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bioregulator · metabolic

Pancragen

Also known as: KEDW, Lys-Glu-Asp-Trp-NH2, lysyl-glutamyl-aspartyl-tryptophanamide, Pankragen

Human trial draft

A synthetic tetrapeptide amide (Lys-Glu-Asp-Trp-NH2) developed as a pancreatic bioregulator and studied almost entirely for glucose metabolism. It has more evidence behind it than most Khavinson cytogens — one small uncontrolled study in older adults, a nine-animal monkey study and a rat diabetes model — but the compound's developer or his institute appears on every one of those reports, none has been replicated by an unconnected group, and PubMed indexes only nine records for the name in total.

Sequence
KEDW

Lys-Glu-Asp-Trp · 4 residues · 575.62 Da (computed)

Lysine at position 1 (terminal).

single source C26H37N7O8

Sequence source: PubMed MeSH Supplementary Concept 'lysyl-glutamyl-aspartyl-tryptophanamide', to which the query term Pancragen maps, corroborated by the title of PMID 21246099: 'Study of biological activity of Lys-Glu-Asp-Trp-NH2 endogenous tetrapeptide'. Both rungs come from the same PubMed indexing chain, and PubChem holds no record for either name, so this is recorded as single-source rather than verified.

Khavinson lineage

Bioregulator context

Target tissue: pancreas (endocrine)

That a four-residue peptide corresponding to a regulatory motif of pancreatic tissue can restore the endocrine function of the ageing pancreas, and that this is one instance of a general rule by which short peptides regulate transcription in the tissue they derive from.

Proposed to raise expression of the transcription factors that drive differentiation of acinar and islet cells — Pdx1, Ptf1a, Pax6, Pax4, Foxa2, Nkx2.2 — and thereby restore insulin-secreting capacity lost with age. The transcription-factor evidence comes from cell culture; the glucose effects come from separate animal and human work, and no study links the two.

Claimed vs established

Mechanism

Claimed

Restores the endocrine function of the ageing pancreas and corrects insulin resistance by stimulating differentiation of islet and acinar cells.

Actually established

Nothing has been established in humans.

Honest appraisal

How good is the evidence

Human trial 0 human RCTs · 1 human trials · 3 animal

Better than most compounds in this family, which is a low bar. The strongest single item is a 2011 report from Kiev in 30 healthy older adults and 33 older patients with type 2 diabetes, where fasting and post-load glucose, insulin and an insulin-resistance index all fell in the treated diabetic patients and did not change in those untreated; it was not randomised, not blinded, and its senior author is the compound's developer. Below that sit a nine-animal rhesus monkey study, a streptozotocin rat model, and cell-culture work on pancreatic differentiation markers. Nothing has been replicated outside the originating network.

Where this evidence comes from

Khavinson is an author on all five studies cited here. The human study comes from the Institute of Gerontology in Kiev with Khavinson as second author; the monkey work comes from the Research Institute of Medical Primatology in Sochi, again with Khavinson attached and the peptide supplied by the Saint Petersburg Institute of Bioregulation and Gerontology, which the paper names outright. Four of the five appeared in Bulletin of Experimental Biology and Medicine or Advances in Gerontology. There is no study of this compound by a group with no connection to its developer.

What is said vs what was shown

Claims, one at a time

Each claim carries its own evidence tier. A compound is never simply "well studied" — some of its claims may be, others not at all.

ClaimVerdictEvidenceBasis
Corrects insulin resistance and impaired glucose tolerance in older people mixed Human trial One prospective, non-randomised, unblinded study in 63 older adults reported significant falls in fasting and post-load glucose, insulin and insulin-resistance index in treated type 2 diabetic patients, with no change in untreated patients. The developer is a co-author, allocation is not described in the abstract, and no independent group has repeated it.
Restores the endocrine function of the ageing pancreas mixed Animal Reported in nine old rhesus monkeys, of which five received the peptide, with normalisation of insulin and C-peptide alongside a fall in basal glucose; the active comparator glimepiride produced a stronger glucose effect. Supported at cell level by increased expression of islet and acinar differentiation factors in aged cultures. Both strands are developer-affiliated, and the monkey study's own conclusion that the compound is 'effective and safe' rests on five treated animals over a short course.
Lowers blood glucose and protects the vascular endothelium in diabetes mixed Animal In streptozotocin-diabetic rats, a hypoglycaemic effect was reported for the oral route and normalised mesenteric capillary adhesion for the intramuscular route, with no change in capillary permeability. A single developer-authored study in an acute chemical model of diabetes, which is a poor proxy for type 2 diabetes in people.
Acts as a tissue-specific epigenetic regulator of pancreatic gene expression mixed In vitro Increased expression of Pdx1, Ptf1a, Pax6, Pax4, Foxa2 and Nkx2.2 was reported in young and aged pancreatic cell cultures. The observation is a change in marker expression in a dish; the interpretation that a four-residue peptide reaches and regulates those promoters directly is not established by it.
Primary sources

