Pancragen: what the studies show, status and safety
Summary
Pancragen is a synthetic chain of four amino acids from a St Petersburg institute, assigned to the pancreas and sold for blood sugar. No trial of it has ever been registered anywhere. People received it on three recorded occasions, none registered, none blinded and none independently reviewed, and on the best documented of them only half of twelve participants showed the reported change. It is approved as a medicine nowhere and banned in sport at all times.
Key findings at a glance
- No trial in people has ever been registered. A registry query on 20 September 2026 returned zero for Pancragen, Pankragen and KEDW, as an intervention and as free text. A control query for semaglutide returned 755 studies [1].
- The whole literature is about a dozen papers. PubMed returns nine records under the name, Europe PMC six that concern the substance. Almost every one comes from the originating group or its co-authors, and no laboratory outside that circle has repeated a single finding [2].
- People received it on three recorded occasions, none of them registered. There is a 2011 report on older people with type 2 diabetes and a 2013 report on twelve older people with impaired glucose tolerance. The third is an example inside the inventors' patent, covering 36 patients [3], [4], [5].
- In the best documented of those, the reported change appeared in half. Twelve people took 500 micrograms twice a day for four weeks. The authors report a significant fall in glucose during a 75 gram glucose test in 50 per cent of them, with no control group and no effect sizes [4].
- The 2011 report gives no numbers for the peptide. It states that fasting glucose, glucose tolerance, insulin and an insulin resistance index improved, without a dose, a route, a duration, a group size or a single figure. Its only stated figure concerns melatonin, which was 70 per cent lower in the diabetic group [3].
- In old monkeys, a licensed tablet outperformed it. Five animals received 50 micrograms a day into the muscle for ten days and four received glimepiride by mouth. Both lowered fasting glucose; the licensed drug had the stronger and longer effect [6].
- It exists in none of the reference chemical databases. No PubChem record, no CAS number, no regulator substance code, no entry in the open knowledge base. Control queries for a sister peptide work in every one of them [7], [8], [9].
- The studied molecule and the traded powder are declared differently. Every paper and the patent describe the amide form, Lys-Glu-Asp-Trp-NH2. Western sellers declare the free acid. No published work has tested the free acid [5], [10], [11].
- In Russia it is a food, not a medicine. Capsules and tablets carry 100 micrograms of a peptide complex, and the entry says in its own words that it is not a medicinal product [12].
- Circulating injection schedules run 200 to 500 times higher. Sales pages give 2 to 5 milligrams a day for 20 to 30 days, against the 10 micrograms a day for ten days of the patent example [5], [13].
- Banned in sport around the clock under the class that catches every substance no health authority has approved [14].
What it is
Pancragen is a laboratory-made tetrapeptide: lysine, glutamic acid, aspartic acid and tryptophan, joined in that order and usually written KEDW. Four amino acids and a mass of 575.62 make it a very small molecule, chemically close to an ordinary fragment of digested protein. The American medical library indexes it under the sequence rather than the trade name [5], [10].
It comes from the St Petersburg Institute of Bioregulation and Gerontology, the group around Vladimir Khavinson, who patented it from December 2003 with three colleagues. The international application lapsed, and the family now carries the status "ceased". Every later paper on the substance has Khavinson or one of his co-authors on it [5], [15], [2].
The words "bioregulator" and "cytogen" belong to that institute and its distributors. A cytogen, in that house vocabulary, is a synthetic short peptide as opposed to a mixture extracted from animal tissue. Neither word appears in any pharmacopoeia, in any medicines classification or in any regulator's definition [16], [17].
Two identity problems deserve stating at the outset. The published work describes the amide form, capped at one end, while Western sellers declare their powder as the uncapped free acid. The Russian capsule declares only a "peptide complex" listed as its four amino acids [5], [11], [12].
Quick facts
| Field | Value | Ref |
|---|---|---|
| Name | Pancragen; Панкраген in Russia; no international non-proprietary name | [12], [10] |
| Other names | Lys-Glu-Asp-Trp, KEDW, KEDW-NH2, pancragene, "Pankragen forte" for the 500 microgram form | [10], [4] |
| Class | Synthetic tetrapeptide; "bioregulator" and "cytogen" are the maker's own words | [16] |
| Chain | Lys-Glu-Asp-Trp, four amino acids, amide cap at the tryptophan end | [5], [10] |
| Formula and mass | C26H37N7O8, 575.62 for the amide form described in the patent | [5] |
| Chemical record | None; PubChem has no entry under any name or either formula | [7] |
| CAS registry number | None found | [7] |
| Code with the American regulator | None; a control search in the same database works | [8] |
| Entry in the open knowledge base | None under either spelling | [9] |
| Half-life | Never published, for any route or species | [18] |
| Registered studies in people | None | [1] |
| Approval status | Approved nowhere, for nothing | [8], [12] |
| Sold as | Capsules and tablets in Russia; 10 to 50 mg vials of powder in the West | [12], [11] |
| Originating group | St Petersburg Institute of Bioregulation and Gerontology | [5] |

How it works
Nobody knows. No receptor has been identified for it, no binding has ever been measured, and every mechanism on offer is either a computer calculation or a description of what changed in a dish.
The account given by the originating group runs as follows. The peptide would enter the cell through a carrier protein and reach the nucleus. There it would settle on a particular stretch of DNA, or on the tails of the proteins that package it, and change which genes are read. Each step rests on different and mostly indirect evidence.
- Getting into the cell. A 2023 calculation scored the capped peptide at two carrier models, at −21.78 and −20.57. A companion paper lists it among the stronger candidate blockers of one amino acid carrier. Both are docking scores, and no transport of this molecule has ever been measured [18], [16].
- Settling on DNA. One paper from the group puts it on a stretch written "acct". Another paper from the same group puts the same molecule on "GGCAG" in the wide groove of the double helix. The two answers contradict each other, and both come from calculations [19], [20].
- Sitting on packing proteins. Fluorescence measurements show it binding all four types of histone tested. The histones came from wheat, a plant model rather than human chromatin, and it was one of six peptides examined [21].
- Switching on pancreatic genes. In ageing human pancreatic cell cultures it raised the readout of several genes that steer how pancreatic cells mature, among them PDX1, PAX4, PAX6, FOXA2 and NKX2.2 [22], [23].
- Changing DNA labelling. A follow-up measured the chemical tags on those gene promoters. For three genes the tags moved with the readout; for PAX4 they did not move at all, and for FOXA2 they moved without any link to the readout. The authors conclude that "some other mechanisms" must be at work [24].
