Lys-Glu-Asp-Trp (KEDW), a Khavinson short peptide proposed as a β-cell and glucose-tolerance bioregulator. Russian preclinical work plus one small elderly-T2DM cohort study, no Western clinical replication. Investigational.
Pancragen is the synthetic Khavinson tetrapeptide Lys-Glu-Asp-Trp, supplied as the C-terminal amide form H-Lys-Glu-Asp-Trp-NH2 (KEDW-NH2) — four amino acids. It was synthesized at the St. Petersburg Institute of Bioregulation and Gerontology as an analog of a four-residue motif found across natural insulinotropic polypeptides, with the C-amide added to protect it from gastrointestinal proteinases. Identity is verified through the NLM MeSH supplementary concept "lysyl-glutamyl-aspartyl-tryptophanamide" and roughly ten PubMed-indexed Khavinson-group papers naming Pancragen with the KEDW sequence (Khavinson 2010 PMID 21246099; Goncharova 2014 PMID 25946840 in rhesus monkeys; Khavinson 2007 PMID 18642713; founding paper Khavinson 2005 PMID 16671579).
Pancragen sits in the Khavinson short-peptide family alongside Cartalax (AED), Prostamax (KEDP), Testagen (KEDG), Epitalon (AEDG), and Pinealon (EDR). Each is positioned as a tissue-specific bioregulator. The parent in this case is Suprefort (A-1), a bovine-pancreas polypeptide-complex extract sold as an oral capsule under the Cytomax line. Both synthetic Pancragen and Suprefort are sold in Russia as БАД (biologically active food additives), not as registered Russian pharmaceuticals. Suprefort has zero PubMed-indexed primary research on the extract itself — a different (worse) parent-extract evidence profile than Prostamax has, where the prostate-extract parent (Prostatilen) is a registered Russian drug with its own RCT trail.
The most consequential framing point is what Pancragen is not. It is not insulin and does not bind the insulin receptor. It is not a GLP-1 receptor agonist or a structural analog of GLP-1 — the "insulinotropic" framing in the founding paper refers to a sequence-motif mimetic shared across multiple insulinotropic polypeptides, not GLP-1R binding. It is not a sulfonylurea, DPP-4 inhibitor, metformin, or SGLT2 inhibitor. PMID 28509500 directly compared pancragen and glimepiride in old rhesus monkeys and described their mechanisms as distinct. Pancragen is not an alternative to semaglutide, tirzepatide, or retatrutide.
The Khavinson framework holds that short peptides penetrate the cell membrane and nuclear envelope, bind DNA promoter regions and histone N-terminal tails, and modulate tissue-specific gene expression. The framework is computationally docked rather than crystal-structure validated — no published X-ray or NMR structure of KEDW bound to DNA exists.
Within that framework, the direct findings on KEDW span DNA binding, transcription factor regulation, and downstream pancreatic biology. Computational docking shows KEDW binds preferentially to the GGCAG sequence in the DNA major groove (Tarnovskaya 2014 PMID 24770759), with sequence-specific major-groove binding and more permissive minor-groove binding. The founding paper (Khavinson 2005 PMID 16671579) proposed direct interaction with preproinsulin gene promoter sequences (ggcagg and cctgcc) and showed partial restoration of insulin synthesis in alloxan-diabetic rats. Histone-tail binding has been shown for KEDW with wheat histones H1, H2B, H3, H4 (Vanyushin lab, PMID 23581987 — wheat histones reflect the lab's plant-genetics background, not human equivalence).
Downstream, KEDW upregulates the canonical β-cell-fate transcription factors Pdx1, Pax4, Pax6, Foxa2, and Nkx2.2 in young and aged human pancreatic cell cultures (Khavinson 2013 PMID 23486591), with the effect more pronounced in aged cultures — the Khavinson-framework "geroprotector signature." DNA-methylation patterns of the PDX1, PAX6, and NGN3 promoter regions also shift in pancreatic cell cultures, correlating with expression changes (Ashapkin 2015 PMID 25761685). At sub-nanogram concentrations (0.05 ng/mL), KEDW supports pancreatic explant outgrowth in young and aged rat tissue (PMID 17152728).
In vivo, IM pancragen normalized mesenteric capillary adhesion in STZ-diabetic rats without modifying capillary permeability, and oral pancragen produced a pronounced hypoglycemic effect (Khavinson 2007 PMID 18642713). The Goncharova rhesus-monkey trials (PMIDs 25946840, 28509500) used 50 µg/animal/day IM × 10 days in old female monkeys and showed normalization of glucose tolerance plus insulin and C-peptide dynamics.
