Cortagen (AEDP): the evidence, and the human data inside a patent

What is Cortagen?

The molecule: four residues in a row, L-alanyl-L-glutamyl-L-aspartyl-L-proline. Papers print it as Ala-Glu-Asp-Pro, chemists shorten that to AEDP, and the granted patent writes the same thing as H-Ala-Glu-Asp-Pro-OH.

Where the name came from: the peptide was obtained by directed synthesis based on the amino acid analysis of Cortexin, a natural brain cortex peptide preparation, which is the origin its own authors give for it (Anisimov, 2004). The cortex in Cortexin is why this compound has a nerve literature and its siblings do not.

The independent structural record: PubChem holds it as CID 18439621, molecular formula C17H26N4O9, molecular weight 430.4, with an IUPAC name ending in pyrrolidine-2-carboxylic acid. Pyrrolidine-2-carboxylic acid is proline, so the fourth residue is settled by a database entry rather than by the authors' own wording.

The name collision to avoid: AEDP and AEDG are one letter apart and they are two different molecules. AEDG is Epitalon, PubChem CID 219042, formula C14H22N4O9. Anything filing Cortagen under AEDG has merged the two records.

What changes when Epitalon's last amino acid becomes proline?

The distance between them: Epitalon is Ala-Glu-Asp-Gly. Cortagen is Ala-Glu-Asp-Pro. Three of the four residues are identical and in the same order, and only the terminal one differs. The two PubChem formulas differ by three carbons and four hydrogens, and that is the whole gap. The papers spell the other peptide Epithalon and the chemical databases spell it Epitalon; both names sit on the same molecule, and this page keeps whichever spelling the source it is quoting used.

Why that is unusual here: peptides in this group are rarely tested against a near-twin. This one has been, repeatedly, by one group and its collaborators. Four of those experiments can be read as a comparison, and the table below holds those four and only those four. The criterion for getting into it is narrow and worth stating outright: the abstract has to report what each peptide did on its own, and it has to print both sequences inline so there is no doubt about which molecule was which.

The one place Cortagen was not left out: in that fourth experiment all five peptides tested activated ribosome genes and decondensed densely packed chromatin fibrils. What Cortagen is missing from is the narrower finding, decondensation of chromosome 1 pericentromeric structural chromatin, which the paper attributes to Epithalon, Livagen and Prostamax (Khavinson, 2004). Reporting the row as "Cortagen did nothing" would overstate what the abstract says. Nineteen years later a co-author of that 2004 paper leads one that reports the narrower finding differently: in cultured lymphocytes from donors aged 75 to 88, human tissue in a dish, four bioregulators including both Epitalon and Cortagen decondensed total heterochromatin and activated ribosomal genes but, in that paper's own words, "does not cause deheterochromatinized of pericentromeric structural heterochromatin" (Lezhava, 2023). That abstract does not separate the four peptides, so it cannot become a table row, but it does mean the endpoint row four turns on is not settled in the other peptide's favor either.

Which experiments the criterion leaves out, and which way they went: the same PubMed query returns five further papers that gave both peptides in one experiment. They are lipid peroxidation in rat serum and cerebral cortex, in vivo (Kozina, 2007); lymphocyte-activating factor production by mouse peritoneal macrophages, in vitro (Gumen, 2006); interleukin-2 gene expression in rat hypothalamic structures, in vivo (Kazakova, 2005); rat explant culture, in vitro, the Russian companion to the tissue-matching paper below (Khavinson, Adv Gerontol 2002); and the 2023 chromatin paper just described. None of the five clears the criterion, because none reports the two peptides apart from each other: each abstract names them as a group and gives one combined result. That cuts both ways. They are not five more losses for this compound, and they are not wins either. They are experiments in which nobody can say, from the published summary, which of the two did what.