The patent adds a broader claim, that the substance raises insulin secretion and the sensitivity of tissue to insulin. A later paper from the group calls it a mimetic of insulinotropic peptides, meaning a stand-in for the gut signals that prompt insulin release. That phrase describes a hypothesis, not a measured receptor effect [5], [20].
Computed docking scores for the capped peptide from one 2023 paper, not measurements: a more negative number means a better calculated fit. No transport of this molecule has ever been measured. Source [18].
There is a size problem underneath all of this. A chain of four amino acids carries very little information, far too little to pick out one gene in a whole genome. Its four building blocks also circulate freely in the blood as ordinary amino acids, and short chains are cut quickly by enzymes in blood and gut [16].
One boundary is worth drawing against the neighbouring products. The same institute also sells extracted tissue mixtures under a separate label, which are not single molecules at all. Pancragen is a defined synthetic chain, and the two categories should not be read as evidence for each other [17].
What the studies found
The record is a handful of small papers from one research school, two of them in monkeys and two of them in people, plus a patent that carries the most detailed numbers of all. Nothing in it was registered, blinded or repeated elsewhere [1], [2].
Literature searches and a registry query run on 20 September 2026. The three human reports are the two Kyiv papers and the patent example; none of them is registered. Sources [1], [2].
The two Kyiv reports, the only published human record
Unregistered observation The 2011 report covers 30 healthy older people and 33 older patients with type 2 diabetes. Its one concrete figure is not about the peptide at all: night-time melatonin production was 70 per cent lower in the diabetic group than in healthy people of the same age [3].
Unregistered observation The authors then state that in the diabetic patients fasting glucose, glucose during a standard tolerance test, plasma insulin and an insulin resistance index all fell, while participants who received nothing showed no change. The abstract gives no dose, no route, no duration, no figures and no account of how the groups were formed [3].
Unregistered observation The 2013 report screened 150 people, 39 young, 42 middle-aged and 69 older. Twelve of the older group with impaired glucose tolerance took 500 micrograms twice a day for four weeks. Glucose was measured at 0, 30, 60 and 120 minutes after 75 grams of glucose [4].
Unregistered observation The result is reported as a significant fall in plasma glucose during that test "in 50 percent" of the twelve, so in six people. There was no control group, no randomisation and no blinding, and no effect size, spread or p-value is given [4].
Neither report can show whether the substance works. Both have the inventor as a co-author, neither appears in any trial registry, and neither states an ethics approval number. They are observations of what happened, published without the numbers that would let anyone check them [1], [3], [4].
The patent example, which is not a trial
Patent example, not a study The patent describes 36 patients, seven men and 29 women, aged 16 to 83, of whom 23 had type 1 and 13 had type 2 diabetes; 32 were on insulin. Sixteen received 10 micrograms into the muscle daily for ten days, against 16 controls [5].
Patent example, not a study The document reports that eight of the treated group used less insulin, six kept the same amount and two needed more, while 14 of 16 controls needed more. Four further patients took 100 micrograms twice a day by mouth for ten days [5].
These figures cannot be read as clinical evidence, and the reasons are structural. A patent application is examined for novelty, not for medical results. There is no randomisation, no blinding, no registration, no ethics record, no sample size calculation and no statistical test of any kind [1], [5].
They should not be read as an achievable outcome either. The document records no blood sugar monitoring, no safety endpoint and no rule by which those insulin changes were made. Insulin and other glucose-lowering treatments are prescribed and adjusted by a doctor, and nothing on this page is a reason to change any of them.
Animals, where most of the work sits
Animal data In old female rhesus monkeys, 50 micrograms per animal a day into the muscle for ten days raised the rate at which glucose cleared from the blood and moved insulin and C-peptide patterns towards those of young animals. Part of the effect was still reported three weeks later [25].
Animal data The 2015 monkey comparison is the most informative of the set, and not in the substance's favour. Five animals received it into the muscle and four received the licensed tablet glimepiride by mouth, each for ten days. Both lowered fasting glucose; glimepiride had the stronger and more sustained effect [6].
Animal data In rats with chemically induced diabetes, the substance given by mouth lowered blood sugar during treatment. Given into the muscle it normalised how cells stuck to the lining of small blood vessels, but left the leakiness of those vessels unchanged. Neither abstract states a dose or a group size [26].
Alloxan-diabetic rats, 3 micrograms per animal into the abdomen daily for 11 days, 21 animals. These figures appear only in patent US7491703B2 and have never been published in a journal or reproduced by anyone. Source [5].
Cells in a dish
Cell culture In ageing human pancreatic cell cultures the substance raised the readout of genes that steer how pancreatic cells mature. From that result the authors conclude it could be an effective tool in treating diabetes and pancreatitis, which is a long way past what a dish can show [22].
Cell culture A Russian-language paper from the same group reports higher levels of the enzymes MMP2 and MMP9, of PCNA and Ki67, both markers of cell division, and lower p53. The rise in those two enzymes is read as favourable here, while the same group treats blocking MMP-9 as favourable for other peptides [27].
Animal tissue The earliest paper, from 2006, added 0.05 nanograms per millilitre to organ cultures of pancreas, heart, lung and prostate from rats aged three weeks and 18 months. Each of four peptides was reported to act on its own assigned tissue. The abstract carries no figures [28].
The negative and missing results
- The vessel leakiness endpoint did not move. In the rat study, the measure that would matter most for diabetic complications was explicitly unchanged [26].
- The gene labelling story does not hold together. PAX4 readout changed without any change in labelling, and FOXA2 labelling changed without any link to readout [24].
- The licensed comparator won. In the only experiment where the substance was set against an approved medicine, the approved medicine had the stronger effect [6].
- Two papers give two different DNA targets for the same molecule, both from calculations by the same group [19], [20].
- One abstract reports no result at all. A 2010 paper on the substance's biological activity describes the method and stops there [29].
- A second rat paper is a single sentence. It states that an effect on pancreatic tissue was found, without a dose, a group size or a figure [30].
What is still unknown
- Everything about how the body handles it. No half-life, no absorption, no distribution, no breakdown and no excretion data exist, for any route or any species [18].
- Whether the oral route works at all. The Russian product is swallowed, the patent and monkey work inject, and nobody has measured whether anything is absorbed [12], [5].
- Whether any of it can be reproduced. No laboratory outside the originating circle has repeated a single finding; the one recent mention elsewhere simply cites the group's work [2], [31].
- What happens beyond four weeks. The longest recorded human exposure is 28 days [4].