The audit-critical finding sits in PMID 23734516 (Khavinson group, Adv Gerontol 2012): in aged human pancreatic cells, KEDW-NH2 upregulates MMP2, MMP9, serotonin, CD79α, Mcl1, PCNA, and Ki67 while downregulating p53. The Khavinson interpretation is "restoration of youthful tissue dynamics"; the oncology-conservative reading is "elevated proliferation pressure with anti-apoptotic and matrix-degrading shifts." Both are mechanistically tenable. See the Cancer concern section.
Net read: KEDW is a putative DNA-binding bioregulator that drives β-cell-fate transcription, normalizes glucose tolerance in aging and diabetes models, and shifts the cell-cycle / apoptosis balance toward proliferation. All mechanism claims are computationally supported, not biophysically validated.
All evidence is preclinical or single-cohort Russian observational. There is no Western RCT, no Phase 1/2/3, and no clinicaltrials.gov entry.
| Claim | Source | Evidence Tier |
|---|---|---|
| Insulin synthesis restoration | PMID 16671579 | Alloxan-diabetic rats |
| β-cell differentiation factor upregulation | PMID 23486591 | In vitro human cells |
| Hypoglycemic effect (oral) + capillary protection (IM) | PMID 18642713 | STZ-diabetic rats |
| Pancreatic explant outgrowth at 0.05 ng/mL | PMID 17152728 | Rat organotypic culture |
| Glucose tolerance normalization in primates | PMIDs 25946840, 28509500 | Old rhesus, n=5–9 per study |
| Pancragen vs. glimepiride head-to-head | PMID 28509500 | Old rhesus, n=5 vs 4 |
| Reduced fasting glucose, OGTT, insulin, IR index in elderly T2DM | PMID 22448364 | Single Russian Korkushko cohort, n=33 |
| Stem-cell β-cell lineage modulation | PMID 39871657 | 2025 review, no new data |
The Korkushko cohort (PMID 22448364) is the closest thing to human evidence and worth reading honestly: 33 T2DM patients plus 30 healthy elderly controls. The abstract does not describe the design as randomized, blinded, or placebo-controlled. Effect sizes are not extracted; dose, duration, and route are not specified. HbA1c and hard glycemic / cardiovascular / microvascular endpoints are not reported. No follow-up paper has been published in the 14 years since. It's a single small Russian-group cohort, not a powered RCT, and shouldn't be cited as confirmation of efficacy.
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Start Tracking FreeNo human RCT of synthetic Pancragen has been published. The dose ranges below reflect the Russian rhesus-monkey IM dose extrapolated to human weight, plus vendor and community convention — not validated clinical protocols.
The closest animal anchor is the Goncharova rhesus-monkey trials (PMIDs 25946840, 28509500), which used 50 µg/animal/day IM × 10 days in old female monkeys (5–8 kg body weight). Naive body-weight scaling to a 70-kg human yields ~0.4–0.7 mg/day equivalent; allometric (BSA) scaling gives a smaller number. Neither is validated by a human PK study.
| Route | Common Range | Cycle |
|---|---|---|
| Subcutaneous | 100–400 µg/day | 10–20 days on, 2–4 cycles per year |
| Oral capsule | 100–400 µg/day | 10–20 days on, 2–4 cycles per year |
| Intramuscular | ~50–500 µg/day | 10 days on, repeat per year |
The KEDW-NH2 amide form is GI-protected by design (per the founding paper), so oral dosing is plausible — but oral PK has not been formally measured in humans. The parent extract Suprefort is dosed at 1 capsule (~10 mg natural peptides) twice daily × 30 days per vendor literature; Suprefort and synthetic Pancragen are not interchangeable.
Concurrent use with insulin, sulfonylureas, GLP-1 RAs, or DPP-4 inhibitors is uncharacterized in published research. Theoretical hypoglycemia risk in combination — physician supervision required for diabetic users on prescription therapy.
Standard short-peptide SC reconstitution. For a 5 mg vial in 2 mL bacteriostatic water: 2.5 mg/mL, so 1 unit on a U-100 insulin syringe = 25 µg, and a 100 µg dose = 4 units. For a 10 mg vial in 2 mL: 5 mg/mL, 1 unit = 50 µg, 100 µg dose = 2 units.
Lyophilized vials are stable at room temperature short-term; refrigerate for longer storage. Reconstituted vials should be refrigerated and used within 28 days. Oral capsules store dry at room temperature, away from light.
For the full reconstitution protocol, see the Bacteriostatic Water guide.
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There is no PubMed-indexed safety or pharmacovigilance paper on synthetic Pancragen. No FAERS or EudraVigilance entries. The Goncharova monkey papers report no adverse events over 10-day IM courses in 5–9 monkeys, and the Korkushko human cohort paper doesn't extract adverse events in the abstract. Suprefort vendor literature reports "well-tolerated" — БАД-tier marketing language, not pharmacovigilance.