What the four rows are and are not: four consistent results from one group in St Petersburg, published across six years in the same journal family. That is internal consistency, not independent replication. The nearest thing to a repeat we retrieved is the 2023 paper above, run at Tbilisi State University, which is a different laboratory but not an independent group, since it is led by a co-author of the row it revisits and it does not separate the two peptides. It is the same single-source shape as a molecule whose entire record is one laboratory's output, with one difference that works in this compound's favor: the single source ran the comparison itself, and published the result that flattered its other peptide. What the rows settle is narrow and still worth having. Within the work that exists, one terminal residue changes the answer, so treating these peptides as interchangeable is not something their own data supports.

Why does the nerve work belong to this peptide?

The reason, from the group's own tissue experiment: Cortagen, Epithalon, Livagen and Vilon each stimulated growth of explants from the tissue whose peptide complex was used as the template for their synthesis, respectively brain cortex, subcortical structures, liver and thymus (Khavinson, 2001). Cortagen's template was cortex, which is where its results have stayed ever since.

The two hardest numbers on this page: in rats given 10 micrograms per kilogram of cortagen intramuscularly for 10 days after the sciatic nerve was transected and sutured, growth rate and conduction velocity in the regenerating nerve fibers rose by 27 percent and 40 percent respectively (Turchaninova, 2000). That is a rat surgical model, the figures are the abstract's own, and no equivalent measurement exists in a person.

The follow-up nobody can read: a second paper by an overlapping author group, on the delayed effect of cortagen on the restoration of injured nerve function, is indexed in Doklady Biological Sciences for 2002 (Kolosova, 2002). PubMed carries no abstract for that record and the full text sits behind a paywall we did not clear, so it supports the existence of a sustained line of work and no number at all.

The cortex experiment inside the patent: 73 cerebral cortex fragments from chicken embryos aged 10 to 11 days were cultured for two days, then exposed to the tetrapeptide or to Cerebrolysin across ten concentrations. The tetrapeptide raised the explant area index by 40 plus or minus 7 percent at 20 nanograms per milliliter against control, while Cerebrolysin needed 100 nanograms per milliliter to reach 30 plus or minus 2 percent. Chicken embryo tissue in a dish, reported by the applicant.

Has Cortagen been tested in people?

Once, and not in the literature. Searching PubMed for the query cortagen across all fields on 4 August 2026 returns 15 records, and the same query narrowed with the clinical trial and randomized controlled trial publication-type filters returns none. Querying the United States trial registry the same day returns a single study, and opening it shows an enteral nutrition trial in patients with pancreatic disease that has nothing to do with this peptide, matched on a token rather than on the compound. The registered count is zero.

Where the human data actually sits: Example 10 of United States patent 7,189,701 B1, granted 13 March 2007. It describes a trial in 35 patients with remote complications of craniocerebral injury, one to ten years after the injury, split into three groups: 10 on standard treatment, 15 on standard treatment plus 1 microgram of the tetrapeptide intramuscularly once a day for 10 days, and 10 on standard treatment plus Cerebrolysin.

What it measured: attention, with a proof test taken before and after treatment. Reviewed symbols went from 1505.1 plus or minus 134.7 before treatment to 2519.6 plus or minus 105.3 in the tetrapeptide arm, against 1977.4 plus or minus 186.4 on conventional treatment and 2193.3 plus or minus 120.6 on Cerebrolysin, with healthy volunteers at 2969.6 plus or minus 91.2. Mistakes fell from 12.9 plus or minus 1.5 to 6.3 plus or minus 1.1. The table's own footnote marks the tetrapeptide arm at P less than 0.05 against conventional treatment. A second arm of the same example read electroencephalograms and reported a larger rise in the alpha index in that group.

What a patent is: a real document, dated, granted, indexed and quotable, which is more than most claims about this compound can offer. It is also written by the applicant to secure a monopoly. This one names no randomization, no blinding, no registration and no statistical test beyond the significance marker on the table, and it was never refereed by anyone outside the patent office. Treating it as equal to a published trial is one error. Pretending it does not exist is the other.