- What is in the material sold. With no pharmacopoeia monograph and no official reference substance, a traded vial can be measured against nothing [11].
Side effects and safety
There is no safety record. That is not the same as being well tolerated: it means nothing has ever been systematically collected that could be reported [1], [2].
- No adverse event reports exist. The American pharmacovigilance database returned no record for the name on 20 September 2026, and no case report was found in the literature [8], [2].
- The one reassurance on offer comes from the inventors. A monkey paper concludes that the substance is effective and safe. It rests on five treated animals over ten days, with no dummy-treated group and no safety measurements reported [6].
- No toxicology has been published. There is no acute or chronic toxicity study, no dose escalation and no established no-effect level, for any species [2].
- The obvious risk has never been looked at. The substance is described as lowering blood sugar. Whether it can push blood sugar too low has not been examined in any of the published work, and no monitoring scheme appears anywhere [5], [20].
- Nothing is known about interactions. That gap matters because the patent example and the Russian sales material both describe people using it alongside glucose-lowering medicines [5], [32].
- The injected form is the least controlled of all. Vials of 10 to 50 milligrams are sold outside any pharmaceutical quality system, with sterility, endotoxin content and actual peptide content unknown [11].
Data gaps run right through the file. Nothing is known about immune reactions to the substance itself, about cancer risk, about effects on reproduction, or about pregnancy, breastfeeding, children and reduced liver or kidney function [2].
One mismatch is a hazard in its own right. A vial holds 10 to 50 milligrams, while the only injected amount ever given to a person was 10 micrograms a day. A vial therefore holds one to five thousand times that amount, which makes a measuring error the expected outcome rather than a rare one [5], [11].
Diabetes and impaired glucose tolerance are conditions that need proper medical care. Nothing on this page describes a treatment, and questions about managing blood sugar belong with a doctor.
Doses used in studies
The doses below are simply what the cited studies gave, listed so that the results can be understood. They are not advice on how to use anything.
Four lines in this table involve people, and they come from three sources: two rows from a single example inside a patent application, and one row each from the two unregistered Kyiv observations. None of them comes from a registered or reviewed trial. They are listed because they exist, not because they show anything.
| Study | Model | Amount | Route | Duration | Ref |
|---|---|---|---|---|---|
| Organ culture, 2006 | Pancreas and other tissue from rats aged 3 weeks and 18 months | 0.05 ng/ml | Added to the culture fluid | Not stated | [28] |
| Patent example 2 | Alloxan-diabetic rats, 21 animals | 3 µg per animal | Into the abdomen | 11 days | [5] |
| Patent example 4 | Alloxan-diabetic rats, 23 animals | 1 µg against 10 µg per animal | Into the abdomen | 7 days | [5] |
| Monkey study, 2014 | Old female rhesus monkeys | 50 µg per animal per day | Into the muscle | 10 days | [25] |
| Monkey study, 2015 | 5 old female rhesus monkeys | 0.05 mg per animal per day | Into the muscle | 10 days | [6] |
| Patent example 8, first subgroup, in people and not a study | 16 patients with diabetes against 16 controls | 10 µg | Into the muscle | 10 days, once daily | [5] |
| Patent example 8, second subgroup, in people and not a study | 4 patients with type 2 diabetes | 100 µg, one tablet | By mouth, before meals | 10 days, twice daily | [5] |
| Kyiv report 2013, unregistered observation in people | 12 older people with impaired glucose tolerance | 500 µg | By mouth | 4 weeks, twice daily | [4] |
| Kyiv report 2011, unregistered observation in people | Older people with type 2 diabetes | Not stated in the abstract | Not stated | Not stated | [3] |
| Patent description, wording rather than a tested amount | Not tied to any experiment | 0.1 to 30 µg per kg of body weight | Parenteral or by mouth | Not specified | [5] |
| Russian retail supplement, not a study | No study model; the manufacturer's own product figure | 100 µg of the peptide complex per capsule | By mouth | Not a study figure | [12] |
A concentration in a dish cannot be converted into an amount for a body, and neither can an amount given to a rat or a monkey. Between the smallest and the largest figure in this table lies a factor of many thousands, and no dose-finding study explains any of it [2].
The last patent line needs particular care. The figure quoted is the wording of the patent description, and it was never tested as a dose. The patent's own claims print the same range in units a thousand times larger. That alone is reason enough not to treat the document as a source on amounts [5].
The schedules circulating on sales pages sit outside all of this. One Russian trade page gives 2 to 5 milligrams a day for 20 to 30 days as an injection [13].
That is 200 to 500 times the only injected amount ever given to a person, and 40 to 100 times the monkey amount. It is derived from no study, because no study of that kind exists [5], [13].
Development and approval status
There is no development programme. Nothing was ever filed with a medicines regulator, no phase of clinical testing began, and the patent family that started it all has lapsed [1], [15].
A patent in 2003, and no clinical development since
- 2003Patent filed by the St Petersburg groupPriority filing of 10 December for a tetrapeptide said to regulate blood glucose, ref [5]
- 2005International application publishedFiled in 15 countries and regions; the family later lapsed and now carries the status ceased, ref [15]
- 2006 to 2007First tissue culture and rat papersOrgan cultures at 0.05 ng/ml, then rats with chemically induced diabetes, refs [28], [26]
- 2009United States patent grantedGranted 17 February; a property right, not an approval, ref [5]
- 2011First report of people receiving it30 healthy and 33 diabetic older people in Kyiv, with no dose, duration or figures given, ref [3]
- 2012 to 2015Cell culture, gene labelling and monkey workPancreatic cell cultures, then old rhesus monkeys where a licensed tablet had the stronger effect, refs [22], [24], [6]
- 2013Second and last human report12 older people with impaired glucose tolerance, four weeks, the reported change in half of them, ref [4]
- 20 September 2026Registers checkedNo approval in any market, no registered trial, no substance code anywhere, refs [1], [8]
- 2003 the St Petersburg group files the patent family claiming a blood-glucose-regulating tetrapeptide [5].
- 2005 the international application is published, covering 15 countries and regions; it later lapses [15].
- 2006 and 2007 the first tissue culture and rat papers appear, all from the same circle [28], [26], [30].
- 2009 the United States patent is granted, six years after filing [5].
- 2011 the first report of people receiving the substance is published in Kyiv, without figures [3].
- 2013 the second and last human report describes twelve people over four weeks [4].
