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A specimen of the Other drawer Drawer G · Other

Pancragen

Research Only

A synthetic tetrapeptide (Lys-Glu-Asp-Trp) developed by Russian scientist Vladimir Khavinson for pancreatic support. Claimed to modulate pancreatic tissue gene expression and support insulin-producing beta cell function. No Western clinical validation.

KEDW · Lys-Glu-Asp-Trp · Pancreatic tetrapeptide · Pancreas bioregulator

Research evidence
Low

Mostly preclinical · 1 human study

Preclinical
75%
Clinical
13%

Based on 8 cited sources

Evidence Score48/100
Early / limited
Research Depth45/100
Mechanism54/100
Plausibility69/100
Global Coverage40/100
Community Experience23/100
Effectiveness31/100

clinically demonstrated · very-low confidence

Demonstrated effect magnitude — not a recommendation or safety claim.

Research Depth 45 (1A 18 / 1B 4 / 1C 5 / 1D 11 / 1E 7): best human tier is a controlled observational study in elderly with vs without treatment, n~63 (30 healthy + 33 T2D), Korkushko/Khavinson 2011 (22448364) showing reduced fasting/GTT glucose, insulin and HOMA-IR — n<100, high RoB (small, open-label, no randomization/blinding), N in the 50-300 band, directness strong (right population + glycemic outcome). 1E credits a substantial multi-study preclinical program: STZ-diabetic rats (18225766, 18642713, 21246099), old-rhesus NHP (28509500, 25946840), and pancreatic cell-culture work. Mechanism 54 (2A 20 / 2B 17 / 2C 8 / 2D 9): KEDW is a defined tetrapeptide with a named molecular target — DNA motif binding (acct / GGCAG, 25761685, 24770759) and histone interaction (23581987) — driving PDX1/PAX6/PAX4/NGN3 transcription-factor and methylation changes (23486591, 23734516); binding is docking-predicted rather than Ki/IC50-measured and no knockout abolition, but functional gene-expression confirmation and in-vivo mammalian validation (rats, monkeys) are present; dose-response only single-model. Plausibility 69 (3A 24 / 3B 21 / 3C 12 / 3D 12): mechanism -> surrogate (glucose/insulin/ C-peptide normalization) established in animals and the small human study, surrogate -> benefit inferred; coheres with established PDX1/beta-cell biology; class analogy from sibling Khavinson tetrapeptides; tightly scoped pancreatic/glycemic claim, not a cure-all. Global Coverage 40 (4A 17 / 4B 11 / 4C 12 / 4D 0): findings extend beyond the single St. Petersburg lab — independent human work from Institute of Gerontology Kiev (Ukraine), NHP work from the Sochi primatology institute, Moscow co-authorship (Vanyushin/ Belozersky), and a 2025 India review (39871657) — ~12-15 KEDW/pancragen studies total across 2-3 countries; no regulator approval or trial registration (4D 0). Community Experience 23 (5A 3 / 5B 6 / 5C 5 / 5D 9): negligible documented real-world use of pancragen specifically; no recurring adverse signal but minimal exposure data. Effectiveness basis clinical (very-low): the 2011 study reports significant but small-to-moderate glycemic/ insulin-resistance improvement on surrogate endpoints; an NHP head-to-head found glimepiride more potent, so effect is modest and not superior to standard of care — single small unblinded human study caps confidence at very-low.

Scored June 2026 How we rate →
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Evidence Level
low
Not approved for human use by any regulatory agency
Limited human clinical trial data
Consult a healthcare provider before use
Not FDA Approved WADA Prohibited
Identity
SCALE · 1:1 N-TERMINUS C-TERMINUS 4 AA · 562.60 Da
Also Known As
KEDW • Lys-Glu-Asp-Trp • Pancreatic tetrapeptide • Pancreas bioregulator
Class
Tetrapeptide
Length
4 amino acids
Mol. weight
562.60 Da
Sequence
KEDW
Molecular Structure
K
E
D
W
Hydrophobic
Polar
Positive
Negative

Mechanism of Action

Pancragen (Lys-Glu-Asp-Trp) is proposed to regulate pancreatic tissue through peptide bioregulation mechanisms.

Proposed Mechanisms

  1. Beta Cell Support - Claimed to support insulin-producing cell function
  2. Gene Expression Modulation - Proposed effects on pancreatic gene expression
  3. Metabolic Regulation - Claimed involvement in glucose metabolism pathways

Important Limitations

  • No Western clinical validation or regulatory approval
  • All research from Russian institutions
  • NOT a diabetes treatment
  • No controlled human clinical trials
Mechanism Pancreatic beta cell gene expression modulation
Emerging 2 direct studies
Benefit suggested to support pancreatic function
Evidence Level
Very Low
2 Animal
1 In Vitro
Mechanism Confidence
Established
Supported
Emerging
Evidence Level
High
Moderate
Low
Very Low
Synergistic
Compatible
Caution
Avoid

Both Khavinson bioregulator peptides with distinct targets - Pancragen for pancreas, epithalon for pineal/longevity.

Vilon

Compatible
Compatible

Fellow bioregulator peptides from Russian research with different tissue targets.

Research Note: Interaction data is based on published literature, mechanistic understanding, and theoretical considerations. Most peptide combinations lack direct clinical study. This information is for educational purposes only and does not constitute medical advice. Always consult qualified healthcare providers.

8 Sources 1 Human 6 Preclinical

Full reference list available on request. All citations link to PubMed for verification.

This dossier synthesizes available evidence from peer-reviewed literature, regulatory documents, and clinical trial registries. Evidence strength ratings follow a modified GRADE approach.

For complete methodology details, see our Methodology page.

Important Disclaimer

This dossier is for educational purposes only and does not constitute medical advice. Always consult a qualified healthcare provider before making health decisions.

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