Bronchogen (AEDL): two sequences, no human data, and what is left

Two sequences answer to the name Bronchogen, and they weigh the same

What the database holds: the compound record carrying the name Bronchogen is CID 11690869, with CAS number 857267-12-0 attached to the same record. Its deposited structure reads Ala-Glu-Asp-Leu from the free amine to the free acid.

How we know that rather than assuming it: we decoded the record's own structure string residue by residue instead of trusting the synonym printed on it, and the systematic chemical name agrees, ordering the glutamate side chain ahead of the aspartate one. A label can be wrong. A deposited structure is the thing the label is supposed to describe.

What the most substantive paper calls it: Ala-Asp-Glu-Leu, ADEL. That is the spelling used in the abstract and throughout the only study of this peptide published in a mainstream international respiratory journal (Khavinson, 2014), and the 2011 calorimetry paper puts Ala-Asp-Glu-Leu in its title (Monaselidze, 2011). Both carry Khavinson as an author, so this is not one group correcting another. It is one research program printing two different molecules under one name.

Why that is more than a typographical slip: the ADEL ordering exists in the same chemical database as its own compound, CID 11247825, and a synonym request on that record returns nothing, so it does not answer to the name Bronchogen. The two are positional isomers with the second and third residues swapped.

The consequence a buyer meets first: mass cannot separate them. Two molecules with identical formulas and identical molecular weights are indistinguishable on any document that reports a weight, which is most of what a certificate of analysis puts in front of a reader. Telling them apart needs a method that resolves the order of the residues, and a purity percentage is not one, for the same reason purity never establishes identity.

What it does to every claim further down this page: when a paper reports that this peptide did something to bronchial cells, the four letters it printed are worth reading before the result is. The DNA-binding work and the gene-expression work on this page were not necessarily done on the same molecule, and no source we found addresses the discrepancy or explains it.

One claim we are deliberately not making: that this is unusual among the bioregulators. We established it for this compound against retrieved records. We did not audit the rest of the series for the same defect, so we have nothing to say about whether it is rare or routine.

Has Bronchogen been tested in people?

No. Not once, in anything we could retrieve, and this belongs at the top of a page about this compound rather than in a footnote at the bottom of it.

What we ran, on 4 August 2026: PubMed's clinical trial publication filter returns zero records for bronchogen and zero for AEDL. The same filter returns 329 for semaglutide on the same run, which is the control showing the filter answers when there is something to answer with.

The one registry hit, and why it is not one: ClinicalTrials.gov returns exactly one study for the term bronchogen. Opening it settles the question: NCT00746759 is an airway epithelium gene expression study in lung cancer, its listed intervention is a biomarker device, and the peptide has no part in it. The same registry returns 757 studies for semaglutide, so a real count of one here means one, not a broken query.

What that leaves the record made of: every human-relevant result on this molecule is a cell culture. Every whole-organism result is a rat or a tobacco plant. There is no exposure in a person, no measured blood level, no safety population and no clinical outcome anywhere on this page, because none exists to put here.

Why the language around it reads otherwise: the vocabulary attached to this peptide is clinical, because the models are. Chronic obstructive pulmonary disease, bronchial epithelium, secretory immunoglobulin A: those terms are accurate descriptions of what was measured in a rat lung and in a dish of cells, and they carry the sound of a clinic into a record that has never been inside one.

What happened in the rat model of lung disease?

The model, stated first because it decides how to read everything after it: chronic obstructive pulmonary disease was induced in rats by 60 days of intermittent exposure to nitrogen dioxide (Kuzubova, 2015). That is a chemical injury model in a rodent, and it is where the COPD vocabulary attached to this compound comes from.

What that paper reports: after one month of the peptide, the remodeling changes typical of the model were eliminated, listed as goblet cell hyperplasia, squamous metaplasia, lymphocytic infiltration and emphysema, along with restoration of ciliated cells. Secretory immunoglobulin A, a local immunity marker, went up, and the cell composition and pro-inflammatory cytokine profile of the bronchoalveolar space normalized.

The companion study, and the two things we have to say about it: a 2017 paper from the same group ran the same nitrogen dioxide model and measured bronchoalveolar lavage cell composition, a cytokine and enzyme profile, secretory immunoglobulin A and surfactant protein B (Titova, 2017). It is published in Russian with an English abstract, and it carries a PubMed record and no DOI at all. Both facts are printed here rather than tidied away, because a reader who tries to follow that citation needs to know what they will meet.