Why does a mouse paper contain a sentence about humans?

Because the sentence is background, not a finding. A 2004 microarray study of gene expression in mouse hearts opens by stating that "In humans, Cortagen demonstrated a pronounced therapeutic effect upon the structural and functional posttraumatic recovery of peripheral nerve tissue" (Anisimov, 2004). The abstract carries no reference for it, and the study it introduces contains no human arm.

What that paper did measure: expression of 15,247 transcripts in the hearts of female CBA mice aged 6 months, given Cortagen for 5 consecutive days. 234 clones, 1.53 percent of the total, changed significantly, matching 110 known genes, with maximum up and down regulation of plus 5.42 and minus 2.86. The authors compare the pattern with Vilon, Epitalon and melatonin and report both shared and Cortagen-specific effects. All of it is mouse heart tissue.

Why the sentence is worth tracing: a claim about humans, printed in an English-language journal, inside a paper about mice, is the easiest thing in this literature to lift out of context. The only document we found that could stand behind it is the patent above. So the human claim and the 35-patient patent study are the same evidence met at two removes, and a reader who has seen the sentence has not seen a second study.

The general shape of the problem: it is the same failure that turns rodent figures into human expectations everywhere else in this field, which is why reading an animal number across to a person gets its own section on other pages here. On this compound the crossing happened inside a peer-reviewed introduction, which makes it harder to spot, not easier.

What did the one study with no author from the originating group find?

A dose response that does not run in a straight line. A behavioral team at the Istituto Superiore di Sanita in Rome gave CD-1 mice Cortagen by injection into the abdominal cavity at 0, 0.01, 0.03 and 0.10 milligrams per kilogram, then ran locomotor habituation and the elevated plus maze (Adriani, 2009). Only the middle amount, 0.03, raised locomotion, on the first administration and again after repeated dosing. The amount below it and the amount above it did neither.

The comparison it was built around: Cortagen acted from day one, while Cortexin, the extract it was derived from, needed five days. Cortexin was anxiolytic when given once and anxiogenic on repeat, whereas Cortagen showed few anxiety-related effects at the amount that moved locomotion.

Three caveats that travel with it, all of them printed by the paper itself: the groups held 8 animals each; the authors set the level of significance at p less than 0.10, treating the 0.05 to 0.10 range as a "significant tendency", which is looser than the usual threshold; and the acknowledgements state the work was supported by Geropharm Ltd., the Russian company that supplied both compounds, with one co-author affiliated to it. The paper also states there is no conflict of interest to disclose. Both of those facts belong to the reader rather than to us.

Why the non-monotonic result matters more than the effect: when a middle amount does something and the amounts on either side do not, no line can be drawn through the points and no figure from this experiment can be scaled up or down. It quietly removes the more-is-better assumption without handing anyone a number, and every figure in it came out of a mouse.

Is Cortagen approved anywhere?

What we queried and what came back: the openFDA drug labeling endpoint returned NOT_FOUND for cortagen on 4 August 2026. The same endpoint returned 18 labels for semaglutide on the same run, so the query mechanism was working rather than silently failing. In the records we could reach, no United States label exists under this name, which means there is no regulator assessment of what any material sold as this compound contains, and a purity percentage on a certificate does not establish identity.

Two registers we could not reach, which is a different sentence: the European Medicines Agency medicine search returned a page whose body did not contain its own query term even for a control substance, and the Russian State Register of Medicines returned a blank search form in which the control term Cortexin, itself a registered Russian medicine, also failed to appear. Both queries failed rather than returned nothing. So this page says we could not retrieve those two registers, and never that the compound is absent from them.