- 2014 and 2015 two small monkey studies appear, the second comparing it against a licensed tablet [25], [6].
| Market | Status | Note | Ref |
|---|---|---|---|
| United States | Not approved | No substance code, no label, no adverse event file; never put forward for pharmacy compounding | [8], [33] |
| European Union | Not approved | No assessment report and no trial; the agency's own search could not be read on the day of checking | [1], [34] |
| Germany | Not approved | An unlicensed injectable preparation may not be placed on the market | [34] |
| United Kingdom | Not approved | The register returned only a page shell, so the finding rests on every other register | [34] |
| Australia | Not approved | Absent from the Poisons Standard, which is not permission to supply | [35] |
| Canada | Not approved | The medicines database returns nothing, while a control query works | [36] |
| Switzerland | Not approved | No authorisation identified, and no register query was possible | [34] |
| Russia | Not approved | Capsules and tablets are sold as a food supplement, which is not a medicine licence | [12] |
Three rows need care. The Australian entry means the substance was never scheduled, not that it may be supplied; unapproved research peptides are treated there as prescription-only material in practice. The European, British and Swiss entries rest on absence everywhere else, because those registers could not be read [35], [34].
The Russian row is the one most often misread. A food supplement is cleared as a food and passes no test of whether it works. The entry names a manufacturer, gives capsule and tablet sizes, and states plainly that the product is not a medicinal product [12].
One further sales claim belongs here for completeness. A Russian trade page describes an examination of 42 patients in 2007, with blood sugar said to normalise in all of them within five to ten days, and makes further claims about those patients' diabetes medicines. No publication and no registry entry exists for any of it [32].
All registers were checked on 20 September 2026. The wider legal picture is under are peptides legal and FDA-approved peptides.
Anti-doping
Pancragen is prohibited at all times, in and out of competition. It is not named on the 2026 list. Class S0 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" [14].
That classification is a judgement call about where the substance belongs, but not a difficult one, because there is no approval anywhere to argue about. Substances in S0 are specified substances, which affects how a sanction is measured rather than whether the ban applies [14].
One boundary is worth naming. The 2026 list also prohibits "Insulins and insulin-mimetics" in a separate class. Pancragen is described as a mimetic of the gut signals that prompt insulin release, not of insulin itself, so that class does not catch it. No anti-doping body is known to have ruled on the point [14], [20].
German anti-doping law reads differently. Its annex lists banned substances one by one and names no pancreatic tetrapeptide, so possession is not an offence there. That is a gap in a closed list, not a permission [37].
No validated test for detecting it in a sample has been published, and detecting a four-part chain of ordinary amino acids would be demanding [2]. The full picture is at peptides banned in sport.
Compared with related peptides
| Peptide | Relation to Pancragen | What the checks behind this page found |
|---|---|---|
| Pancragen | — | Lys-Glu-Asp-Trp, 575.62; nine PubMed records, no registered trial, approved nowhere [1], [2], [5] |
| Vesugen | A three-part sibling from the same series, tested in the same experiment | Lys-Glu-Asp; in that comparison it acted on connective tissue cells while Pancragen acted on pancreatic ones [23] |
| Bronchogen | The lung-assigned sibling, the third arm of that same experiment | Ala-Glu-Asp-Leu; used by the group as the contrast that makes the tissue-specificity claim [23] |
| Cortagen | A four-part cytogen of the same laboratory, assigned to the brain cortex | Ala-Glu-Asp-Pro; same naming pattern, same evidence problem, different assigned organ [16] |
| Epitalon | The group's best-known peptide, and the yardstick for how thin this file is | Ala-Glu-Asp-Gly; hundreds of papers and database entries against a handful here [7], [2] |
| Semaglutide | A licensed peptide medicine for the same area of the body | 755 registered studies against zero for Pancragen in the same registry query [1] |
The comparison is not about strength, because no head-to-head measure of effect exists against any of them. Two rows do the real work: semaglutide shows what a developed medicine for blood sugar looks like in a registry, and epitalon shows that even inside the same institute this molecule has drawn a fraction of the attention [1], [2].
The Vesugen and Bronchogen rows explain a recurring argument. The group's tissue-specificity claim rests on three peptides acting on three different tissues in one experiment, which is a single unreplicated result rather than a principle [23].
Common misconceptions
- "There are human studies, so it has been tested in people." Three occasions are recorded, none registered, none blinded, none with a stated ethics approval and none reporting effect sizes. Two are observations and one sits inside a patent application [1], [3], [4], [5].
- "The patent's 36 patients are clinical evidence." A patent is examined for novelty and inventiveness, not for medical results. That example appears in no registry and no journal, and the family has since lapsed [5], [15].
- "It is registered in Russia." It is registered there as a food, in capsules and tablets, and the entry states that it is not a medicinal product. A food registration involves no test of whether a product works [12].
- "The capsule and the injection are the same thing." The Russian supplement carries 100 micrograms of a peptide complex plus fillers. The Western vial holds 10 to 50 milligrams of powder for injection. No data connects the two [12], [11].
- "The powder sold in the West is the studied molecule." Every paper and the patent describe the amide form. Sellers declare the free acid, which differs in charge and in how fast enzymes cut it, and has never been tested [5], [10], [11].
- "It is a mimetic of insulin." The phrase in the literature is mimetic of insulinotropic peptides, meaning the gut signals that prompt insulin release. It is a hypothesis from a calculation paper, and no receptor has been identified [20].
- "The epigenetic mechanism is established." Two papers from the same group name two different DNA targets, and the group's own labelling study found two genes that behave the other way [19], [20], [24].
- "Bioregulator and cytogen are official categories." They are house words of one institute and its distributors, absent from every pharmacopoeia, classification and regulator definition [16], [17].
- "It is not on the doping list, so it is allowed." It is not named, but class S0 catches every substance no health authority has approved, which is exactly its situation [14].
- "Searching KEDW shows plenty of research." Two of the six PubMed hits for that string are false: an author's email address and a set of author initials in unrelated cardiology papers [38].
- "The islet organoid paper is about this peptide." That 2023 paper tests a different peptide taken from collagen, and cites this one only in passing [39].
Frequently asked questions
What is Pancragen?
It is a synthetic chain of four amino acids, lysine, glutamic acid, aspartic acid and tryptophan, written Lys-Glu-Asp-Trp or KEDW. The published work and the patent describe it with an amide cap at one end, formula C26H37N7O8 and mass 575.62. It comes from a St Petersburg institute that calls such molecules bioregulators and cytogens, house words with no standing in any official classification.
Has Pancragen ever been tested in people?
