Cortagen: what the studies show, status and safety
Summary
Cortagen is a synthetic chain of four amino acids from a St Petersburg institute. No trial in people has ever been registered, and the only account of people taking it sits in a patent. In its makers' own head-to-head tests it usually came last. It is the one peptide of that series sold as no product at all.
Key findings at a glance
- No registered trial, anywhere. On 15 September 2026 the ClinicalTrials.gov registry returned nothing for the name, for the code AEDP or for the sequence [1].
- The only human account sits in the inventors' own patent. Two of its examples describe people: fifteen patients with old head injuries and twelve with vascular dementia, 27 in all. Both claim benefit; neither names randomisation, blinding or a placebo [2].
- The one peptide of its series sold as no product at all. Its own institute lists six licensed medicines, and this is not among them. The Russian capsule catalogues do not carry it either [3], [4].
- It did nothing in the head-to-head test its makers ran. In hypophysectomised chicks Epithalon corrected every measured shift in blood, immunity and clotting. Cortagen, one amino acid apart, "do not affect the parameters studied" [5].
- Last of 26 in its makers' own transport calculation. At the carrier PEPT2 it scored +17.28, the only positive value in that table and the worst rank in it [6].
- Circulating injection amounts run far above the patent figures. Trade pages name amounts tens to hundreds of times the largest amount the patent ever gave a person. They come from no study, and the same pages say so [7], [8].
- Banned in sport, and abandoned as a drug candidate. Category S0 catches any drug-like substance no health authority has approved for people [9]. The patent itself lapsed for non-payment of fees [2].
What it is
Cortagen is a laboratory-made peptide of four amino acids: alanine, glutamic acid, aspartic acid and proline, written Ala-Glu-Asp-Pro or AEDP [10]. It comes from the St Petersburg Institute of Bioregulation and Gerontology, the group around Vladimir Khavinson [2].
It was not isolated from anything. The group designed the sequence from an amino acid analysis of Cortexin, a preparation made from the brain cortex of calves [11]. Such an analysis counts building blocks; it does not reveal which sequences a mixture actually contains.
The words bioregulator, cytogen and ultrashort peptide run through that literature. They are house terms of the same institute, used by no pharmacopoeia and no regulator [12], [13].
Quick facts
| Field | Value | Ref |
|---|---|---|
| Chain | Ala-Glu-Asp-Pro, four amino acids | [10], [2] |
| Formula and mass | C17H26N4O9, 430.4 g/mol | [10] |
| Structure key | InChIKey PLTRIMAUDDQYRV-NAKRPEOUSA-N | [10] |
| Code in the literature | AEDP; no laboratory number found for it | [13] |
| Chemical record | PubChem CID 18439621, holding four synonyms | [10] |
| Registry number | CAS 335591-03-2, from a secondary source only | [10], [14] |
| Code with the American regulator | None | [15] |
| Curated chemistry records | No ChEBI, no ChEMBL, no DrugBank entry | [14] |
| Water-loving character | Calculated XLogP −6.5, polar surface 216 Ų | [10] |
| How long it lasts in the body | No published value, for any route or species | [6] |
| Registered studies in people | None | [1] |
| Approval status | Approved nowhere, for nothing | [3], [15] |
| Sold as | Vials of freeze-dried powder for research use only | [16] |
| Originating group | St Petersburg Institute of Bioregulation and Gerontology | [2] |
How it works
Nobody knows. No receptor has been identified, no measurement in any living person exists, and the peptide's entry into a cell has never been observed [17], [6].
The group's own account runs as follows, each step to be weighed on its own evidence.
- Acting on genes. The peptide would enter the nucleus, settle on stretches of DNA and change which genes are read [17], [18]. No binding measurement and no uptake experiment has ever been published for it.
- Tissue specificity. In rat explant cultures each peptide of the series was said to stimulate growth in the tissue its parent extract came from [12], [19]. That effect depended on concentration and was never reproduced outside the group.
- Riding on transport proteins. Computer modelling only, and the result is poor. In the group's 2023 run AEDP scored −20.95 at the carrier LAT1, rank 23 of 26, and +17.28 at PEPT2, the last of 26. A positive score means no favourable fit at all. The authors call the PEPT2 figures preliminary, because only one structure of that carrier existed to dock against [6].
- Changing gene activity. A microarray in mouse heart tissue found 234 of 15,247 clones altered, or 1.53 per cent, mapping to 110 known genes [11]. The organ was the heart, not the brain, and no second method confirmed the signals.
- Repairing nerves. One rat experiment on a cut sciatic nerve reports faster fibre growth and faster conduction, described in full below [20].
Two facts sit awkwardly under all this. With a calculated XLogP of −6.5, the molecule is far too water-loving to cross membranes unaided [10].
The group also set itself a threshold: a score below −15 marks likely transport. In their earlier table, published in 2022 and calculated separately from the 2023 run, AEDP reached only −12.11 and misses that mark, where Pinealon reached −30.29 [13]. The two LAT1 figures come from two different calculations, and the peptide sits near the bottom of both.
What the studies found
Cell cultures, rodents, chicks, one frog experiment and a computer model: that is the whole record. PubMed holds 15 entries across 26 years, and not one reviewed study in people [21], [1].
Nerve repair in rats
Animal data This is the only published paper with exact figures for the substance on its own. Rats whose sciatic nerve had been cut and stitched received 10 µg per kilogram into a muscle daily for ten days. Fibre growth rose by 27 per cent and conduction speed by 40 per cent [20]. The abstract gives no group sizes, no spread and no p-values, and the full text is not freely available. In 26 years no laboratory outside that circle has repeated it, and a follow-up paper by the same group carries no abstract in PubMed at all, so it counts only as evidence that the work happened [22].
Gene activity in the heart
Animal data Six-month-old female mice received injections on five consecutive days. A microarray covering 15,247 transcripts found 234 clones with altered expression, 1.53 per cent of the total, mapping to 110 known genes. The strongest changes were a 5.42-fold rise and a 2.86-fold fall [11].
The organ studied was the heart, chosen because the authors wanted to explain cardiovascular observations. A single snapshot of gene activity, unconfirmed by a second method, generates hypotheses rather than settling mechanisms.
Where it did nothing
Animal data Chicks whose pituitary had been removed at birth developed anaemia, immune deficiency and abnormal clotting. The paper reports that Epithalon, which differs by one amino acid, removed every one of those shifts over 40 days of injections. Of Cortagen it says the peptide "do not affect the parameters studied" [5].