What is documented: United States patent 7,189,701 B1, granted 13 March 2007 on a Russian priority application of 20 October 1999, filed through the international system on 25 May 2000, assigned to the St Petersburg Institute of Bioregulation and Gerontology, a public research organization. Its named inventors are Khavinson, Morozov, Malinin and Grigoriev. A separate Russian patent, RU2155063C1, is reported by Adriani and colleagues as covering the compound; the Russian patent database refused our requests, so that one appears here as their statement and not as something we checked.

What the patent claims cover, and why the range is not a protocol: claim 9 covers administering the tetrapeptide "in a dose in a range of 0.01 to 100 ug/kg of the body weight at least once a day", and the description names a period of 10 to 40 days. A ten-thousand-fold span exists to make a claim hard to design around, not to tell anyone what to do, and it appears here as a quoted claim boundary rather than in any chart, table or calculator on this site.

Where the evidence runs out

Seven limits, and together they are the reason this page is the length it is:

• One laboratory wrote all of this but one study. Of the primary work cited here, every item except the Rome mouse study carries Khavinson or an immediate colleague as an author, and that includes the 2023 Tbilisi chromatin paper, whose lead author co-wrote the 2004 one it follows. Nobody unconnected to that circle has repeated the nerve result, the chicken result or the chromatin result in anything we retrieved.
• Two of the papers were read only in translated summary. The chicken study and the rat ischemia study are Russian-language articles. PubMed carries English abstracts for both and those abstracts are all we read, so nothing here rests on their methods sections.
• The human evidence is one document and one document only. Thirty-five patients, inside a patent, unrefereed, with no registration and no independent report of the same trial anywhere we searched.
• One relevant paper is paid for and unread. A 2015 article named for this compound and heterochromatin exists in the International Journal of Peptide Research and Therapeutics (Lezhava, 2015). No abstract is distributed, it is indexed in neither literature database we queried, and the publisher refused our request. It is listed below for its existence and nothing is drawn from it.
• One record in the search results is not about this compound. The PubMed query above, the term cortagen queried across all fields on 4 August 2026, returns 15 records, and all 15 are in the reference list below, so nothing it found is sitting unaccounted for. One of them is listed only to be discounted: PMID 26902350, a 2016 rat ischemic preconditioning study whose abstract, keyword list and subject headings name only "neurospecific protein preparations" and never this peptide (Zarubina, 2016). Its full text is paywalled, so we can neither confirm nor rule out that the compound appears inside, and no claim on this page rests on it.
• Nothing here is a measured blood level. There is no pharmacokinetic study in the set: no half-life, no bioavailability, no exposure figure, in any species, that we could retrieve.
• Identity is a separate unsolved problem. None of the above says anything about what is in material sold under this name, and no regulator anywhere holds a document describing what should be.

What the record is not: evidence that the compound fails. A small, mostly single-group, mostly preclinical literature is an absence of the information that would settle the question either way, which is a different thing from a negative result. A compound that genuinely failed leaves a much heavier paper trail, as the carcinogenicity data behind one abandoned development program shows. The one comparison here that is settled, four times over, is the one against its near-twin.

How this page is sourced

Which document each claim came out of: the sequence and structure come from two PubChem records and the granted patent, which agree with each other; the four head-to-head results from four primary papers, and the five same-query papers the comparison criterion excludes, each read as its PubMed abstract; the nerve figures from the 2000 rat paper's abstract; the cortex explant, toxicology and 35-patient figures from the patent's own numbered examples, read in the granted document itself; the mouse behavior findings from the Rome paper, read in full as an open-access file; and the absence statements from named database queries run on 4 August 2026 and printed with their results.

Twenty-two sources: fifteen journal articles carrying a PubMed record, ten of which also carry a linked DOI; one open-access article carrying a DOI and no PubMed record; one paywalled article listed for its existence only; one granted patent, located through its Europe PMC patent record; two chemical database entries; and two dated database queries whose results are the claim they support.

One paper, two DOIs, and why that is worth saying out loud: the 2000 sciatic nerve study is registered twice, as 10.1023/A:1017532001908 and as 10.1007/BF02682018. Both resolve to the same article at the same publisher. Both are printed in its entry below, so a citation check reading either one finds it rather than reading the pair as two separate papers.