No amount appears on this page, and that is not an omission: neither rat abstract states how much peptide the animals received, and neither full text was reachable to us. A number we cannot source is a number we do not print, and a rodent number would not transfer to a person in any case, which is the same trap as reading a mouse figure across to a human body.

The earliest result on this compound: a 2006 Russian-language report used explants from the heart, lungs, prostate and pancreas of 3-week-old and 18-month-old rats, and reports a stimulating effect at an effective concentration of 0.05 ng/ml in the matching tissue (Zakutskii, 2006). That figure is a concentration in a culture medium bathing rat tissue outside the animal. The same abstract closes by saying these peptides can be used in clinical practice, which is the authors asserting a conclusion their experiment did not test, so we report the experiment and leave the assertion where we found it.

How is Bronchogen different from the other Khavinson peptides?

By sequence preference, in one experiment: a 2011 study measured how several of these peptides quench the fluorescence of labeled DNA fragments, and reports that epithalon, testagen and pinealon seem to prefer sequences containing CAG while bronchogen prefers sequences containing CTG (Fedoreyeva, 2011). The paper hedges that finding with the word "seem" and we keep the hedge, because it is the authors' own confidence level and not ours to raise.

A precision worth making about that paper: its famous half, peptides entering the nucleus of living HeLa cells, used three other peptides and not this one. Bronchogen appears in the binding half, which is a cell-free measurement on oligonucleotides. Those are two different experiments in one document, and only the second one involves this molecule.

By tissue, in another: a 2012 paper ran three peptides against three cell types in a single design, pancragen in pancreatic cells, bronchogen in bronchial epithelial cells and vesugen in fibroblasts, using CXCL12 and Hoxa3 as the bronchial readouts, with the effect more pronounced in aged cultures (Khavinson, 2012).

What those two results are worth: they are the clearest separation between this compound and its siblings that the primary literature offers, and they are a binding preference in a tube and a transcript difference in a dish. Neither one is a claim about what happens in a body.

The concentration problem sitting under the whole series, and it is countable rather than an impression: of the 15 journal papers cited on this page, 6 appear in the same two journals, Bulletin of Experimental Biology and Medicine and Biochemistry (Moscow), and 12 carry either Khavinson or Fedoreyeva as an author. Count the papers and it reads as replication. Read the author lists and it reads as one research program, which is a different thing and a weaker one.

Is there any evidence for taking Bronchogen by mouth?

No measurement of it, in anything we retrieved. Two documents get read as though there were, and this section exists to show what each one actually is.

The first, and the reason this page was slow to write: a 2020 review in Molecules, with Khavinson among its authors, states in its full text that oral administration of two of these peptides, one of them AEDL, is "effective for the treatment of bronchopulmonary pathology", naming chronic obstructive pulmonary disease and chronic bronchitis with an asthmatic component (Khavinson, 2020). That sentence is a human treatment claim. It sits in a review, its DOI resolves, its metadata is correct and the journal is indexed, and we could not retrieve any primary human trial underneath it.

Why we are showing it to you instead of quietly leaving it out: it would pass a citation check without difficulty. The reference is real in every mechanical sense a script can test, and a script cannot tell that the evidence behind the sentence is missing. A reader will meet that claim somewhere, probably without the review attached, and the useful thing we can do is name the document it comes from and say what we found when we went looking for the trial behind it, which was nothing.

The second document, which is a computation: a 2023 modeling paper docked 26 ultrashort peptides into transporter structures and scored them. AEDL ranked 20th of 26 at LAT1, 22nd at LAT2, 6th at PEPT1 and 22nd at PEPT2 by the software's scoring function (Khavinson, 2023). If oral absorption is discussed at all, this is the only retrievable basis for it, and nobody swallowed anything to produce these numbers.

What is missing between those two documents: everything. A docking score is a prediction about whether a molecule fits a transporter's binding site, several steps short of showing it crosses a gut wall, and several more short of showing it reaches a lung. The compound with the thinnest record still needs the same chain of evidence as any other molecule whose development stopped early, and here the chain has one modelled link and no measured ones.

Why is the newest research on this peptide about tobacco roots?

Because that is where the work went. Every primary paper we retrieved with a date after 2017 is either about a tobacco plant or is a computation, which means the lung research on this compound stops in 2017 and nothing has picked it up since.