Not in a registered trial. A registry check on 20 September 2026 returned nothing under any spelling of the name. People received it on three recorded occasions: two reports from a Kyiv research group and one example inside the inventors' patent. None was registered, blinded or independently reviewed, and none reports effect sizes.
What did the human reports of Pancragen actually show?
Very little that can be checked. The 2011 report gives no dose, no route, no duration and not a single figure for the peptide's effect. The 2013 report describes twelve older people with impaired glucose tolerance taking it for four weeks, with the reported change appearing in half of them. Neither is a controlled trial, and neither can show whether the substance works.
Is Pancragen approved as a medicine anywhere?
No, in no country. Register checks on 20 September 2026 found no approval in the United States, the European Union, Germany, the United Kingdom, Australia, Canada, Switzerland or Russia. In Russia it is sold as a capsule and tablet food supplement, and the entry states in its own words that it is not a medicine.
Does the Pancragen patent mean it has been approved or proven?
No. A granted patent is a property right over an invention, examined for novelty and inventiveness rather than for effect, safety or the right to sell. No medicines regulator took part in granting it, and the international family lapsed years ago.
Is the Pancragen sold in the West the same molecule that was studied?
Not as declared. The published work and the patent describe the amide form, Lys-Glu-Asp-Trp-NH2. Western sellers declare their powder as the free acid, H-Lys-Glu-Asp-Trp-OH. That cap changes charge and how quickly enzymes cut the chain, and no published work has tested the free acid.
How much Pancragen has ever been given to a person?
Three amounts have been described: 10 micrograms into the muscle for ten days and 100 micrograms twice a day by mouth for ten days, both in a patent example, and 500 micrograms twice a day by mouth for four weeks in the 2013 report. None of the three comes from a registered or reviewed trial. Injection schedules circulating on sales pages run to 2 to 5 milligrams a day, hundreds of times the injected figure, and come from no study.
Is Pancragen banned in sport?
Yes, at all times, in and out of competition. The name is not printed on the 2026 prohibited list. Class S0 covers any pharmacological substance that no government health authority has approved for human use, which describes this one exactly.
What are the side effects of Pancragen?
Nobody knows, because no study has ever collected them. There is no published toxicology, no adverse event report in the American database and no case report in the literature. The obvious question for a substance said to lower blood sugar, whether it can push blood sugar too low, has never been examined.
Is the Russian Pancragen capsule the same as the injectable powder?
No. The Russian product is a food supplement containing 100 micrograms of a peptide complex plus fillers, swallowed as a capsule or tablet. The Western product is a 10 to 50 milligram vial of powder for injection. Several orders of magnitude separate them, and no absorption data exists for either route.
Sources
- ClinicalTrials.gov, API v2, queried 20 September 2026. query.intr for "Pancragen", "Pankragen" and "KEDW" each returned a total count of zero, as did query.term for "pancragen". query.intr for "Lys-Glu-Asp-Trp" returns one unrelated amino acid study (NCT05400733, Texas A&M University). The control query for semaglutide returned 755 studies, so the interface was working. No entry with the sponsor "Hudson Biotech" was found. https://clinicaltrials.gov/api/v2/studies
- PubMed via NCBI E-utilities and Europe PMC REST search, queried 20 September 2026. "Pancragen" returns nine PubMed records through the MeSH mapping, "Lys-Glu-Asp-Trp" seven, "Lys-Glu-Asp-Trp-NH2" eight, "KEDW" six of which two are false hits, and "pancragene" one. Europe PMC returns 23 records for "pancragen", six of which concern the substance. All relevant abstracts were read in full. No pharmacokinetic study, no toxicology study, no case report and no doping-control detection method was found. Authorship of the entire body of work rests with the St Petersburg institute and its co-authors.
- Korkushko OV, Khavinson VKh, Shatilo VB, Antonyk-Sheglova IA, Bondarenko EV (2011). Prospects of using pancragen for correction of metabolic disorders in elderly people. Bulletin of Experimental Biology and Medicine 151(4):454-456. PMID 22448364. DOI 10.1007/s10517-011-1354-4. Abstract read 20 September 2026: 30 healthy older people and 33 older patients with type 2 diabetes; nocturnal melatonin production "significantly reduced by 70%" in the diabetic group against healthy people of the same age; reported falls in fasting glucose, glucose during a standard tolerance test, plasma insulin and an insulin resistance index, with "no changes in carbohydrate metabolism indices" in participants receiving nothing. The abstract states no dose, no route, no duration, no treated group size, no randomisation, no blinding and no figures. The study appears in no trial registry.
- Korkushko OV, Chizhova VP, Shatilo VB, Khavinson VK (2013). The tetrapeptide pankragen forte efficiency in elderly people with prediabetic state. Advances in Gerontology 26(2):297-308. In Russian with English abstract. PMID 28976155. Abstract read in both languages 20 September 2026: 150 people screened, 39 young, 42 middle-aged and 69 older; twelve of the older group with impaired glucose tolerance received "500 mkg 2 times a day (morning and evening) for 4 weeks"; a 75 gram oral glucose tolerance test was measured fasting and at 30, 60 and 120 minutes alongside HbA1c, proinsulin, HOMA-IR, the Matsuda index and HOMA-%; the reported result is a significant fall in plasma glucose "in 50 percent" of the twelve. No control group, no randomisation, no blinding, no effect sizes and no registration.
- Khavinson VKh, Malinin VV, Grigoriev EI, Ryzhak GA. Tetrapeptide regulating blood glucose level in diabetes mellitus. US 7,491,703 B2; priority 10 December 2003, granted 17 February 2009; applicants Access Bioscience CJSC and "peptid Products" LLC. Full text read 20 September 2026: the sequence "Lys-Glu-Asp-Trp-NH2 SEQ ID NO:1", formula C26H37N7O8 and "molecular weight 575.62"; the synthesis through protected intermediates; examples 2 to 7 in alloxan-diabetic rats, including 3 micrograms per animal into the abdomen for 11 days in 21 animals with a reported 38.4 per cent fall in blood glucose and 36.4 per cent mortality against 70 per cent in controls; and example 8 in 36 patients, seven men and 29 women aged 16 to 83, of whom 16 received 10 micrograms in 1 ml of saline into the muscle once daily for ten days against 16 controls, and four with type 2 diabetes received 100 micrograms as one tablet twice daily before meals for ten days. The description states a range of "0.1-30 μg/kg of the body weight at least once a day", while claim 8 of the same document prints the same range in milligrams per kilogram. A patent application is examined for novelty and inventiveness, not for medical results, and none of these experiments has been published in a journal or entered in any registry. https://patents.google.com/patent/US7491703B2/en
- Goncharova ND, Ivanova LG, Oganyan TE, Vengerin AA, Khavinson VK (2015). Correction of impaired glucose tolerance using tetrapeptide (Pancragen) in old female rhesus monkeys. Advances in Gerontology 28(3):579-585. In Russian with English abstract. PMID 28509500. Abstract read 20 September 2026: nine clinically healthy old female rhesus monkeys aged 20 to 25 years; five received 0.05 mg per animal per day into the muscle for ten days and four received glimepiride 4 mg per animal per day by mouth for ten days. Both lowered basal blood glucose; glimepiride had "the more expressed and delayed hypoglycemic effect". The authors conclude the tetrapeptide is "effective and safe", a conclusion five treated animals without a dummy-treated group cannot carry. No p-values or group statistics appear in the abstract.