Where the numbers on this page were actually read: the patent figures were taken from the granted document rather than from any summary of it, which is how the assignee named above was corrected: it is the St Petersburg Institute of Bioregulation and Gerontology, not the company that later funded the Rome study. Reading a document instead of a description of it is the same discipline that separates a certificate read line by line from one somebody has told you about.

The standard: how a citation is verified here, and who reads a page before it goes out, is written up on the methodology page. A literature this thin is exactly where that standard has to hold.

Last reviewed: 4 August 2026.

1. 1

   Turchaninova LN, Kolosova LI, Malinin VV, Moiseeva AB, Nozdrachev AD, Khavinson VK. Effect of tetrapeptide cortagen on regeneration of sciatic nerve. Bull Exp Biol Med. 2000;130(12):1172-1174. doi:10.1023/A:1017532001908, registered a second time as doi:10.1007/BF02682018. PMID 11276314. Rat sciatic nerve transection and suture model, and the source of the 27 and 40 percent figures. Read as the English abstract retrieved through the NCBI programmatic interface on 4 August 2026; the full text is paywalled.

2. 2

   Kolosova LI, Moiseeva AB, Turchaninova LN, Malinin VV, Polyakov EL, Nozdrachev AD, Khavinson VKh. The delayed effect of cortagen on the restoration of injured nerve function. Dokl Biol Sci. 2002;384:183-184. doi:10.1023/A:1016098302564. PMID 12134478. PubMed holds no abstract for this record and the full text is paywalled, so it is cited for the existence and the title of a follow-up study and for nothing else.

3. 3

   Khavinson VK. Tissue-specific effects of peptides. Bull Exp Biol Med. 2001;132(2):807-808. doi:10.1023/A:1013058701974. PMID 11713572. Rat organotypic explant culture, in vitro. The source for the tissue-matching result that places cortex work with this peptide rather than with its siblings.

4. 4

   Kuznik BI, Pateiuk AV, Baranchugova LM, Rusaeva NS. Effects of epithalon and cortagene on immunity and hemostasis in neonatally hypophysectomized chicken and old birds. Adv Gerontol. 2008;21(3):372-381. PMID 19432169. Russian-language article with an English abstract indexed in PubMed; no DOI is registered and the full text was not retrieved. The paper defines cortagene as differing from epithalon only by proline replacing glycine, which is what makes it the load-bearing head-to-head.

5. 5

   Kazakova TB, Barabanova SV, Khavinson VKh, Glushikhina MS, Parkhomenko EP, Malinin VV, Korneva EA. In vitro effect of short peptides on expression of interleukin-2 gene in splenocytes. Bull Exp Biol Med. 2002;133(6):614-616. doi:10.1023/A:1020210615148. PMID 12447482. Mouse splenocytes, in vitro. Prints all three sequences inline, which is one of the independent confirmations of Ala-Glu-Asp-Pro.

6. 6

   Khavinson VKh, Rybakina EG, Malinin VV, Pivanovich IY, Shanin SN, Korneva EA. Effects of short peptides on thymocyte blast transformation and signal transduction along the sphingomyelin pathway. Bull Exp Biol Med. 2002;133(5):497-499. doi:10.1023/A:1019830308824. PMID 12420072. Mouse thymocytes, in vitro. The sharpest of the four comparisons: Cortagen "produced no such effects".

7. 7

   Khavinson VKh, Lezhava TA, Malinin VV. Effects of short peptides on lymphocyte chromatin in senile subjects. Bull Exp Biol Med. 2004;137(1):78-81. doi:10.1023/B:BEBM.0000024393.40560.05. PMID 15085253. Cultured leukocytes from human donors aged 75 to 88, in vitro. Human tissue, never a human trial, and the distinction is load-bearing.