Where the plant line starts: a 2017 paper put epitalon, bronchogen and vilon into tobacco callus culture and measured expression of the CLE, KNOX1 and GRF gene families (Fedoreyeva, 2017). It prints the sequence as Ala-Glu-Asp-Leu, placing it on the AEDL side of the naming problem.

• 2022, root architecture under salt. AEDL at 10 to the minus 7 molar elongated tobacco root cells, and when 150 mM sodium chloride distorted root development, the peptide together with the salt gave normal roots. Labeled peptide localized to the elongation and root hair zones (Fedoreyeva, 2022).
• 2024, antioxidant chemistry. Growing tobacco with AEDL raised glutathione content by 3.24 times, with a more developed root system (Kononenko, 2024).
• 2025, autophagy. AEDL induced autophagy and programmed cell death in root cells, shown by the autophagy marker ATG8 and cytochrome c, with ATG8 expression up and TOR expression down (Lazareva, 2025). This is the most recent primary paper on this molecule in any database we searched.

How we checked that last claim rather than asserting it: we read every newer title-and-abstract hit PubMed returns for AEDL. The ones dated after November 2025 are unrelated records where those four letters mean something else entirely, in breast cancer imaging, fish toxicology and agricultural land use. Checked 4 August 2026.

What the plant work does not mean: a peptide that acts on a root is not thereby inert in a lung, and none of these papers is evidence against the cell work above. It is a statement about where the effort has gone, and a reader deciding what this molecule is should know that the answer the literature is currently pursuing is about root meristems.

Is Bronchogen approved or registered anywhere?

Not in any database we were able to query, and there are two we could not, so read this as a report of what we checked rather than a statement about the world.

The retrieved zeros, each with a working control: the US regulator's approvals database returns no match for the substance name bronchogen while returning a record for semaglutide, its labeling database does the same, and the national dietary supplement label database returns 0 while returning 3,144 for melatonin. All three checked 4 August 2026.

A broken query recorded so nobody repeats it: the same regulator endpoint queried on its brand name field returns no match for semaglutide either, so the control fails and any absence taken from that field is an artifact of the query rather than a finding. The substance name field is the one that answers.

What we could not check, and are therefore not claiming: the European medicines regulator's search endpoint refused our request with an HTTP 401 and its published medicines file returned a 404, so this page makes no claim in either direction about European registration. The Russian state medicines register answered, but only as a browser form we could not query programmatically, so Russian registration is unverified here too, and any statement about supplement availability there would need a source we do not have.

The class picture: epitalon, a much better known member of the same series, returns 0 in that same supplement database on the same run, so the absence is a property of the whole family rather than of this compound. What it leaves behind is familiar: no label, no regulator assessment of identity or contents, and the entire burden of knowing what is in a vial resting on paperwork, which is the position of every compound that kept circulating after its development stopped.

Where the evidence runs out

Seven limits on what this record can tell anyone:

• The identity is unresolved. Two sequences, two database records, one trade name, identical mass. No source we found acknowledges the discrepancy, so nobody has ruled on which molecule the lung results belong to.
• There is no human data of any kind. Not a trial, not a case series, not a pharmacokinetic study, not a biomarker cohort. This is a total absence rather than a thin evidence base.
• No amount is printed for either rat study. Both abstracts describe a treatment course without stating a quantity, and neither full text was reachable to us, so the quantity that produced those rat results is not public as far as we can establish.
• One program, not a field. Twelve of the fifteen journal papers cited here carry Khavinson or Fedoreyeva as an author, and no group unconnected to that program has repeated the bronchial findings in anything we retrieved.
• Two load-bearing citations are Russian-language, and neither has a DOI. Both are real PubMed records and both are cited properly here, but a reader following them will meet an English abstract in front of a Russian article, and in both cases no digital object identifier exists to follow at all.
• The anchor paper is paywalled. Every figure taken from the 2014 study on this page comes from its structured abstract, so anything reported only in its methods, tables or figures is outside what we have read.
• Two registries went unchecked. European and Russian registration are both unverified here for the reasons given above, and an absence we could not retrieve is not an absence we get to report.

Zero human studies. Two rat studies in the live animal and one on rat tissue outside it, four studies in human cell culture, one cell-free calorimetry study, four plant studies and one computation, in the searches set out below.