Cell data In mouse thymocytes, Vilon had the strongest effect on cell division and altered how interleukin-1beta acted. Epithalon was weaker. "Cortagen produced no such effects" [23].
Where it came last
Cell data In mouse spleen cells all three peptides raised interleukin-2 messenger RNA. The authors rank them plainly: "Vilon and Epithalon were most potent, while Cortagen produced a less pronounced effect" [24]. A later rat study found the same gene modulated in the hypothalamus, without naming doses or direction [25].
Cell data In white blood cells from people aged 75 to 88, five peptides loosened tightly packed chromatin and switched on ribosomal genes. Only three loosened the packed region of chromosome 1 and only two that of chromosome 9, and Cortagen was in neither group [26].
Cell data A frog experiment points against the name. In pluripotent tissue from an early Xenopus embryo, AEDG steered development towards epidermis and nerve tissue, AEDP towards mesenchyme and epidermis [27], [28]. The primary paper for it could not be found.
Cell data A group in Tbilisi confirms that loosening for four peptides including AEDP and reports more sister chromatid exchanges near the chromosome tips [29], [30]. All of this used donated human cells in a dish. Nobody was treated.
Results that point against the marketing
Animal data In rats, injections of Epithalon and Cortagen lowered the products of fat oxidation and the oxidative damage to proteins, but the same abstract reports this "paralleled by suppression of antioxidant activity" in serum and cortex [31]. Falling damage alongside a suppressed defence needs explaining, and it does not support the label antioxidant.
The one account of people
Everything ever said about the peptide working in people traces to a single document, and that document is not a study. Two examples of the patent describe patients, 27 treated in all.
The first covers 35 people whose head injury lay one to ten years back, split three ways: ten on standard care, ten on standard care plus Cerebrolysin, and 15 on standard care plus 1 µg of the tetrapeptide into a muscle daily for ten days [2].
It does report measured numbers. On a pen-and-paper attention test the tetrapeptide group reviewed 2,519.6 ± 105.3 symbols against 1,977.4 ± 186.4 on standard care, with 6.3 ± 1.1 mistakes against 10.5 ± 1.9 (p below 0.05 for both).
The alpha rhythm index on the electroencephalogram reached 47.9 ± 3.1, against 39.6 ± 4.1 on standard care, 42.4 ± 3.9 with Cerebrolysin and 52.9 ± 3.2 in healthy volunteers. Improvement is claimed for 71 per cent of the patients.
The second example is smaller and weaker. Twelve people aged 69 to 76 with vascular dementia received 3 µg into a muscle once daily for 30 days, with no control group at all.
The comparison there is against the patients' own state before treatment. The patent reports improvement from the fourth or fifth day and calls the result a reverse development of symptoms in 74.8 per cent of them [2].
The numbers are not the weak point here; where they come from is. Neither example mentions randomisation, blinding, a placebo or an endpoint fixed in advance, and neither was ever peer reviewed.
Both were written by the people who own the right they support, and a patent is examined for novelty and inventive step, never for benefit. Those 30 days are also the longest the substance has knowingly been given to a person.
A 2004 paper in an international journal states that the peptide showed "a pronounced therapeutic effect" on nerve recovery in people [11]. No such publication exists in PubMed, Europe PMC or the trial registry, and the patent's two human examples concern head injury and vascular dementia rather than peripheral nerves [21], [1].
Work from outside the institute
Animal data One group not attached to the institute, at a military medical academy, ran its own animal work. In rats with chronic brain ischaemia, both Cortexin and Cortagen speeded the recovery of normal behaviour and limited fat oxidation in brain tissue [32]. That abstract gives no doses, no group sizes and no figures, and it does not separate the two preparations.
A critical Russian review from the same year lists the peptide among preparations with paradoxical effects, acting differently when given into the body than into the brain [33].
What is still unknown
- Whether any of it reaches the brain. An independent Russian review states plainly that nobody knows which peptides of these preparations cross the barrier and which do not [34].
- How the body handles the substance: no half-life, no absorption figure and no excretion data, for any route or species [6].
- Whether a receptor exists at all, and whether the epigenetic account holds outside a computer model [17].
- What happens beyond six months in an animal, the longest exposure ever documented, and documented only in a patent [2].
- Whether the changes seen in human chromatin in a dish mean anything in a living body [26].
Side effects and safety
No safety profile exists, and that is not a clean bill of health. There is no reviewed toxicology in any species and no entry in the American adverse event database [15].
What has actually been observed
- No reports in the pharmacovigilance system. The American adverse event database holds nothing for the name [15]. A substance that is neither approved nor prescribed generates no spontaneous reports.
- The only toxicity figures sit in a patent. Sixty-six mice were split into six groups of eleven: five received single amounts of 1 to 5 mg per kilogram into a muscle, one received saline. None died within 14 days.
- Longer animal dosing, also only in the patent. The same example describes 60 rats dosed daily for 90 days and a further group dosed daily for six months, reporting no pathological changes in either. The patent says this work followed the Russian rules for preclinical safety testing, an assertion nobody outside the inventors has checked [2].
- A warning signal in the nerve experiment. Alongside the shortened response latency, the patent's mouse experiment on a compressed nerve records a tendency towards suppressed muscle contraction in response to acetylcholine [2]. Dampened signalling at the nerve-muscle junction sits oddly in a preparation meant to repair nerves, and nobody followed it up.
- A suppressed antioxidant defence. What a lasting suppression of the body's own antioxidant defence would mean, as reported in the rat study above, nobody has examined [31].
Because no reviewed study in people exists, no side effect in people has ever been recorded either [1].
What is missing
- No reviewed toxicology and no no-effect level. The patent's own animal work is the only source of numbers, and it was never published or independently repeated [2].
- No data on cancer risk or on reproduction, which given the claimed action on gene activity is the serious gap [26], [17].
- No data on immune reactions, drug interactions, pregnancy, breastfeeding, children, or liver and kidney impairment.
- No official reference standard. Without a pharmacopoeia monograph, a regulator code or a curated chemistry entry, traded material cannot be measured against anything [14], [15].
The injectable form carries risks of its own. Vials sold for research are made under no pharmaceutical quality system, so sterility, endotoxin content and actual peptide content are unknown [16], and injecting non-sterile material brings the usual risks of abscess, vein inflammation and blood-borne infection.
Doses used in studies
The doses below are simply what the cited sources gave, listed so that the results can be understood. They are not advice on how to use anything, and the human figures come from patent examples, not from reviewed studies.