8. 8

   Anisimov SV, Khavinson VKh, Anisimov VN. Elucidation of the effect of brain cortex tetrapeptide Cortagen on gene expression in mouse heart by microarray. Neuro Endocrinol Lett. 2004;25(1-2):87-93. PMID 15159690. No DOI is registered for this record. Mouse heart tissue. The source of the transcript figures, of the Cortexin origin statement, and of the background sentence about humans that this page traces.

9. 9

   Zarubina IV, Shabanov PD. Cortexin and cortagen as correcting agents in functional and metabolic disorders in the brain in chronic ischemia. Eksp Klin Farmakol. 2011;74(2):8-15. PMID 21476278. Russian-language article with an English abstract indexed in PubMed; no DOI registered, full text not retrieved. Rats stratified by hypoxia resistance. The authors' own framing is that the drugs can be used, which is a suggestion rather than a demonstration.

10. 10

    Khavinson VKh, Malinin VV, Chalisova NI, Grigor'ev EI. Tissue-specific action of peptides in tissue culture of rats of various ages. Adv Gerontol. 2002;9:95-100. PMID 12096446. Russian-language article with an English abstract indexed in PubMed; no DOI is registered and the full text was not retrieved. Rat explant culture, in vitro. The Russian companion to the tissue-matching paper above. It gives Cortagen, Epitalon, Livagen and Vilon in one experiment and reports a combined tissue-specific result, so it carries no comparison between the first two and is not in the table.

11. 11

    Kazakova TB, Barabanova SV, Novikova NS, Glushikhina MS, Khavinson VKh, Malinin VV, Korneva EA. Synthesis of IL-2 mRNA in cells of rat hypothalamic structures after injection of short peptides. Bull Exp Biol Med. 2005;139(6):718-720. doi:10.1007/s10517-005-0388-x. PMID 16224591. Rat brain, in vivo, read by in situ hybridization on paraffin sections. Names Vilon, Epithalon and Cortagen as a group and reports one modulating result for the three, which is why it is excluded from the comparison table.

12. 12

    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. Bull Exp Biol Med. 2006;142(3):360-362. doi:10.1007/s10517-006-0366-y. PMID 17426849. Mouse peritoneal macrophages, in vitro. Same shape as the entry above: three peptides given, one combined result, no separation between Epithalon and Cortagen. The contrast the abstract does draw is between resident and lipopolysaccharide-stimulated cells, not between peptides.

13. 13

    Kozina LS. Effects of bioactive tetrapeptides on free-radical processes. Bull Exp Biol Med. 2007;143(6):744-746. doi:10.1007/s10517-007-0230-8. PMID 18239817. Rats, in vivo, measured in serum and cerebral cortex. Reports epithalon and cortagen together in a single sentence, with no result attributed to either one alone, so it is excluded from the comparison table on the same criterion as the three entries above.

14. 14

    Lezhava T, Jokhadze T, Monaselidze J, Buadze T, Gaiozishvili M, Sigua T, Khujadze I, Gogidze K, Mikaia N, Chigvinadze N. Epigenetic modification under the influence of peptide bioregulators on the "old" chromatin. Georgian Med News. 2023;(335):79-83. PMID 37042594. No DOI is registered. Cultured lymphocytes from donors aged 75 to 88, human tissue in a dish, never a trial. Run at Tbilisi State University with no Khavinson author, but led by a co-author of the 2004 chromatin paper above. The source of the quoted pericentromeric heterochromatin finding, and the nearest thing to a later look at that endpoint we retrieved. Read as the English abstract retrieved through the NCBI programmatic interface on 4 August 2026; the full text was not retrieved.

15. 15

    Adriani W, Granstrem O, Romano E, Koroleva S, Laviola G. Modulatory effects of Cortexin and Cortagen on locomotor activity and anxiety-related behavior in mice. The Open Neuropsychopharmacology Journal. 2009;2:22-29. doi:10.2174/1876523800902010022. Open access; the full article was downloaded and read on 4 August 2026. Not indexed in PubMed. The only primary study here led from outside the originating group, and the source of the p less than 0.10 threshold, the group size of 8, and the funding statement.

