F tier · safety concern
The entire human record is a single non-randomised, non-blinded, placebo-free comparison in 33 elderly type 2 diabetes patients from the originating collaboration, with zero registered trials on ClinicalTrials.gov and no replication by any laboratory not co-authored by Khavinson in nearly two decades.
pancragen
Pancragen is the pancreas-directed member of the Khavinson short-peptide series, published as the tetrapeptide amide Lys-Glu-Asp-Trp-NH2. Its evidence consists of in vitro work on pancreatic cell differentiation markers, a streptozotocin diabetes model, glucose-tolerance experiments in old rhesus monkeys, and one small uncontrolled human observation in elderly type 2 diabetes. Every one of those reports is co-authored by Khavinson and appears in Bulletin of Experimental Biology and Medicine or Advances in Gerontology.
// we supply this one
available as a research reagent
≥ 98% HPLC · lyophilised powder · batch certificate published. Grade F above is our own and is not adjusted because we stock it.
the explanation
Pancragen is a four-amino-acid peptide from a Russian institute, sold as a pancreas and blood-sugar peptide. There is real laboratory work behind it, including experiments in aged monkeys, but the only human data is one small study in 33 older diabetic patients where the comparison group simply received nothing — no placebo, no randomisation. No trial has ever been registered and no laboratory outside the originating group has repeated any of it.
regulatory status
No medicinal approval anywhere; unlicensed in the UK; research reagent only
Pancragen holds no marketing authorisation as a medicine in the UK, EU or US, and no MHRA, EMA or FDA assessment of it exists. A ClinicalTrials.gov query returns zero registered studies of Pancragen. In Russia it is distributed within the consumer peptide range associated with Khavinson's institute rather than as a registered medicine, and Khavinson's own 2014 review of clinical results for the group's bioregulators does not include it. It is not named on the WADA Prohibited List. In the UK it is not a licensed medicine, not a prescription-only medicine, not a controlled drug and not an authorised supplement ingredient; lawful supply is as a laboratory reagent not for human consumption.
how it works · proposed mechanism
The proposed mechanism is nuclear entry and promoter-level regulation of pancreatic transcription factors, producing tissue-specific restoration of islet and acinar function with age. The supporting data are real but confined to cultures, a chemically induced rodent diabetes model and a small primate experiment. None of it demonstrates the pathway in humans.
Differentiation-factor expression in ageing pancreatic culture
In ageing pancreatic cell cultures, pancragen was reported to raise expression of acinar (Pdx1, Ptf1a) and islet (Pdx1, Pax6, Pax4, Foxa2, Nkx2.2) differentiation factors. The authors propose these transcription factors as its pharmacological target. This is a marker-expression readout, not a functional insulin-secretion outcome.
Rodent chemically induced diabetes
Biological activity of Lys-Glu-Asp-Trp-NH2 was assessed during ontogeny and in streptozotocin-induced diabetes, with reported effects on glucose level, capillary permeability and adhesion in a separate rat diabetes experiment. Streptozotocin models beta-cell destruction rather than human type 2 disease, so translational reach is limited.
Old rhesus monkey glucose tolerance
In old female rhesus monkeys the peptide was reported to increase glucose disappearance rate and normalise plasma insulin and C-peptide responses to a glucose load, with partial persistence after withdrawal. This is the strongest preclinical result in the set. It is a single small primate experiment, co-authored by Khavinson, published in Advances in Gerontology.
Pineal-melatonin framing of the human claim
The human report attributes insulin resistance in the elderly to reduced nocturnal melatonin production and positions pancragen as a corrective. The design cannot support that causal chain: melatonin was measured cross-sectionally in separate healthy and diabetic groups, and the peptide comparison was unrandomised and uncontrolled.
what’s reported
evidence shape
7 sourcesThe composition of the cited literature by study type. This describes the shape of the evidence, not its quality — and it does not by itself set the grade.