Almost every line is an animal experiment or a figure from the patent held by the inventors, and so are the two lines describing people.
| Study | Model | Amount | Route | Duration | Ref |
|---|---|---|---|---|---|
| Turchaninova 2000, nerve repair | Rat, cut sciatic nerve | 10 µg/kg | Into a muscle | Daily, 10 days | [20] |
| Anisimov 2004, heart gene activity | Mouse, six months old | Not stated in the abstract | Injection, route not stated | Daily, 5 days | [11] |
| Khavinson 2021, review of the series | Cells in a dish | 2 to 200 ng/ml | Added to the culture fluid | — | [17] |
| Patent example 9, nerve compression | 22 mice, 7 of them treated | 10 µg/kg | Into the abdominal cavity | Daily, 8 days | [2] |
| Patent example 4, fat oxidation in the cortex | 20 rats | 1 µg, not per kilogram | Into the abdominal cavity | Daily, 5 days | [2] |
| Patent example 2, single-amount toxicity | 66 mice, six groups of 11 | 1 to 5 mg/kg, once | Into a muscle | Single administration | [2] |
| Patent example 2, repeated dosing | 60 rats | 1 µg/kg, 0.3 mg/kg and 3 mg/kg | Into a muscle | Daily, 90 days | [2] |
| Patent example 2, long-term dosing | Rats, number not stated | 1 µg/kg, 0.1 mg/kg and 1 mg/kg | Into a muscle | Daily, 6 months | [2] |
| Patent example 10, people | 15 patients, old head injury | 1 µg, not per kilogram | Into a muscle | Daily, 10 days | [2] |
| Patent example 11, people | 12 patients, vascular dementia | 3 µg, not per kilogram | Into a muscle | Daily, 30 days | [2] |
A concentration in a dish cannot be converted into an amount for a body, and neither can an animal figure. The patent also claims a range of 0.01 to 100 µg per kilogram over 10 to 40 days [2]. A span of four orders of magnitude is legal breadth, not dose-finding.
The gap between those patent figures and what circulates among users is the striking number on this page. One overview page names 1 to 2 mg per administration, calling it "community convention, not a trial dose", and another names 100 to 200 µg [7], [8].
The largest amount the patent ever gave a person was 3 µg. The circulating figures therefore run from roughly thirty to several hundred times that.
Those figures come from no study, because no study exists from which to derive them. The same pages say so themselves, in the words "no human trials" and "every reported effect is animal or cell-culture" [7].
Development and approval status
A patent, fifteen papers, no development programme
- 1999Patent priority filedFour inventors from the St Petersburg institute claim the sequence L-Ala-L-Glu-L-Asp-L-Pro
- 2000The only paper with exact figuresRats, cut sciatic nerve: fibre growth 27 per cent faster, conduction speed 40 per cent higher
- 2004Microarray in mouse heart, and an unsupported human claim234 of 15,247 clones altered; the same paper asserts an effect in people that no publication supports
- 2007Patent granted in the United StatesIts examples hold the only toxicity figures and the only account of people taking the substance, 27 patients across two of them
- 2008No effect where its sibling workedHypophysectomised chicks: Epithalon corrected every shift, Cortagen none
- 2022The makers own calculation places it near the bottomLAT1 score of minus 12.11, rank 26 of 27, short of the binding threshold the same authors set
- 2023Last of 26 at a second carrierPEPT2 score of plus 17.28, the only positive value in the table
- 15 September 2026Registers checkedNo approval anywhere, no registered trial, no regulator code, and the patent long gone: lapsed for non-payment, with its twenty-year term ending in 2020 in any case
There is no development programme behind Cortagen. No sponsor has filed anything and no phase of testing has begun.
The patent is recorded as expired for non-payment of fees, and its twenty-year term would have run out on 25 May 2020 in any case [1], [2]. What exists is a thin line of laboratory papers and a vial sold for research.
| Market | Status | Note | Ref |
|---|---|---|---|
| United States | Not approved | No substance code, no label, no adverse event file; never put forward for pharmacy compounding | [15], [35] |
| European Union | Not approved | No authorisation and no trial; the agency's own register could not be read on the day of checking | [36] |
| Germany | Not approved | Neither a licensed medicine nor a lawful food; the imported preparation falls under novel food rules | [36] |
| United Kingdom | Not approved | The register returned only a page shell, so the finding rests on every other register | [36] |
| Australia | Not approved | Absent from the Poisons Standard, which is not permission | [37] |
| Canada | Not approved | The medicines database returns nothing; a control query works | [38] |
| Switzerland | Not approved | No authorisation identified, and no register query was possible | [36] |
| Russia | Not approved | Its own institute lists six licensed medicines and this is not one; no supplement version is sold either | [3], [4] |
Two rows need care. The Australian entry means the substance was never scheduled, not that it may be used; research peptides are treated there much as prescription substances are [37].
The Russian row sets this peptide apart. Its siblings Cartalax, Ovagen and Pinealon are sold there as capsules and this one is not sold at all, while Cortexin, the extract it was designed from, is a licensed medicine whose licence does not transfer [4], [39].
All registers were checked on 15 September 2026. Where a register returned only a page shell, that is recorded as an unverified gap rather than a nil result [36].
Anti-doping
Cortagen is banned at all times, in and out of competition. Category S0 of the 2026 Prohibited List covers "any pharmacological substance which is not addressed by any of the subsequent sections of the List and with no current approval by any governmental regulatory health authority for human therapeutic use" [9].
The name is not printed on the list, and that is not a gap. The clause names drugs "under pre-clinical or clinical development or discontinued", which describes an abandoned candidate with a lapsed patent exactly [9], [2].
German anti-doping law works differently. Its annex names banned substances one by one, and this peptide is not among them, so possession is not an offence under that provision [40]. The sporting ban is unaffected by that.
No published test for detecting it in a sample exists: four ordinary amino acids are hard to tell apart from the products of normal protein digestion, and without any pharmacokinetics nobody knows what window to look in. Further detail is in the overview of peptides banned in sport.
Compared with related peptides
Seven of the 27 ultrashort peptides in table 2 of the 2022 overview by the originating group. A more negative value means a better calculated fit; the same authors call a score below minus 15 the sign of likely transport. Only one peptide in the full table, Normoftal at minus 10.49, scored worse than Cortagen. Source [13].