- PubChem, checked through the NCBI E-utilities index on 20 September 2026 because the PUG-REST interface returned server-busy faults for every query including the control. esearch db=pccompound for "Pancragen", "KEDW", "Lys-Glu-Asp-Trp" and "lysyl-glutamyl-aspartyl-tryptophanamide" each returned zero, while the control query "epitalon" returned four compound records. A formula search for C26H37N7O8, the amide form, returned zero; C26H36N6O9, the free acid, returned exactly one record, CID 73356311, which is the unrelated chymotrypsin substrate Suc-Ala-Ala-Pro-Val-pNA. esearch db=pcsubstance returned zero for the name and the sequence against 55 substance records for the control. No CAS registry number could be found in any of these routes or by search. https://eutils.ncbi.nlm.nih.gov/entrez/eutils/esearch.fcgi?db=pccompound
- United States register checks, 20 September 2026. FDA Global Substance Registration System: "pancragen" and "KEDW" each returned zero records, while the control query "epitalon" returned two, so the substance has no regulator code and no UNII. openFDA drug label, adverse event and NSDE endpoints: not found for the name, against 18 control label hits for semaglutide. DailyMed web services v2: zero entries, database state 18 September 2026, against a control hit for Ozempic. https://gsrs.ncats.nih.gov and https://api.fda.gov
- Wikidata, wbsearchentities in English for "Pancragen" and "Pankragen", queried 20 September 2026: no entity exists under either spelling. "KEDW" returns only surnames and place names. The control query "epitalon" returns Q126487100 and Q27285389. https://www.wikidata.org/w/api.php
- United States National Library of Medicine, MeSH supplementary concept record UID 67531938, "lysyl-glutamyl-aspartyl-tryptophanamide", retrieved through E-utilities 20 September 2026. Entry terms Lys-Glu-Asp-Trp-NH2, KEDW-NH2 and pancragen; heading mapped to Oligopeptides; described as having "homeostatic and endothelioprotective activities". The record is for the amide form. https://eutils.ncbi.nlm.nih.gov/entrez/eutils/efetch.fcgi?db=mesh&id=67531938
- Western research-chemical listings for the substance, retrieved 20 September 2026 from sellers in the United States, the United Kingdom and Canada. Vial sizes of 10, 20 and 50 mg of freeze-dried powder; the sequence is declared as "H-Lys-Glu-Asp-Trp-OH (KEDW)", that is the free acid rather than the amide described in the literature; purity is stated as at or above 99 per cent by the seller without independent testing; the material is labelled for research use only. Trade records, cited only as evidence of what is sold and how it is declared. Not linked.
- Russian medicines directory RLS, entry for Панкраген® in the food supplement section rather than the medicines section, read 20 September 2026. Contents given as "peptide complex AKS-P (lysine, glutamic acid, aspartic acid, tryptophan)", 100 micrograms per capsule, with microcrystalline cellulose, beet sugar, lactose, starch and Tween-80 as fillers; capsules of 0.2 g and 0.275 g and tablets of 0.16 g and 0.3 g; manufacturer named; intake given as one to two capsules once or twice a day for one month, repeated after four to six months; and the explicit statement that the product is not a medicinal product. A validity date of 17 October 2012 is noted. No injectable form is registered there. https://www.rlsnet.ru/baa/pankragen-32632
- Russian trade page for 20 mg vials of the substance, retrieved 20 September 2026. Gives an injection schedule of 2 to 5 mg once daily for 20 to 30 days, under the skin or into the muscle, repeated up to twice a year, names Taiwan as the origin of the material and states on the same page that the product is not a medicine. Trade record, cited only as evidence that such schedules circulate. Not linked.
- World Anti-Doping Agency. The 2026 Prohibited List, in force 1 January 2026, full text checked 20 September 2026. Class S0 Non-Approved Substances: "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", and all substances in that class are specified substances. Section S4.4.2 reads "Insulins and insulin-mimetics, e.g. S519, S597". A full-text search for "pancrag", "KEDW" and "Lys-Glu-Asp" returned no match, while BPC-157 appears in the same text as a control. https://www.wada-ama.org/en/prohibited-list
- Khavinson VKh, Malinin VV, Grigoriev EI, Ryzhak GA. Tetrapeptide regulating blood glucose level in diabetes mellitus. International application WO 2005/056580 A1, filed 9 August 2004, published 23 June 2005, filed in 15 countries and regions. Family status read 20 September 2026: "Ceased". The description states the intended effect as "insulin secretion increase and increase of tissue sensitivity to insulin". https://patents.google.com/patent/WO2005056580A1/en
- Khavinson V, Linkova N, Kozhevnikova E, Dyatlova A, Petukhov M (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 read 20 September 2026: the cytogen and cytomax tables that define the group's own vocabulary, KEDW among the stronger candidate LAT2 inhibitors by calculation, and a reference to a hydrolysis study of AEDG, KE, KEDW and KEDA in saline, Ringer solution, hydrochloric acid and homogenates of stomach, small and large intestine, liver, kidney and spleen, for which no figures for KEDW are reproduced. The original hydrolysis paper was not accessible.
- Khavinson V, Linkova N, Dyatlova A, Kuznik B, Umnov R (2021). Peptides Regulate Cognitive Functions and Gene Expression: A Systematic Review. Molecules 26(23):7053. PMID 34834147. PMCID PMC8619776. Full text read 20 September 2026: places KEDW in the cytogen series of synthesised short peptides as against the cytomax series of tissue-extracted polypeptide complexes, and states that "the KEDW peptide stimulates the maturation of various types of human pancreatic cells". A review by the originating group, cited here for how the group classifies its own products rather than as independent evidence.