Theoretical concerns worth knowing:
The "well-tolerated in Russian use" framing shouldn't be read as safety equivalence — Western pharmacovigilance doesn't exist for this molecule.
The pancreas is one of the highest-stakes target tissues in the Khavinson family. Pancreatic ductal adenocarcinoma (PDAC) is among the most lethal common cancers (5-year survival ~10–13%), and insulinoma is a real if rare β-cell tumor. A peptide that drives β-cell-fate transcription factors alongside PCNA, Ki67, and Mcl1 is mechanistically aligned with β-cell proliferation pressure.
The audit-critical paper is Khavinson 2012 (Adv Gerontol, PMID 23734516). The abstract states KEDW-NH2 increases MMP2, MMP9, serotonin, CD79α, antiapoptotic Mcl1, and proliferation markers PCNA and Ki67, while decreasing proapoptotic p53, in aged pancreatic cell cultures. The Khavinson interpretation is "restoration of youthful tissue dynamics." An oncology-conservative reading is "elevated proliferation pressure with anti-apoptotic and matrix-degrading shifts." Both are mechanistically tenable, and the MMP2/MMP9 upregulation is closely aligned with the PDAC stromal-invasion gain-of-function pattern.
What's never been tested: KEDW on pancreatic cancer cell lines (PANC-1, MIA PaCa-2, BxPC-3, Capan-1, AsPC-1), insulinoma cell lines (RIN-m5F, INS-1, MIN6), or xenograft / genetically-engineered PDAC mouse models (KPC, KC, Pdx1-Cre;LSL-KrasG12D). The cancer question is mechanistically flagged but not directly addressed in indexed literature.
Practical implications: active or prior PDAC, insulinoma, or pancreatic neuroendocrine tumor → absolute contraindication. New-onset diabetes within 36 months in adults over 50 with weight loss or abdominal symptoms → PDAC workup before consideration. Long-standing T2DM with new GI symptoms → gastroenterologist consult.
Three commonly-confused entities. They aren't the same thing.
Pancragen is the synthetic Khavinson tetrapeptide Lys-Glu-Asp-Trp (KEDW). NLM MeSH "lysyl-glutamyl-aspartyl-tryptophanamide." Roughly 10 PubMed-indexed Khavinson-group preclinical papers, anchored on β-cell and glucose-tolerance biology. This guide.
Suprefort (A-1) is a bovine-pancreas polypeptide-complex extract — oral capsule, sold as Russian БАД, Cytomax line under SPIBG patent. The parent extract from which Khavinson positions Pancragen as the synthetic short-peptide mimetic. Zero PubMed-indexed primary research on Suprefort itself, which is a worse parent-extract evidence profile than Prostamax has (where the prostate parent Prostatilen is a registered Russian drug with its own RCT trail).
Adamax is Ac-Met-Glu-His-Phe-Pro-Gly-Pro-AG-NH2 — N-acetyl Semax with an adamantyl-AG cap from P21. Entirely different molecule from Pancragen. Vendor copy occasionally attaches the trade name "Adamax" to the KEDW sequence; that's a misidentification. Adamax has zero PubMed-indexed primary literature; KEDW belongs to Pancragen. See the Adamax guide for the full disambiguation.
| Name | Composition | Family | Target | PubMed |
|---|---|---|---|---|
| Pancragen | KEDW | Khavinson | β-cells / pancreas | ~10 |
| Suprefort (A-1) | Bovine pancreas extract | Khavinson Cytomax | Whole pancreas | 0 |
| Adamax | Ac-MEHFPGP-AG-NH2 | Semax / P21 hybrid | Cognitive | 0 |
Pancragen is a research peptide not approved by the FDA for human use. It is sold only as a research chemical, and StackTrax does not endorse or facilitate personal use.
Quality varies enormously among research-chemical suppliers. At minimum, look for:
StackTrax’s preferred partner NextGen Peptides does not currently carry Pancragenin their catalog, which is why you don’t see a direct purchase link here. Other major research-chemical suppliers carry it; we don’t specifically recommend one for this compound.
Pancragen is the synthetic Khavinson tetrapeptide Lys-Glu-Asp-Trp, supplied as the C-terminal amide form (KEDW-NH2). It was synthesized at the St. Petersburg Institute of Bioregulation and Gerontology as an analog of a four-residue motif found across natural insulinotropic polypeptides, with the C-amide added to protect it from gastrointestinal proteinases. Identity is verified through NLM MeSH and roughly ten PubMed-indexed Khavinson-group papers. It sits alongside Cartalax, Prostamax, Testagen, Epitalon, and Pinealon as a tissue-specific bioregulator; the parent extract is Suprefort (A-1), a bovine-pancreas polypeptide-complex sold as Russian BAD.