Counts as of 15 September 2026. The literature records include reviews and papers in which the peptide is one of several tested. Sources [21], [1].
| Peptide | Relation to Cortagen | What the checks behind this page found |
|---|---|---|
| Cortagen | — | Ala-Glu-Asp-Pro, 430.4 g/mol; scored −12.11 in the group's own LAT1 table, the lowest shown here [10], [13] |
| Epitalon | Same series, differing only in the last amino acid | Ala-Glu-Asp-Gly, 390.35 g/mol; scored −20.38, and corrected every shift in the chick experiment where Cortagen corrected none [41], [13], [5] |
| Pinealon | A tripeptide of the same series, assigned to the pineal gland | Glu-Asp-Arg; scored −30.29 in the same table, against −12.11 here [13] |
| Cartalax | A tripeptide of the same series, assigned to cartilage | Ala-Glu-Asp; scored −26.65, and is sold in Russia as capsules where Cortagen is not [13], [4] |
| Chonluten | Another peptide of the same series, assigned to the lung and stomach | Glu-Asp-Gly; the best score in that table at −30.30 [13] |
| Cortexin | The cortex extract Cortagen was designed from | A licensed Russian medicine; in the one independent animal study the two were tested side by side [39], [32] |
The comparison is not about strength. It shows where Cortagen sits among its neighbours, and the answer is at the bottom of their own table. Two rows matter especially: Epitalon, which differs by a single amino acid and won the only head-to-head animal test [5], and Cortexin, the licensed preparation whose licence is routinely misread as covering the peptide [39].
Common misconceptions
- "Cortagen is Cortexin, or a pure form of it." Cortexin is a licensed Russian mixture of hundreds of polypeptides from calf brain cortex [39]. Cortagen is a single peptide designed from an amino acid analysis of it, which is a construction proposal, not an isolated fraction [11].
- "Cortagen is Epitalon, or AEDG." Epitalon is Ala-Glu-Asp-Gly and Cortagen is Ala-Glu-Asp-Pro [10], [41]. One trade page still carries Cortagen under the heading "AEDG Peptide Complex" [8], and the chick experiment above shows that the swap changes everything [5].
- "Cortagen is a tripeptide like Pinealon or Cartalax." It has four amino acids, and that matters: the gut carrier PEPT1 moves two- and three-part peptides, which makes the oral route claimed in the patent additionally doubtful [10], [6], [2].
- "It worked in people, it says so in a journal." That sentence appears in a 2004 abstract and rests on nothing: no human study of this peptide exists in PubMed, Europe PMC or the trial registry [11], [21], [1].
- "It is well researched, there have been papers since 2000." Fifteen PubMed records in 26 years, ten of them authored by Khavinson or Malinin and most of the rest by the immediate circle [21]. Within that literature the peptide loses most direct comparisons [5], [23], [24].
- "It is an antioxidant." The group's own rat study reports the opposite alongside the desired effect: antioxidant activity in serum and cortex was suppressed [31].
- "A granted patent means it was checked by an authority." Patent offices examine novelty, inventive step and industrial applicability, never benefit or safety [2]. Tables, error margins and p-values do not change what the document is: a property right written by the people it benefits. It has also expired for non-payment of fees.
Frequently asked questions
Has Cortagen ever been tested in a clinical trial?
No. On 15 September 2026 the ClinicalTrials.gov registry returned nothing for the name, for the code AEDP or for the sequence. The only account of people taking it sits in two examples of a patent held by its inventors, covering 27 treated patients in all, and neither example mentions randomisation, blinding or a placebo.
What is Cortagen made of?
Four amino acids: alanine, glutamic acid, aspartic acid and proline, written Ala-Glu-Asp-Pro or AEDP. The chemical record gives the formula C17H26N4O9 and a mass of 430.4 g/mol. That makes it a tetrapeptide, not a tripeptide.
Is Cortagen the same as Cortexin?
No. Cortexin is a licensed Russian medicine, a mixture of polypeptides extracted from the brain cortex of calves. Cortagen is a single synthetic peptide whose sequence was designed from an amino acid analysis of that mixture. The licence for the extract does not carry over.
Is Cortagen the same as Epitalon?
No, though they differ by one amino acid. Epitalon is Ala-Glu-Asp-Gly and Cortagen is Ala-Glu-Asp-Pro, glycine against proline at the tail. That single swap mattered: in hypophysectomised chicks Epithalon corrected every measured shift and Cortagen corrected none.
Is Cortagen approved as a medicine anywhere?
No, in no country. There is no authorisation in the United States, the European Union, Germany, the United Kingdom, Australia, Canada, Switzerland or Russia. Its own institute lists six licensed medicines and this is not one of them, and no Russian supplement version exists either.
What did the animal studies of Cortagen find?
One clear positive result and several blanks. In rats with a cut sciatic nerve, fibre growth was 27 per cent faster and conduction speed 40 per cent higher. In chicks it changed nothing, in mouse thymocytes nothing, and in a frog experiment it steered tissue away from nerve rather than towards it.
Why does Cortagen score badly in its makers' own transport calculations?
In their 2022 table the peptide reached only −12.11 at the carrier LAT1, rank 26 of 27. The same authors call a score below −15 the sign of likely transport. In the 2023 follow-up it came last of 26 at the carrier PEPT2, with the only positive value in the table.
What are the side effects of Cortagen?
Unknown, because nobody has looked properly. There is no reviewed toxicology in any species and no entry in the American adverse event database. The only toxicity figures sit in the patent held by the inventors, which is not a reviewed publication, and no laboratory outside that circle has ever checked them.
Is Cortagen banned in sport?
Yes, at all times, in and out of competition. Category S0 of the 2026 Prohibited List covers any drug-like substance that no health authority has approved for use in people, and names discontinued candidates explicitly. Cortagen is not printed on the list, and that absence is not a loophole.