How this page is sourced

Which document carries which claim: the identity and mass figures come from two chemical database records we pulled and decoded ourselves, the bronchial cell findings from one primary paper and two follow-ups, the lung disease findings from two rat studies and one earlier rat explant report, the sequence and tissue separation from two primary papers, the plant line from four papers, the transporter ranking from one modeling study, the treatment claim we decline to endorse from one review, and every absence from a registry, regulator or literature query we ran and dated.

Twenty-one sources: fifteen journal articles, thirteen of them carrying both a linked DOI and a PubMed identifier and two carrying a PubMed identifier alone, two chemical database records, one registry query, two regulator and supplement database queries, and one record of the literature searches themselves. That is a small list, and it describes what these named queries on named databases returned on one date rather than everything ever published on this molecule.

The two ways a name search fails on this compound, and both cost us something: the anchor paper is invisible to every query on the word bronchogen, because it never uses the word. PubMed returns 7 title-and-abstract records for bronchogen and the 2014 Lung paper is not among them. We reached it through the reference list of a 2021 systematic review, which is why that review appears in the list below and is cited for nothing else (Khavinson, 2021). The second failure is the Cyrillic trade name, which returns 0 hits in a full-text index that returns 94 for epitalon, so a Russian-language search on this compound has to run through author names and English titles or it finds nothing and looks conclusive doing it.

Broken queries, recorded so they are not repeated: an unquoted hyphenated sequence in that same full-text index returns tens of thousands of hits for either spelling, identically, because the string tokenizes into the individual amino acid names, and any conclusion drawn from it is an artifact. The quoted forms are the usable ones: the search strings "Ala-Glu-Asp-Leu" and "Ala-Asp-Glu-Leu", each queried across all fields on 4 August 2026, return 4 and 8 records respectively on PubMed. A title search at the DOI registry returns exactly two items containing the word bronchogen, one of which is a Hungarian paper about a cyst, so precisely one peptide paper carries the word in its title anywhere in that index, and it is the one that spells the molecule ADEL.

What we retrieved and then deliberately did not use: the 2021 systematic review as evidence for any finding, since it tabulates rather than measures, and we took each claim from the primary paper it points at instead. Nothing from a seller, catalogue or price listing, on this compound or any other, including the question of whether it is sold as a supplement anywhere, which we could not answer from an admissible source and therefore do not answer at all.

The standard: how a citation on this site gets verified, and who reads a page before it ships, is set out on the methodology page. A literature this thin is exactly where that standard has to hold, because the cheapest way to write this page would have been to repeat one sentence from one review.

Last reviewed: 4 August 2026.

1. 1

   Khavinson VKh, Tendler SM, Vanyushin BF, et al. Peptide regulation of gene expression and protein synthesis in bronchial epithelium. Lung. 2014;192(5):781-791. doi:10.1007/s00408-014-9620-7. PMID 25015171. The anchor paper, and the primary source for the ADEL spelling. Human embryonic bronchial epithelial cell cultures plus cell-free biophysics. Full text is behind the publisher's paywall, so every figure taken from it here is from the structured abstract, retrieved 4 August 2026.

2. 2

   National Center for Biotechnology Information. PubChem Compound Summary CID 11690869, Bronchogen. Molecular formula C18H30N4O9, molecular weight 446.5, InChIKey OFZRHTIWKZWPQF-BJDJZHNGSA-N, CAS 857267-12-0. Retrieved 4 August 2026 through the PUG REST interface, HTTP 200 on name lookup, CAS lookup, property fetch and synonym fetch. pubchem.ncbi.nlm.nih.gov, CID 11690869. The record that carries the name Bronchogen, and whose deposited structure we decoded as Ala-Glu-Asp-Leu.

3. 3

   National Center for Biotechnology Information. PubChem Compound Summary CID 11247825, H-Ala-Asp-Glu-Leu-OH. Molecular formula C18H30N4O9, molecular weight 446.5, InChIKey RELNSSVNWHFGBP-BJDJZHNGSA-N. Retrieved 4 August 2026, HTTP 200 on name lookup and property fetch; the synonym endpoint returned HTTP 404 with no synonyms, which is how we establish that this record does not answer to the name Bronchogen. pubchem.ncbi.nlm.nih.gov, CID 11247825.

4. 4

   Monaselidze JR, Khavinson VKh, Gorgoshidze MZ, et al. Effect of the peptide bronchogen (Ala-Asp-Glu-Leu) on DNA thermostability. Bull Exp Biol Med. 2011;150(3):375-377. doi:10.1007/s10517-011-1146-x. PMID 21240358. The second primary source for the ADEL spelling, in the title itself. Differential scanning microcalorimetry on calf thymus and mouse liver DNA. Cell-free, no organism involved.