- 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 read 20 September 2026: KEDW-NH2 carries calculated ICM docking scores of −21.78 against the model 7B00 and −20.57 against 7PN1. These are calculations, not measurements; no transport assay and no competition experiment for this peptide appears here or anywhere else searched, and no pharmacokinetic data exists for any route or species.
- Khavinson VK, Lin'kova NS, Tarnovskaya SI (2016). Short Peptides Regulate Gene Expression. Bulletin of Experimental Biology and Medicine 162(2):288-292. PMID 27909961. DOI 10.1007/s10517-016-3596-7. Abstract read 20 September 2026: molecular docking of short peptides to DNA, reporting that "peptides KEDW and AED" bind the "acct" sequence. This differs from the binding site proposed by the same group in the molecular mechanics paper above for the same molecule.
- Tarnovskaya SI, Yakutseni PP, Khavinson VKh (2014). Study of interactions between DNA and tetrapeptides using methods of molecular mechanics. Bulletin of Experimental Biology and Medicine 156(5):689-693. PMID 24770759. DOI 10.1007/s10517-014-2426-z. Abstract read 20 September 2026: a molecular mechanics calculation proposing that the tetrapeptide can interact with the major as well as the minor groove of DNA, with "Sequence GGCAG is the putative binding site". The same abstract contains the sentence "Tetrapeptide Lys-Glu-Asp-Trp is a mimetic of insulinotropic peptides and reduces the blood glucose level". No structural determination and no binding assay accompanies it.
- Fedoreyeva LI, Smirnova TA, Kolomijtseva GY, Khavinson VKh, Vanyushin BF (2013). Interaction of short peptides with FITC-labeled wheat histones and their complexes with deoxyribooligonucleotides. Biochemistry (Moscow) 78(2):166-175. PMID 23581987. DOI 10.1134/S0006297913020053. Abstract read 20 September 2026: Lys-Glu-Asp-Trp binds all four histone types tested, judged by fluorescence quenching, with binding depending on histone type, peptide sequence and oligonucleotide. The histones come from wheat, a plant model rather than human chromatin, and the peptide is one of six examined.
- Khavinson VKh, Durnova AO, Polyakova VO, Tolibova GH, Linkova NS, Kvetnoy IM, Kvetnaia TV, Tarnovskaya SI (2013). Effects of pancragen on the differentiation of pancreatic cells during their ageing. Bulletin of Experimental Biology and Medicine 154(4):501-504. PMID 23486591. DOI 10.1007/s10517-013-1987-6. Abstract read 20 September 2026: raised expression of Pdx1 and Ptf1a in acinar cells and of Pdx1, Pax6, Pax4, Foxa2 and Nkx2.2 in islet cells, in young and aged human pancreatic cultures. No concentrations, effect sizes, group sizes or p-values are given. The authors conclude the peptide may be "an effective tool in the treatment of diabetes mellitus and pancreatitis", which the experiment cannot support.
- Khavinson VKh, Linkova NS, Polyakova VO, Kheifets OV, Tarnovskaya SI, Kvetnoy IM (2012). Peptides tissue-specifically stimulate cell differentiation during their aging. Bulletin of Experimental Biology and Medicine 153(1):148-151. PMID 22808515. DOI 10.1007/s10517-012-1664-1. Abstract read 20 September 2026: in human embryonic pancreatic cells the tetrapeptide stimulated CXCL12 and Hoxa3, while Bronchogen (Ala-Glu-Asp-Leu) acted on bronchial epithelium and Vesugen (Lys-Glu-Asp) on prostate fibroblasts. The effect is reported as more pronounced in aged cultures. No concentrations or figures are given, and the experiment has not been repeated elsewhere.
- Ashapkin VV, Linkova NS, Khavinson VKh, Vanyushin BF (2015). Epigenetic mechanisms of peptidergic regulation of gene expression during aging of human cells. Biochemistry (Moscow) 80(3):310-322. PMID 25761685. DOI 10.1134/S0006297915030062. Abstract read 20 September 2026: in ageing human pancreatic cultures, promoter methylation of PDX1, PAX6 and NGN3 changed in line with expression; PAX4 methylation changed neither with culture age nor under the peptide although expression changed; FOXA2 promoter methylation was affected "though without any correlation with gene expression levels". The authors conclude that PAX4 and FOXA2 are governed "by some other mechanisms".
- Goncharova ND, Ivanova LG, Oganian TÉ, Vengerin AA, Khavinson VKh (2014). Impact of tetrapeptide pancragen on endocrine function of the pancreas in old monkeys. Advances in Gerontology 27(4):662-667. In Russian with English abstract. PMID 25946840. Abstract read 20 September 2026: 50 micrograms per animal per day into the muscle for ten days in old female rhesus monkeys raised the glucose disappearance rate and normalised insulin and C-peptide dynamics after a glucose load, with part of the effect still present three weeks after stopping. No group sizes and no p-values are given.
- Khavinson VKh, Gavrisheva NA, Malinin VV, Chefu SG, Trofimov EL (2007). Effect of pancragen on blood glucose level, capillary permeability and adhesion in rats with experimental diabetes mellitus. Bulletin of Experimental Biology and Medicine 144(4):559-562. PMID 18642713. DOI 10.1007/s10517-007-0377-3. Abstract read 20 September 2026: oral administration produced a "pronounced hypoglycemic effect" during treatment, while administration into the muscle normalised endothelial adhesion in mesenteric capillaries but did not change capillary permeability. No dose, group size or statistics appear in the abstract.
- Khavinson VKh, Sevost'ianova NN, Durnova AO, Lin'kova NS, Tarnovskaia SI, Dudkov AV, Kvetnaia TV (2012). Tetrapeptide stimulates functional activity of the pancreatic cells in aging. Advances in Gerontology 25(4):680-684. In Russian. PMID 23734516. Abstract read 20 September 2026: H-Lys-Glu-Asp-Trp-NH2 raised MMP2, MMP9, serotonin, CD79alpha, Mcl1, PCNA and Ki67 and lowered p53 in aged human pancreatic cell cultures. The rise in the two matrix metalloproteinases is presented as favourable here, while the same group presents inhibition of MMP-9 as favourable for other peptides.
- Zakutskiĭ AN, Chalisova NI, Ryzhak GA, Aniskina AI, Filippov SV, Zeziulin PN (2006). The tissue-specific effect of synthetic peptides-biologic regulators in organotypic tissues culture in young and old rats. Advances in Gerontology 19:93-96. In Russian. PMID 17152728. Abstract read 20 September 2026: organotypic cultures of pancreas, heart, lung and prostate from rats aged three weeks and 18 months, with an effective peptide concentration of 0.05 ng/ml; each of four peptides is reported to stimulate its own assigned tissue against control explants. No figures are given.