Sources
- ClinicalTrials.gov, API v2. Queries on 15 September 2026: intervention "Cortagen" total count 0, "Kortagen" 0, "AEDP" 0, "Cortexin" 0, free text "Khavinson" 0 and "peptide bioregulator" 0. The free-text hit NCT06852014 and the sequence hits NCT05214872 and NCT05400733 were opened individually and have no connection to the substance. The sponsor "Hudson Biotech" holds eight mock records, none of them on this substance. Control query "semaglutide" returns 752 studies. https://clinicaltrials.gov/api/v2/studies
- Khavinson VK, Morozov VG, Malinin VV, Grigoriev EI (2007). Tetrapeptide stimulating functional activity of neurons, pharmacological agent based thereon and method of use thereof. US patent 7,189,701 B1. Priority 20 October 1999, filed 25 May 2000, granted 13 March 2007; applicant Nostiji Klinika Instituta Bioregulyatsii Gerontologii OOO, later GEROPHARM Ltd; legal status "expired, fee related", with the anticipated end of the twenty-year term on 25 May 2020. Full description read at the source on 15 September 2026. Claims L-Ala-L-Glu-L-Asp-L-Pro and dosing "from 0.01 to 100 µg/kg of the body weight, at least once a day for a period necessary for attaining a therapeutic effect — from 10 to 40 days", by the parenteral, intranasal or oral route. Example 2 holds all the toxicity work and states that it followed the Russian rules for preclinical safety assessment of 29 December 1997: acute, 66 male mice of 20 to 23 g in six equal groups of 11, five groups given a single intramuscular 0.25 ml injection at 1, 2, 3, 4 and 5 mg/kg and one given saline, with no deaths within 14 days and no change in condition, behaviour, movement, coat or excretions; subacute, 60 rats of 150 to 250 g given 1 µg/kg, 0.3 mg/kg or 3 mg/kg intramuscularly in 0.5 ml saline daily for 90 days; chronic, rats of the same weight given 1 µg/kg, 0.1 mg/kg or 1 mg/kg intramuscularly daily for six months, with the closing statement that neither the subacute nor the chronic study revealed pathological changes. Example 3, 73 chicken-embryo cortex fragments in culture, area index 40 ± 7 per cent above control at 20 ng/ml. Example 4, 20 rats given 1 µg into the abdominal cavity daily for 5 days, with diene conjugates falling from 40.19 ± 2.55 to 29.67 ± 1.93 nmol/g and protein oxidation from 7.53 ± 0.40 to 4.81 ± 0.09 µmol/mg (p below 0.01). Example 9, 22 male mice of 25 to 30 g, 7 treated and 15 controls, 10 µg/kg into the abdominal cavity daily for 8 days from the third day after compression of the fibular nerve: the electrical threshold of the regenerating nerve improved "by 30–50 per cent", the latent period of the M-response shortened by 89 per cent in the intact and 59 per cent in the regenerating preparation, and a tendency towards suppressed acetylcholine-induced contraction was recorded. Example 10, 35 patients whose head injury lay one to ten years back, in three groups: 10 on standard care, 15 on standard care plus 1 µg of the tetrapeptide into a muscle daily for 10 days, and 10 on standard care plus Cerebrolysin; attention test 2,519.6 ± 105.3 reviewed symbols and 6.3 ± 1.1 mistakes in the tetrapeptide group against 1,977.4 ± 186.4 and 10.5 ± 1.9 on standard care (p below 0.05), alpha index 47.9 ± 3.1 against 39.6 ± 4.1 on standard care, 42.4 ± 3.9 with Cerebrolysin and 52.9 ± 3.2 in healthy volunteers, and subjective improvement claimed in 71 per cent of cases. Example 11, 12 patients aged 69 to 76 with vascular dementia, 3 µg into a muscle once daily for 30 days, compared only against their own state before treatment; improvement reported from the fourth to fifth day and "reverse development of the pathologic symptoms" in 74.8 per cent. Neither human example names randomisation, blinding, a placebo or an endpoint fixed in advance, and neither has ever been published in a journal. A property right, not a reviewed publication. https://patents.google.com/patent/US7189701B1/en
- St Petersburg Institute of Bioregulation and Gerontology, page of licensed medicines, retrieved 15 September 2026. Lists exactly six approved products with registration numbers: Thymalin ЛС-00026, Thymogen PN002408/01, Retinalamin ЛС-000684, Cortexin Р N003862/02, Pineamin ЛП-003202 and Samprost Р N001849/02. Cortagen is not among them. https://gerontology.ru/medications
- Russian trade catalogue checks, retrieved 15 September 2026. Product searches for "Кортаген" on the two Russian distribution sites returned no product, while the same catalogues list Cartalax, Ovagen, Vesugen and Pinealon as capsule products. Trade record, cited as evidence of what is and is not sold. Not linked.
- Kuznik BI, Pateiuk AV, Baranchugova LM, Rusaeva NS (2008). Effects of epithalon and cortagene on immunity and hemostasis in neonatally hypophysectomized chicken and old birds. Advances in Gerontology 21(3):372-381. PMID 19432169. In Russian. The operated birds developed anaemia, cellular and humoral immune deficiency, hypercoagulation and inhibited fibrinolysis. Injections of Epithalon over 40 days removed those shifts completely, while of Cortagen the abstract states that it "do not affect the parameters studied". Also the source of the spelling "cortagene (Ala-Glu-Asp-Pro) which is distinguished from epithalon by a different terminal aminoacid (with Gly being replaced by Pro)".
- Khavinson VK, Linkova NS, Rudskoy AI, Petukhov MG (2023). Feasibility of transport of 26 biologically active ultrashort peptides via LAT and PEPT family transporters. Biomolecules 13(3):552. PMID 36979488. PMCID PMC10046148. DOI 10.3390/biom13030552. Full text and tables 2, 3, 5 and 7 read. AEDP scored −20.95 at LAT1, rank 23 of 26; −22.15 at LAT2, rank 14; −12.65 at PEPT1, rank 25; and +17.28 at PEPT2, rank 26 and last. Molecular docking only, with no experimental transport measurement, and the authors call the PEPT2 results preliminary because only one structure was available. No pharmacokinetic data for the substance exists in this or any other publication found.
- Western trade overview page for Cortagen, retrieved 15 September 2026. Names 1 to 2 mg per administration described in its own words as "community convention, not a trial dose", once daily in courses of 10 to 20 days, and states on the same page "No human trials", "Every reported effect is animal or cell-culture", "There is no human evidence to predict a subjective effect" and "There are no human clinical trials and no FDA evaluation". Also gives 20 mg for 46.95 US dollars, or 2.35 dollars per milligram. Trade record, cited only as evidence that such figures circulate. Not linked.
- Second trade overview page for Cortagen, retrieved 15 September 2026. Gives the sequence correctly as "Cortagen (AEDP tetrapeptide, Ala-Glu-Asp-Pro, Brain Cortex Peptide)" and expressly corrects the confusion with AEDG, while its own page title reads "AEDG Peptide Complex"; cited as the documented instance of that mix-up. Also names 100 to 200 micrograms per administration under the skin. Trade record, cited only as evidence that such figures circulate. Not linked.