⚠ the catch
Pancragen's identity is often reported wrongly, and its human evidence is one uncontrolled series. The published molecule is the amidated tetrapeptide Lys-Glu-Asp-Trp-NH2 — not Lys-Glu-Asp-Gly, which is Testagen, and not Crystagen, which is a separate immune-directed member of the family that some retail listings conflate with it. The single human study enrolled 33 elderly patients with type 2 diabetes and compared them against patients who simply received nothing: no randomisation, no placebo, no blinding, no stated duration, and outcomes limited to glucose, insulin and an insulin-resistance index rather than any hard endpoint. Zero trials have ever been registered on ClinicalTrials.gov, and all nine PubMed-indexed papers are co-authored by Khavinson and published in two journals closely tied to the originating institute. No CAS number could be verified.
key published findings
- ClinicalTrials.gov contains zero registered studies of Pancragen (verified by registry query).
- Sequence confirmed from primary literature as Lys-Glu-Asp-Trp published in the C-terminal amide form; PubChem gives C26H37N7O8 and 575.6 for H-Lys-Glu-Asp-Trp-NH2 (CID 68451868), and no CAS number could be verified.
- The commonly repeated assignment of Lys-Glu-Asp-Gly (KEDG) to Pancragen is wrong — KEDG is Testagen — and conflation with Crystagen in some listings is also unsupported.
- The only human study is a non-randomised, placebo-free comparison in 33 elderly type 2 diabetes patients versus 30 healthy controls, reporting reduced fasting and post-load glucose, insulin and insulin-resistance index.
- In old female rhesus monkeys pancragen reportedly increased glucose disappearance rate and normalised insulin and C-peptide dynamics, with partial persistence after withdrawal — the strongest preclinical result in the series.
- All nine PubMed-indexed papers naming pancragen are co-authored by Khavinson; Khavinson's own 2014 clinical-results review of the family's bioregulators does not include it.
limitations of the evidence
- Single uncontrolled human series with an untreated rather than placebo comparator; no randomisation, no blinding, no reported duration.
- Zero independent replication: every retrieved study lists Khavinson as an author, and the primate work is a collaboration with him rather than an external check.
- Publication venue is concentrated in Bulletin of Experimental Biology and Medicine and Advances in Gerontology, both closely associated with the originating group and thinly indexed in the West.
- The published molecule is a C-terminal amide while much of the research market sells the free acid KEDW, a genuine chemical difference that no vendor documentation resolves.
- No CAS registry number, no human pharmacokinetics and no half-life data exist, so exposure after administration is entirely uncharacterised.
- Sources are shared with the other Khavinson bioregulators in this index because these compounds are described in one common body of literature; shared reviews are not independent support for pancragen specifically.
documented safety signals
- No formal toxicology, adverse-event surveillance or human safety dataset was located for pancragen.
- Absence of reported harm reflects absence of monitored human exposure rather than demonstrated safety.
- The claimed effect is glucose-lowering, so any real activity carries an inherent hypoglycaemia risk that has never been characterised in a controlled setting.
- The peptide is proposed to act on pancreatic differentiation transcription factors; effects on proliferative signalling in a tissue prone to neoplasia have not been studied over any meaningful horizon.
identity
| full name | Pancragen (lysyl-glutamyl-aspartyl-tryptophanamide; H-Lys-Glu-Asp-Trp-NH2) |
| category | Metabolic |
| modality | peptide |
| formula | C26H37N7O8 |
| molar mass | 575.6 g/mol |
| sequence | Lys-Glu-Asp-Trp (KEDW); published as the C-terminal amide H-Lys-Glu-Asp-Trp-NH2 |
laboratory handling
| storage | Lyophilised powder is stored desiccated at -20 °C and protected from light. Once reconstituted, laboratory practice is refrigeration at 2-8 °C for short-term use, or aliquoting and freezing to avoid repeated freeze-thaw cycles. Handling information only; this material has no approved human use. |
| solubility | Short hydrophilic peptide, readily soluble in sterile or bacteriostatic water and in dilute aqueous buffer. Lot-specific solubility is stated on the certificate of analysis. |
Handling information describes laboratory practice for a research reagent. It is not a preparation guide for use in humans.
the receipts
7 citedPubChem, NCBI · 2026 · official
ClinicalTrials.gov, US National Library of Medicine · 2026 · official
Bulletin of Experimental Biology and Medicine · 2011 · clinical study
Bulletin of Experimental Biology and Medicine · 2013 · preclinical
Advances in Gerontology · 2014 · preclinical
Bulletin of Experimental Biology and Medicine · 2010 · preclinical
Molecules · 2021 · systematic review
others in Metabolic