- Khavinson VKh, Gapparov MM, Sharanova NE, Vasilyev AV, Ryzhak GA (2010). Study of biological activity of Lys-Glu-Asp-Trp-NH2 endogenous tetrapeptide. Bulletin of Experimental Biology and Medicine 149(3):351-353. PMID 21246099. DOI 10.1007/s10517-010-0944-x. Abstract read 20 September 2026: two sentences describing rat ontogenesis and streptozotocin diabetes as a model of accelerated ageing and an assessment through apoptosis-related metabolic parameters, with no result, no direction of effect and no figure stated. The title describes the tetrapeptide as endogenous; no independent confirmation that it occurs naturally in the human pancreas was found.
- Kvetnoi IM, Ryzhak AP, Kostyuchek IN, Tafeev YA (2007). Effect of tetrapeptide pancragene on functional morphology of the pancreas in rats with experimental diabetes mellitus. Bulletin of Experimental Biology and Medicine 143(3):368-371. PMID 18225766. DOI 10.1007/s10517-007-0114-y. Abstract read 20 September 2026: a single sentence reporting a regulating effect on the morphology and function of pancreatic tissue, with no dose, no group sizes and no figures.
- Vishwanath R, Biswas A, Modi U, Gupta S, Bhatia D, Solanki R (2025). Programmable short peptides for modulating stem cell fate in tissue engineering and regenerative medicine. Journal of Materials Chemistry B 13(8):2573-2591. PMID 39871657. DOI 10.1039/d4tb02102a. Abstract read 20 September 2026: the only recent mention of KEDW from outside the originating circle, referring to the group's published work without contributing any data of its own.
- Russian trade article claiming clinical results for the product, retrieved 20 September 2026. It describes an examination said to have taken place at a medical centre of the St Petersburg institute in September and October 2007, covering 42 treated patients, 18 with chronic pancreatitis and 24 with type 2 diabetes, against 25 controls, with blood sugar said to normalise in all treated patients within five to ten days. The same page makes claims about patients reducing and stopping their glucose-lowering medicines; those claims are not reproduced here, because no examination behind them exists in PubMed, in Europe PMC or in any registry, and decisions about prescribed treatment belong with a doctor. Trade record, cited only as evidence of an unsupported marketing claim. Not linked.
- United States Food and Drug Administration. Bulk Drug Substances Nominated for Use in Compounding Under Section 503A of the Federal Food, Drug, and Cosmetic Act. Downloaded and checked in full text 20 September 2026: no match for "pancrag", "lys-glu", "KEDW" or "tryptophan" in any of the three categories, while the dipeptide alanyl-L-glutamine appears as a control showing that short peptides are listed there when nominated. https://www.fda.gov/media/94155/download
- Registers that could not be read on 20 September 2026, documented here rather than treated as confirmed negative findings: the European Medicines Agency search returned HTTP 403 directly and HTTP 401 through a fetching tool; the British medicines register returned only the JavaScript shell of its search page, with the control query for semaglutide returning an identical response of exactly 122,696 bytes; the Swiss page returned HTTP 404; the Australian goods register returned HTTP 500; and the Russian state medicines register and the Russian register of supplement certificates could not be queried successfully. The findings for those markets therefore rest on the absence of any entry in every register that could be read and on the absence of any clinical development. Under German and European law, an unlicensed preparation for injection may not be placed on the market in any case.
- Commonwealth of Australia. Therapeutic Goods (Poisons Standard—June 2026) Instrument 2026, authorised version registered 27 and 28 May 2026, full text checked 20 September 2026: no entry for "Pancragen", "KEDW", "Lys-Glu" or "tryptophanamide", and no general heading covering peptides. The control term "alanylglutamine" appears twice in the same text, so short peptides are indeed listed there by name when they are scheduled at all. Absence from the standard means the substance was never scheduled, not that it may be supplied.
- Health Canada, Drug Product Database API, brand-name query for "pancragen" on 20 September 2026: empty result, while the control query for Ozempic returns DIN 02471469. https://health-products.canada.ca/api/drug/drugproduct/
- Germany, annex to section 2(3) of the Anti-Doping Act, official text as published in the Federal Law Gazette 2023 I no. 67, read in full 20 September 2026: no entry for "pancrag", "KEDW" or "Lys-Glu-Asp". Section II on peptide hormones, growth factors, related substances and mimetics lists erythropoiesis-stimulating agents and HIF activators, chorionic gonadotrophin and luteinising hormone with their releasing factors, corticotrophins, growth hormone with its analogues and fragments, growth hormone releasing hormone, secretagogues and releasing peptides, and growth factors including IGF-1, MGF and TB-500, all by name. The metabolic modulators position lists insulins, PPAR-delta agonists and AMPK axis agonists. No catch-all position covers a pancreatic tetrapeptide.
- False hits on the string "KEDW" in PubMed, checked 20 September 2026. Niaz S et al. (2021), CJEM 23(3):325-329, PMID 33959927, matches through an author email address; Chew DS et al. (2020), Circulation: Cardiovascular Quality and Outcomes 13(12):e007094, PMID 33280436, matches through the author initials "K.E.D.W.". Both are cardiology papers with no connection to the substance.
- Kim J et al. (2023). Extracellular matrix-derived peptide stimulates the generation of endocrine progenitors and islet organoids from iPSCs. Journal of Tissue Engineering 14. PMID 37435573. PMCID PMC10331343. Full text checked 20 September 2026: the peptide tested is WWASKS, derived from collagen type V, and not KEDW, which appears only as a literature citation. It is not an independent confirmation of anything on this page.
Cite this page
The searches and register checks behind this page were run on 20 September 2026. For a substance with almost no scientific record, the date on which those searches came back nearly empty is part of the finding. Three things could still move it: a registered trial, an independent replication of any single result, or a change in the anti-doping classification.
myPeptides Research & Editing. (2026). Pancragen: what the studies show, status and safety. Version 1.0, 20 September 2026. myPeptides Peptide Register. Retrieved from https://mypep.app/peptides/pancragen
How pages in this register are compiled and graded is described under methodology; the full register is at peptides.
| Version | Date | Change |
|---|---|---|
| 1.0 | 2026-09-20 | Initial publication |
Last verified: 20 September 2026. Next review: on any registered trial, on any independent replication of the monkey or human reports, or on any change to the anti-doping classification.