- World Anti-Doping Agency. The 2026 Prohibited List, in force from 1 January 2026, section S0 "Non-approved substances", page 4. Wording: "Any pharmacological substance which is not addressed by any of the subsequent sections of the List and with no current approval by any governmental regulatory health authority for human therapeutic use (e.g. drugs under pre-clinical or clinical development or discontinued, designer drugs, substances approved only for veterinary use) is prohibited at all times." All substances in the class are specified substances. Full text checked 15 September 2026: "cortagen", "kortagen", "korthagen", "ala-glu", "AEDP" and "Asp-Pro" return no match, so the classification follows from the general clause; control check, BPC-157 appears twice. https://www.wada-ama.org/en/prohibited-list
- PubChem. Compound CID 18439621, Cortagen, C17H26N4O9, 430.4 g/mol, InChIKey PLTRIMAUDDQYRV-NAKRPEOUSA-N, calculated XLogP −6.5 and topological polar surface area 216 Ų, CAS 335591-03-2, with four synonyms and six substance records in total. Retrieved 15 September 2026. https://pubchem.ncbi.nlm.nih.gov/compound/18439621
- Anisimov SV, Khavinson VK, Anisimov VN (2004). Elucidation of the effect of brain cortex tetrapeptide Cortagen on gene expression in mouse heart by microarray. Neuro-Endocrinology Letters 25(1-2):87-93. PMID 15159690. Six-month-old female CBA mice, injections on five consecutive days, cDNA microarray over 15,247 transcripts; 234 clones with significantly altered expression, 1.53 per cent of the total, mapping to 110 known genes, maximum upregulation 5.42-fold and maximum downregulation 2.86-fold, with shared and specific effects against Vilon, Epitalon and melatonin. Source of the origin statement "The synthetic tetrapeptide Cortagen (Ala-Glu-Asp-Pro) was obtained by directed synthesis based on amino acid analysis of natural brain cortex peptide preparation Cortexin", and of the unsupported assertion that the peptide showed "a pronounced therapeutic effect upon the structural and functional posttraumatic recovery of peripheral nerve tissue" in people.
- Khavinson VK (2001). Tissue-specific effects of peptides. Bulletin of Experimental Biology and Medicine 132(2):807-808. PMID 11713572. DOI 10.1023/a:1013058701974. Organotypic explant cultures from rat brain cortex, subcortical structures, liver and thymus; the house term appears as "Synthetic peptides (cytogens) Cortagen, Epithalon, Livagen, and Vilon". No concentrations, group sizes or effect sizes are given in the abstract.
- Khavinson VK, Linkova NS, Kozhevnikova EO, Dyatlova AS, Petukhov MG (2022). Transport of biologically active ultrashort peptides using POT and LAT carriers. International Journal of Molecular Sciences 23(14):7733. PMID 35887081. PMCID PMC9323678. DOI 10.3390/ijms23147733. Full text and tables 1 and 2 read. Table 2 lists "Korthagen (AEDP) −12.11 Neuroprotector", rank 26 of 27, alongside Chonluten (EDG) −30.30, Pinealon (EDR) −30.29, Cardiogen (AEDR) −29.81, Cartalax (AED) −26.65, Epitalon (AEDG) −20.38 and Crystagen (EDP) −20.22. Table 1 puts the known LAT1 ligands between −19.67 and −15.00. The threshold is the authors' own: "ICM-Score function values of the studied USPs less than −15 may indicate a high probability of highly efficient binding to the LAT1 transporter." The labels neuroprotector and gastroprotector in that table are the authors' attributions, not findings.
- Curated chemistry database checks, 15 September 2026. ChEBI search for "cortagen": "No compound matches the provided term", control query "semaglutide" returns CHEBI:167574. ChEMBL molecule search, q=cortagen: total count 0, control query returns four hits. CAS Common Chemistry, query for 335591-03-2 and for the name: "API key required" for both the query and the control, so the registry number rests on the PubChem synonym list alone. Wikidata entity Q137538173 carries exactly two statements, that it is a chemical compound and the PubChem identifier, with no registry number, structure key, ChEBI, ChEMBL or DrugBank link and no approval data. No DrugBank record was found; the direct query returned HTTP 403, so the finding rests on the absence of a DrugBank link in PubChem and Wikidata.
- United States register checks, 15 September 2026. FDA Global Substance Registration System, exact-name query for "CORTAGEN": zero records, and zero for the fuzzy full-text query, while the control query "SEMAGLUTIDE" returns five; no substance code exists. openFDA drug label API, search "cortagen": not found, control query for a marketed brand returns four labels. openFDA adverse event database, medicinal product "cortagen": not found. DailyMed web services v2: zero entries, database state 14 September 2026, control query returns one. https://gsrs.ncats.nih.gov
- Western and Chinese research-chemical listings for Cortagen, retrieved 15 September 2026. Freeze-dried powder in vials of 10, 20 and 50 mg, purity stated by the sellers as "99 per cent and above by HPLC" and "third-party tested" with no independent certificate, marked "Research Use Only", at 2 to 6 US dollars per milligram; one Chinese seller asserts manufacture under good manufacturing practice, which is a self-declaration and not a regulatory finding. No Russian capsule or sublingual form exists. Trade record, cited as evidence of what is sold. Not linked.
- Khavinson VK, Popovich IG, Linkova NS, Mironova ES, Ilina AR (2021). Peptide regulation of gene expression: a systematic review. Molecules 26(22):7053. PMID 34834147. PMCID PMC8619776. DOI 10.3390/molecules26227053. Full text read. Lists AEDP among short peptides said to act on gene expression and gives 2 to 200 ng/ml as the working range for these peptides in culture. Contains no binding measurement, no promoter docking and no cell-uptake experiment for this peptide.
- Rubinskii AV, Linkova NS, Chalisova NI, Noskin LA, Marchenko VN, Khavinson VK (2021). Epigenetic regulation of adaptogenesis by pathology and aging. Advances in Gerontology 34(1):10-17. PMID 33993656. In Russian. Names AEDP in a list of epigenetic regulators without adding substance-specific data.
- Khavinson VK, Malinin VV, Chalisova NI, Grigor'ev EI (2002). Tissue-specific action of peptides in tissue culture of rats of various ages. Advances in Gerontology 9:95-100. PMID 12096446. In Russian. Compares the polypeptide complexes Cortexin, Epithalamin, Hepalin and Thymalin with the synthetic peptides Cortagen, Epitalon, Livagen and Vilon in organotypic cultures. The tissue-specific effect is reported "with respect to the applied concentrations", and the abstract names neither the concentrations nor any effect size.