The studies themselves

StudyDesignSubjectsQuality
Prospects of using pancragen for correction of metabolic disorders in elderly people
Korkushko OV, Khavinson VKh, Shatilo VB, Antonyk-Sheglova IA, Bondarenko EV · Bulletin of experimental biology and medicine · 2011 PMID 22448364 		open_label_trial / human 63 — 30 healthy older adults and 33 older patients with type 2 diabetes mellitus Human trial
risk of bias: high
authored by the developer
[Correction of impaired glucose tolerance using tetrapeptide (Pancragen) in old female rhesus monkeys]
Goncharova ND, Ivanova LG, Oganyan TE, Vengerin AA, Khavinson VK · Advances in gerontology = Uspekhi gerontologii · 2015 PMID 28509500 ru		 animal_controlled / monkey 9 — Nine clinically healthy old (20–25 years) female rhesus monkeys (Macaca mulatta); five received Pancragen and four an active comparator Animal
risk of bias: high
authored by the developer
Effect of pancragen on blood glucose level, capillary permeability and adhesion in rats with experimental diabetes mellitus
Khavinson VKh, Gavrisheva NA, Malinin VV, Chefu SG, Trofimov EL · Bulletin of experimental biology and medicine · 2007 PMID 18642713 		animal_uncontrolled / rat — Wistar rats with streptozotocin-induced diabetes mellitus Animal
risk of bias: high
authored by the developer
Effects of pancragen on the differentiation of pancreatic cells during their ageing
Khavinson VKh, Durnova AO, Polyakova VO, Tolibova GH, Linkova NS, Kvetnoy IM, Kvetnaia TV, Tarnovskaya SI · Bulletin of experimental biology and medicine · 2013 PMID 23486591 		in_vitro / cell_culture — 'Young' and 'aged' pancreatic cell cultures In vitro
risk of bias: high
authored by the developer
Study of biological activity of Lys-Glu-Asp-Trp-NH2 endogenous tetrapeptide
Khavinson VKh, Gapparov MM, Sharanova NE, Vasilyev AV, Ryzhak GA · Bulletin of experimental biology and medicine · 2010 PMID 21246099 		animal_uncontrolled / rat — Animals across ontogeny and in streptozotocin-induced experimental diabetes, described by the authors as a model of accelerated ageing Animal
risk of bias: high
authored by the developer
What we do not know
  • No randomised or placebo-controlled trial exists in any species; the single human study was unblinded and its allocation method is not described.
  • No human pharmacokinetic data exists — absorption, half-life, distribution and clearance are uncharacterised for every route, including the oral capsules sold under this name.
  • No database record (PubChem, CAS) exists for this compound, so its molecular mass has never been confirmed against an independent source; the formula given here is computed, not transcribed.
  • Nothing is known about duration: no study followed a treated human or animal beyond the immediate course, and no long-term safety data of any length exists.
  • Whether the glucose effects reported in a chemically induced rat model of beta-cell destruction have any bearing on age-related insulin resistance in people is untested.
  • No study of this compound has been performed by a group unconnected to its developer, so no finding here has been independently replicated.
  • No dose from any cited study is recorded here, because no full text has been read.
  • The Russian-language literature has not been read or translated for this entry, only its English abstracts.
Discussion, not evidence

What people actually report

Read this differently from everything above. Public posts from Reddit and X. Nothing here has been verified beyond confirming the post exists, and community reports are the weakest tier this site recognises. Doses discussed in these threads are deliberately not reproduced.
  • claims about glucose metabolism support
  • interest in combining Pancragen with GLP-1 drugs

What people keep asking

  • What evidence is discussed for glucose metabolism support?
  • Can Pancragen be combined with a GLP-1 drug?