-hronicheskogo-bronhita-molekulyarnye-mehanizmy. Read October 4, 2026. (In Russian, with an English abstract; bronchial cell cultures and a 78-patient clinical study of the capsules.)
21. Khavinson VKh, Grigoriev EI, Ryzhak GA, Ryadnova IYu. Peptide compound restoring the function of respiratory organs. Russian patent RU 2255757 C1; July 10, 2005 (filed June 22, 2004). US counterpart: US 7,625,870 B2, December 1, 2009. patents.google.com/patent/RU2255757C1. Read October 4, 2026. (In Russian; the developers' patent on the tetrapeptide Ala-Glu-Asp-Leu.)
22. Bronchogen® capsules 0.2 g (Russian dietary supplement): product instructions approved by the manufacturer, October 17, 2012, as reproduced in the RLS drug encyclopedia. rlsnet.ru/baa/bronxogen-32631. Read October 4, 2026. (In Russian.)
23. World Anti-Doping Agency. Prohibited List 2026 (in effect January 1, 2026). S0, Non-approved substances. wada-ama.org/sites/default/files/2025-09/2026list_en_final_clean_september_2025.pdf. Read October 3, 2026.

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