- Turchaninova LN, Kolosova LI, Malinin VV, Moiseeva AB, Nozdrachev AD, Khavinson VK (2000). Effect of tetrapeptide cortagen on regeneration of sciatic nerve. Bulletin of Experimental Biology and Medicine 130(12):1172-1174. PMID 11276314. Rats after transection and suture of the sciatic nerve, 10 µg/kg into a muscle daily for 10 days; growth rate of the regenerating fibres 27 per cent higher and conduction velocity 40 per cent higher. The abstract gives no group sizes, no measures of spread and no p-values, and the full text is not freely available. The only published paper reporting exact figures for this substance alone.
- PubMed, NCBI E-utilities, and Europe PMC, REST search, retrieved 15 September 2026. "Cortagen", mapped through MeSH supplementary concept UID 67431545 "alanyl-glutamyl-aspartylprolyine" with entry terms "Ala-Glu-Asp-Pro" and "cortagen", returns 15 PubMed records, the oldest from 2000 and the most recent substance-related one from 2023. Europe PMC returns 17 records, two of them conference abstract volumes without any connection to the substance. "Ala-Glu-Asp-Pro" returns 6 PubMed and 20 Europe PMC records, the latter overwhelmingly sequence fragments in protein structure papers. Europe PMC full-text search for the name returns nothing, because none of the substance-related papers is available as open-access full text. Of the 15 substance-related records, 10 carry Khavinson or Malinin as an author and most of the rest come from the immediate collaboration circle; two come from a fully independent group. https://pubmed.ncbi.nlm.nih.gov/?term=cortagen
- Kolosova LI, Moiseeva AB, Turchaninova LN, Malinin VV, Polyakov EL, Nozdrachev AD, Khavinson VK (2002). The delayed effect of cortagen on the restoration of injured nerve function. Doklady Biological Sciences 384:183-184. PMID 12134478. DOI 10.1023/a:1016098302564. No abstract is held in PubMed, only title and identifier, so neither content nor figures could be verified; cited solely as evidence that the work exists.
- Khavinson VK, Rybakina EG, Malinin VV, Pivanovich IY, Shanin SN, Korneva EA (2002). Effects of short peptides on thymocyte blast transformation and signal transduction along the sphingomyelin pathway. Bulletin of Experimental Biology and Medicine 133(5):497-499. PMID 12420072. DOI 10.1023/a:1019830308824. Vilon had the strongest comitogenic effect on thymocyte proliferation and modulated the comitogenic activity of interleukin-1beta, Epithalon was weaker, and of the third peptide the paper states "Cortagen produced no such effects". On sphingomyelinase activity in thymocyte membranes Vilon likewise acted more strongly than either of the others.
- Kazakova TB, Barabanova SV, Khavinson VK, Glushikhina MS, Parkhomenko EP, Malinin VV, Korneva EA (2002). In vitro effect of short peptides on expression of interleukin-2 gene in splenocytes. Bulletin of Experimental Biology and Medicine 133(6):614-616. PMID 12447482. DOI 10.1023/a:1020210615148. Splenocytes of CBA mice without specific inducers; all three peptides activated interleukin-2 messenger RNA synthesis depending on type, concentration and exposure time, and the ranking is explicit: "Vilon and Epithalon were most potent, while Cortagen produced a less pronounced effect on interleukin-2 mRNA synthesis." No concentrations or effect sizes in the abstract.
- Kazakova TB, Barabanova SV, Novikova NS, Glushikhina MS, Khavinson VK, Malinin VV, Korneva EA (2005). Synthesis of IL-2 mRNA in cells of rat hypothalamic structures after injection of short peptides. Bulletin of Experimental Biology and Medicine 139(6):718-720. PMID 16224591. DOI 10.1007/s10517-005-0388-x. In-situ hybridisation on paraffin sections after injection; the three peptides modulated interleukin-2 gene expression in individual hypothalamic structures depending on timing and route. The abstract names no doses, no direction of change and no effect sizes.
- Khavinson VK, Lezhava TA, Malinin VV (2004). Effects of short peptides on lymphocyte chromatin in senile subjects. Bulletin of Experimental Biology and Medicine 137(1):78-81. PMID 15085253. DOI 10.1023/b:bebm.0000024393.40560.05. Leukocyte cultures from donors aged 75 to 88. All five peptides tested activated ribosomal genes, decondensed tightly packed chromatin fibrils and released age-repressed genes. Differentiating result: the pericentromeric structural chromatin of chromosome 1 was decondensed only by Epithalon, Livagen and Prostamax, and that of chromosome 9 only by Epithalon and Livagen; Cortagen belongs to neither group. Human cells in culture, not treated people, and no concentrations in the abstract.
- Caputi S, Trubiani O, Sinjari B, Trofimova S, Diomede F, Linkova N, Diatlova A, Khavinson V (2019). Effect of short peptides on neuronal differentiation of stem cells. PMID 30791821. PMCID PMC6376556. Full text read. Reports the Xenopus laevis experiment on pluripotent ectoderm of the early gastrula in the words "The AEDG peptide stimulated the differentiation of the polypotent tissue into the epidermis and neural tissue, and the AEDP peptide induced the development of the mesenchyme and epidermis." No concentrations or figures are given, and the primary publication of that experiment with AEDP could not be located. https://www.ebi.ac.uk/europepmc/webservices/rest/PMC6376556/fullTextXML
- Khavinson V, Linkova N, Diatlova A, Trofimova S (2020). Peptide regulation of cell differentiation. Stem Cell Reviews and Reports 16(1):118-125. PMID 31808038. DOI 10.1007/s12015-019-09938-8. Repeats the same Xenopus finding for AEDG and AEDP in a review, without adding primary data.
- Lezhava T, Jokhadze T, Monaselidze J, Buadze T, Gaiozishvili M, Sigua T (2020). Epigenetic modification under the influence of peptide bioregulators on "aged" heterochromatin. Georgian Medical News (309):120-124. PMID 33526740. Lymphocyte cultures from donors aged 75 to 88 and from donors aged 20 to 40; differential calorimetry, nucleolar organiser activity, C-heterochromatin polymorphism and sister chromatid exchanges. AEDG, KEDA, AEDP and the dipeptide KE induced deheterochromatinisation of total, constitutive and facultative heterochromatin, with exchanges rising in the telomeric and falling in the middle arm regions, each peptide acting selectively on different chromosome regions. A group outside the originating institute, but the peptide was not tested on its own and no concentrations appear in the abstract.