16. 16

    Lezhava T, Monaselidze J, Jokhadze T, Gaiozishvili M. Epigenetic regulation of "aged" heterochromatin by peptide bioregulator Cortagen. International Journal of Peptide Research and Therapeutics. 2015;21(1):157-163. doi:10.1007/s10989-014-9443-7. Metadata confirmed at the DOI registry on 4 August 2026; the article itself sits behind a publisher paywall and no abstract is distributed, so this entry supports its existence and its title only.

17. 17

    Zarubina IV, Shabanov PD. Neuroprotective effects of peptides during ischemic preconditioning. Bull Exp Biol Med. 2016;160(4):448-451. doi:10.1007/s10517-016-3193-9. PMID 26902350. Listed as a negative finding: it is returned by a cortagen search, and its abstract, keywords and subject headings name only neurospecific protein preparations. No claim on this page rests on it.

18. 18

    Khavinson VK, Morozov VG, Malinin VV, Grigoriev EI. Tetrapeptide stimulating functional activity of neurons, pharmacological agent based thereon and method of use thereof. United States patent 7,189,701 B1, granted 13 March 2007; Russian priority application 99121778 of 20 October 1999; international application filed 25 May 2000. Assignee: Sankt-Peterburgskaya Obschestvennaya Organizatsiya, the St Petersburg Institute of Bioregulation and Gerontology. Patent record at Europe PMC, US7189701, retrieved 4 August 2026, and the granted document read in full the same day. The source of Example 10 and its 35 patients, of the chicken embryo explant experiment, of the toxicology studies, and of the 0.01 to 100 microgram per kilogram claim range.

19. 19

    National Center for Biotechnology Information. PubChem compound summary, CID 18439621, Cortagen. Retrieved 4 August 2026: molecular formula C17H26N4O9, molecular weight 430.4, IUPAC name terminating in pyrrolidine-2-carboxylic acid. pubchem.ncbi.nlm.nih.gov, CID 18439621.

20. 20

    National Center for Biotechnology Information. PubChem compound summary, CID 219042, Epitalon. Retrieved 4 August 2026: molecular formula C14H22N4O9, molecular weight 390.35, synonym Ala-Glu-Asp-Gly. pubchem.ncbi.nlm.nih.gov, CID 219042. Paired with the entry above, the two records establish the one-residue difference from outside the papers that report it.

21. 21

    ClinicalTrials.gov, United States National Library of Medicine. Registry queried through the version 2 interface on 4 August 2026 for the term cortagen: one record returned, opened, and rejected as a token match on an unrelated enteral nutrition study. clinicaltrials.gov, cortagen query. Verified zero registered studies of this compound.

22. 22

    United States Food and Drug Administration, openFDA. Drug labeling endpoint queried for cortagen on 4 August 2026, returning NOT_FOUND. api.fda.gov, cortagen labeling query. The same endpoint returned 18 labels for semaglutide on the same run, which is the positive control showing the query worked.

Related pages

Nearby on this site: five pages on molecules with thin records, on what a compound is, and on what a laboratory result does and does not establish.

• PE 22-28 explained: another peptide whose entire record is one paper from one laboratory, with the same absence of any human exposure.
• Cardarine (GW501516) explained: the opposite problem, a compound with a heavy document trail that includes the reason its development stopped.
• MOTS-c guide: the animal-to-human reading problem set out at length, on a peptide with more human data than this one.
• What an HPLC purity number misses: why a high percentage on a certificate leaves the identity question completely open.
• How to read a COA: which line on a certificate measures what, and which lines measure nothing at all.

Next in the series: one molecule's paper trail opened up each week in The Decadewise briefing.