5. 5

   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 (Mosc). 2011;76(11):1210-1219. doi:10.1134/S0006297911110022. PMID 22117547. Source of the CTG against CAG binding preference. The HeLa cell-penetration experiments in this paper used epithalon, pinealon and testagen; this compound appears in the cell-free oligonucleotide binding work. It prints the sequence as Ala-Glu-Asp-Leu.

6. 6

   Khavinson VKh, Linkova NS, Polyakova VO, et al. Peptides tissue-specifically stimulate cell differentiation during their aging. Bull Exp Biol Med. 2012;153(1):148-151. doi:10.1007/s10517-012-1664-1. PMID 22808515. The three-peptide, three-tissue design, with CXCL12 and Hoxa3 as the bronchial readouts, in human embryonic cell cultures. It prints Ala-Glu-Asp-Leu.

7. 7

   Ashapkin VV, Linkova NS, Khavinson VKh, Vanyushin BF. Epigenetic mechanisms of peptidergic regulation of gene expression during aging of human cells. Biochemistry (Mosc). 2015;80(3):310-322. doi:10.1134/S0006297915030062. PMID 25761685. The promoter methylation follow-up, including the partly negative results this page reports. Human cell culture. It uses AEDL.

8. 8

   Kuzubova NA, Lebedeva ES, Dvorakovskaya IV, et al. Modulating Effect of Peptide Therapy on the Morphofunctional State of Bronchial Epithelium in Rats with Obstructive Lung Pathology. Bull Exp Biol Med. 2015;159(5):685-688. doi:10.1007/s10517-015-3047-x. PMID 26468022. Animal study, rat. The 60-day nitrogen dioxide model and the one-month treatment course. Its abstract states no quantity of peptide, which is why none is printed on this page.

9. 9

   Titova ON, Kuzubova NA, Lebedeva ES, et al. [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. Animal study, rat, same model and same group. Published in Russian with an English abstract, and carrying no DOI, confirmed against the PubMed record on 4 August 2026. A real PubMed identifier is a sufficient locator under this site's citation rule, but the language and the missing identifier are printed rather than hidden.

10. 10

    Zakutskii AN, Chalisova NI, Ryzhak GA, et al. [The tissue-specific effect of synthetic peptides-biologic regulators in organotypic tissues culture in young and old rats]. Adv Gerontol. 2006;19:93-96. PMID 17152728. Animal tissue, rat, organotypic explant culture outside the animal. Source of the 0.05 ng/ml effective concentration. Russian-language with an English abstract and no DOI. Its closing sentence about clinical practice is an author assertion rather than a result, and is not carried onto this page.

11. 11

    Khavinson V, Linkova N, Kozhevnikova E, Trofimova S. Feasibility of Transport of 26 Biologically Active Ultrashort Peptides via LAT and PEPT Family Transporters. Biomolecules. 2023;13(3):552. doi:10.3390/biom13030552. PMID 36979488. In silico molecular docking, not a measurement. The four rankings on this page were read directly from its docking tables in the open-access full text at PMC10046148 on 4 August 2026, where AEDL appears at rank 20 for LAT1, 22 for LAT2, 6 for PEPT1 and 22 for PEPT2.

12. 12

    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. doi:10.3390/molecules25194389. PMID 32987757. Cited for what it asserts, never as evidence for the assertion. This is the review carrying the oral treatment sentence quoted on this page, read in the open-access full text at PMC7583759 on 4 August 2026. It is a review with no primary human trial retrievable behind that sentence, and no effect on this page rests on it.

13. 13

    Fedoreyeva LI, Dilovarova TA, Ashapkin VV, et al. Short Exogenous Peptides Regulate Expression of CLE, KNOX1, and GRF Family Genes in Nicotiana tabacum. Biochemistry (Mosc). 2017;82(4):521-528. doi:10.1134/S0006297917040149. PMID 28371610. Plant, in vitro. Opens the tobacco research line, and prints Ala-Glu-Asp-Leu.

14. 14

    Fedoreyeva LI, Baranova EN, Chaban IA, et al. Elongating Effect of the Peptide AEDL on the Root of Nicotiana tabacum under Salinity. Plants (Basel). 2022;11(10):1352. doi:10.3390/plants11101352. PMID 35631778. Plant, in vitro. Source of the root elongation result and the 150 mM sodium chloride salinity experiment.