- Lezhava T, Jokhadze T, Monaselidze J, Buadze T, Gaiozishvili M, Sigua T, Khujadze I, Gogidze K, Mikaia N, Chigvinadze N (2023). Epigenetic modification under the influence of peptide bioregulators on the "old" chromatin. Georgian Medical News (335):79-83. PMID 37042594. Confirms the selective deheterochromatinisation by the four peptides and states expressly that they do not deheterochromatinise the pericentromeric structural heterochromatin. The closing phrase about new opportunities in treating diseases of ageing is an expectation of the authors, not a result.
- Kozina LS (2007). Effects of bioactive tetrapeptides on free-radical processes. Bulletin of Experimental Biology and Medicine 143(6):744-746. PMID 18239817. DOI 10.1007/s10517-007-0230-8. Rats, serum and cerebral cortex. Injections of Epithalon and Cortagen lowered the content of lipid peroxidation products and the oxidative modification of proteins, and the abstract adds that this was "paralleled by suppression of antioxidant activity in rat serum and cerebral cortex". No doses and no figures in the abstract.
- Zarubina IV, Shabanov PD (2011). Cortexin and cortagen as correcting agents in functional and metabolic disorders in the brain in chronic ischemia. Eksperimental'naia i Klinicheskaia Farmakologiia 74(2):8-15. PMID 21476278. In Russian. Rats of high and low tolerance to low oxygen, model of chronic brain ischaemia. Both preparations speeded the restoration of disturbed individual behaviour and prevented excessive lipid peroxidation and a fall in antioxidant activity in brain tissue. From the Kirov Military Medical Academy and therefore outside the originating institute; the abstract names no doses, group sizes, effect sizes or p-values, and does not separate the two preparations quantitatively.
- Shabanov PD (2011). Evidence for the neuroprotective effects of polypeptide preparations: unresolved questions. Nervnye Bolezni 2011. A critical review from the same independent group, describing the tetrapeptide as psychotropically active with paradoxical effects when given into the body as against into the brain. https://cyberleninka.ru/article/n/dokazatelnost-neyroprotektornyh-effektov-polipeptidnyh-preparatov-nereshennye-voprosy
- Gulyaeva NV (2018). Molecular mechanisms of action of preparations containing brain peptides: Cortexin. Zhurnal Nevrologii i Psikhiatrii imeni S.S. Korsakova 118(10):93-96. DOI 10.17116/jnevro201811810193. In Russian. An independent assessment of this class of preparations, stating that it is not known which of their peptides cross the blood-brain barrier and which do not.
- US Food and Drug Administration. Bulk drug substances nominated for use in compounding under section 503A of the Federal Food, Drug, and Cosmetic Act, state of 14 May 2026. Downloaded and checked in full text 15 September 2026: neither Cortagen nor Ala-Glu-Asp-Pro nor AEDP appears in any of the three categories, so the substance was never even put forward for review. Control: alanyl-L-glutamine and GHK-Cu, the latter expressly for non-injectable routes only, stand in category 1. https://www.fda.gov/media/94155/download
- European, British, Swiss and Russian register checks, 15 September 2026. The European Medicines Agency search and its control search both returned a JavaScript shell of almost identical size, 76,900 and 77,056 bytes, with no server-rendered results. MHRA Products returned 122,696 bytes for both the search and the control. Swissmedic returned only its entry page, 27,983 bytes, with no usable search. The Russian state medicines register returned only the search form for both the query and the control, so its nil result is not usable, and the Russian supplement register was unreachable. All four are recorded as unverified gaps rather than nil results; the finding of no authorisation rests on every other register checked and on the absence of any registered trial. For Germany the additional finding is that no lawful food status exists either, because no significant consumption in the European Union before 15 May 1997 is documented and the novel food rules therefore apply.
- Therapeutic Goods (Poisons Standard) Instrument 2026, Australia. Full text checked 15 September 2026 for "Cortagen", "Kortagen", "Ala-Glu-Asp-Pro" and "AEDP": no match, and no general heading for peptides exists. Control: alanylglutamine appears. The Australian medicines register could not be reached on the day of checking. Unapproved research peptides are handled there much as prescription substances are, so absence from the standard is not permission.
- Health Canada, Drug Product Database API, brand-name query for "cortagen": empty result. Control query returns six records with DIN 02471469. Retrieved 15 September 2026. https://health-products.canada.ca/api/drug/drugproduct/
- GEROPHARM, product page for Cortexin, retrieved 15 September 2026. Names the company as the sole manufacturer of the original preparation and gives the Russian registration number Р N003862/02 for the polypeptide complex from the brain cortex of calves. https://geropharm.com/portfolio/nevrologiya-psihiatriya/korteksin
- German Anti-Doping Act, annex to section 2 paragraph 3, published as BGBl. 2023 I No. 67. Full text checked 15 September 2026: Cortagen, Ala-Glu-Asp-Pro and AEDP do not appear, and section II lists peptide hormones, releasing factors and growth factors one by one with no catch-all heading for a cortex tetrapeptide. The closing sentence extends the listed substances to their salts, esters, ethers, isomers, mixtures of isomers, complexes and derivatives, and creates no new group. Control: ipamorelin appears. https://www.gesetze-im-internet.de/antidopg/anlage.html
- PubChem. Compound CID 219042, Epitalon, Ala-Glu-Asp-Gly, C14H22N4O9, 390.35 g/mol. Retrieved 15 September 2026, cited to separate the two tetrapeptides. https://pubchem.ncbi.nlm.nih.gov/compound/219042
Cite this page
The register checks and literature searches behind this page were run on 15 September 2026. For a substance with this little record, the date on which those searches came back nearly empty is part of the finding.
myPeptides Research & Editing. (2026). Cortagen: what the studies show, status and safety. Version 1.0, 15 September 2026. myPeptides Peptide Register. Retrieved from https://mypep.app/peptides/cortagen
How pages in this register are compiled and graded is described under methodology; the full register is at peptides.
| Version | Date | Change |
|---|---|---|
| 1.0 | 2026-09-15 | Initial publication |
Last verified: 15 September 2026. Next review: on the appearance of any registered study in people, any independent replication of the animal findings, or any change in the anti-doping classification.