In Russian preclinical work, yes. Oral Pancragen produced a pronounced hypoglycemic effect in STZ-diabetic rats (PMID 18642713). The Goncharova rhesus-monkey trials (PMIDs 25946840, 28509500) used 50 mcg/animal/day IM x 10 days in old female monkeys and showed normalization of glucose tolerance plus insulin and C-peptide dynamics. The closest thing to human evidence is the Korkushko cohort (PMID 22448364): 33 elderly T2DM patients plus 30 healthy elderly controls. The abstract does not describe the design as randomized, blinded, or placebo-controlled. Effect sizes are not extracted; dose, duration, route, HbA1c, and hard clinical endpoints are not reported. No follow-up has been published in the 14 years since. There is no Western RCT.
No to both. Pancragen is not insulin and does not bind the insulin receptor. It is not a GLP-1 receptor agonist or a structural analog of GLP-1; the insulinotropic framing in the founding paper refers to a sequence-motif mimetic shared across multiple insulinotropic polypeptides, not GLP-1R binding. It is not a sulfonylurea, DPP-4 inhibitor, metformin, or SGLT2 inhibitor. PMID 28509500 directly compared pancragen and glimepiride in old rhesus monkeys and described their mechanisms as distinct. Pancragen is not an alternative to semaglutide, tirzepatide, or retatrutide.
Not approved by FDA or EMA. No NDA, no IND, not on the 503A bulks list. In Russia, synthetic Pancragen and the parent extract Suprefort are both sold at the BAD (biologically active food additive) tier, not as registered pharmaceuticals. Not listed by name on WADA 2026; as an unapproved investigational peptide the S0 catch-all applies. Athletes should consult their governing body.
No human RCT of synthetic Pancragen has been published. The closest animal anchor is the Goncharova rhesus-monkey trials at 50 mcg/animal/day IM x 10 days in old female monkeys (5 to 8 kg); naive body-weight scaling to a 70-kg human yields roughly 0.4 to 0.7 mg/day equivalent, with allometric scaling giving a smaller number. Vendor and community ranges are 100 to 400 mcg/day SubQ or oral capsule for 10 to 20 days on, 2 to 4 cycles per year, or roughly 50 to 500 mcg/day IM for 10 days. The KEDW-NH2 amide form is GI-protected by design so oral dosing is plausible, but oral PK has not been formally measured in humans. Suprefort and synthetic Pancragen are not interchangeable.
There is no PubMed-indexed safety or pharmacovigilance paper on synthetic Pancragen and no FAERS or EudraVigilance entries. The Goncharova monkey papers report no adverse events over 10-day IM courses in 5 to 9 monkeys, and the Korkushko human cohort paper does not extract adverse events in the abstract. Theoretical concerns include hypoglycemia in non-diabetic users (the beta-cell support mechanism makes it plausible; monitor blood glucose) and hypoglycemia in combination with insulin, sulfonylureas, or GLP-1 RAs (no interaction studies; physician supervision required). The well-tolerated in Russian use framing should not be read as safety equivalence; Western pharmacovigilance does not exist for this molecule.
The pancreas is one of the highest-stakes target tissues in the Khavinson family. Pancreatic ductal adenocarcinoma has roughly 10 to 13% 5-year survival, and insulinoma is a real if rare beta-cell tumor. The audit-critical paper is Khavinson 2012 (PMID 23734516): in aged human pancreatic cell cultures, KEDW-NH2 increases MMP2, MMP9, serotonin, CD79alpha, antiapoptotic Mcl1, PCNA, and Ki67 while decreasing pro-apoptotic p53. The Khavinson interpretation is restoration of youthful tissue dynamics; the oncology-conservative reading is elevated proliferation pressure with anti-apoptotic and matrix-degrading shifts. KEDW has never been tested on pancreatic cancer or insulinoma cell lines or PDAC mouse models. Active or prior PDAC, insulinoma, or pancreatic neuroendocrine tumor are absolute contraindications; new-onset diabetes within 36 months in adults over 50 with weight loss or abdominal symptoms warrants PDAC workup first.
Not equivalent and not a substitute. Metformin and the GLP-1 receptor agonists (semaglutide, tirzepatide, retatrutide) have decades of large-RCT and real-world outcome data, FDA approval, and characterized cardiovascular and weight endpoints. Pancragen has Russian preclinical work, one small uncontrolled elderly T2DM cohort, no Western RCT, and a flagged pro-proliferative signal in aged pancreatic cells. If you have type-1 diabetes, Pancragen is not a substitute for insulin. Concurrent use with insulin, sulfonylureas, GLP-1 RAs, or DPP-4 inhibitors is uncharacterized and carries theoretical hypoglycemia risk; physician supervision is required for diabetic users on prescription therapy.
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