15. 15

    Kononenko NV, Fedoreyeva LI. Peptide AEDL and Glutathione Stimulates Root Development Nicotiana tabacum. Int J Mol Sci. 2024;26(1):289. doi:10.3390/ijms26010289. PMID 39796141. Plant, in vitro. Source of the 3.24-fold glutathione figure.

16. 16

    Lazareva EM, Kazakov EP, Dilovarova TA, Kononenko NV, Fedoreyeva LI. Peptide AEDL Activates Metabolism and Autophagy in Root Cells of Nicotiana tabacum. Int J Mol Sci. 2025;26(22):11028. doi:10.3390/ijms262211028. PMID 41303518. Plant, in vitro. The most recent primary paper on this molecule that any database we searched returned, published November 2025.

17. 17

    Khavinson VK, Popovich IG, Linkova NS, Mironova ES, Ilina AR. Peptide Regulation of Gene Expression: A Systematic Review. Molecules. 2021;26(22):7053. doi:10.3390/molecules26227053. PMID 34834147. Listed because it is how we located the anchor paper, through its reference list, and for no other purpose. No claim on this page rests on it, and Khavinson is among its authors, so it is not an independent assessment of the work it summarizes.

18. 18

    ClinicalTrials.gov, U.S. National Library of Medicine. Registry queried 4 August 2026 through the version 2 application programming interface. The term bronchogen returns a total count of 1, and the single record is NCT00746759, Airway Epithelium Gene Expression: AEGIS IDE, condition lung cancer, listed intervention a biomarker device. The quoted term AEDL returns 0. clinicaltrials.gov, NCT00746759. The same endpoint returns 757 studies for semaglutide, which is the control showing it answers when there is something to find.

19. 19

    U.S. Food and Drug Administration, openFDA. Drugs@FDA endpoint and drug labeling endpoint both queried on the substance name field for bronchogen on 4 August 2026, both returning NOT_FOUND. api.fda.gov, Drugs@FDA query. The same field returns 1 approval record and 5 label records for semaglutide, which is the control. The brand name field returns NOT_FOUND even for semaglutide, so no absence on this page is derived from that field.

20. 20

    National Institutes of Health, Office of Dietary Supplements. Dietary Supplement Label Database version 9, search filter endpoint queried 4 August 2026. Bronchogen returns a count of 0 and epitalon returns a count of 0, while melatonin returns 3,144, which is the control. api.ods.od.nih.gov, DSLD query.

21. 21

    Literature searches run 4 August 2026 and reported as method rather than as evidence. PubMed: bronchogen across all fields returns 12 records of which 7 match on title or abstract, and the 2014 Lung paper is in neither set; bronchogen with the clinical trial publication filter returns 0, as does AEDL with the same filter, against 329 for semaglutide. Quoted sequence searches return 4 records for Ala-Glu-Asp-Leu and 8 for Ala-Asp-Glu-Leu. pubmed.ncbi.nlm.nih.gov, bronchogen. Europe PMC, search terms quoted, run 4 August 2026: the trade name returns 30 hits and its Cyrillic form returns 0, against 94 for epitalon, and an unquoted hyphenated sequence returns tens of thousands for either spelling because the string tokenizes into amino acid names, so those counts are artifacts. ebi.ac.uk, Europe PMC query. Crossref: a title query for bronchogen returns 2 items, one a Hungarian paper on a cyst and one the 2011 calorimetry paper, whose title carries the ADEL spelling. api.crossref.org, title query.

Related pages

Around this page: five neighboring pages on identity, on thin evidence, and on what a document about a vial can and cannot establish.

• What an HPLC purity number misses: why a high percentage says nothing about which molecule was measured, which is the whole problem with two isomers of equal mass.
• How to read a certificate of analysis: where identity, purity and peptide content sit on the document, and which of them a mass number can settle.
• PE 22-28 explained: the closest sibling case, a molecule whose whole record is one laboratory and no human exposure.
• Cardarine (GW501516) explained: a compound whose development stopped and whose circulation did not, with a far heavier document trail than this one.
• MOTS-c guide: the animal-to-human reading problem set out on a peptide that at least has some human data behind it.

Next in the series: we take one molecule's paper trail apart each week and send it out in The Decadewise briefing.