Pancragen Research

Pancragen is a synthetic short peptide sold as a research chemical, and its sequence is written KEDW-NH2, or Lys-Glu-Asp-Trp-NH2. This page reviews what the published record shows about Pancragen, and it contains no dosing or administration information.

Identity and the C-terminal amide

The NLM authority record for this compound is headed "lysyl-glutamyl-aspartyl-tryptophanamide", and its entry terms include Lys-Glu-Asp-Trp-NH2, KEDW-NH2 and pancragen ^[1]. The matching PubChem record, CID 68451868, has the molecular formula C26H37N7O8 ^[1]. That formula is the C-terminal amide, and the free acid would be C26H36N6O9.

The amide is not written consistently in the literature, and the originating group's 2023 transporter-docking paper writes KEDW-NH2 throughout ^[2]. A US patent naming four of the group's members as inventors claims the amide too, as "Lys-Glu-Asp-Trp-NH2" ^[19]. Several primary papers, including the earlier primate report, instead write the free acid Lys-Glu-Asp-Trp ^[3][5]. So two closely related molecules circulate under one product name, and which one a vial holds cannot be read off that name, only from a batch certificate of analysis.

PubChem CID 68451868 carries no depositor-supplied name or synonym beyond an internal SCHEMBL identifier and no CAS registry number ^[1], so there is no authoritative CAS number for Pancragen.

Pancragen also sits inside a nested set, the KED- series, which runs Vesugen (KED), Livagen (KEDA), Testagen (KEDG), Prostamax (KEDP) and Pancragen (KEDW-NH2) ^[5]. Vesugen is literally the first three residues of Pancragen ^[5], and the published literature does not establish what functionally separates these siblings. It is silent, and this page will not fill that gap. In one animal study, Epitalon (AEDG) eliminated the induced changes measured ^[6]. Cortagen (AEDP) differs from it only at the final residue, and did not affect the parameters studied at all ^[6].

Nearly all of this research came from one group

The central fact a reader needs is quickly stated: a title-and-abstract search of PubMed for the product name returns seven records for Pancragen ^[7]. All seven come from Vladimir Khavinson, the St Petersburg Institute of Bioregulation and Gerontology, or that institute's collaborators ^[7]. That count is a property of the query rather than of the whole corpus ^[7]. PubMed also indexes the transliteration "pankragen", and several further compound-specific papers name only the KEDW sequence ^[7]. Those additional papers, all of them cited on this page, sit inside the same network, and no unaffiliated record has been found ^[7]. Across his whole output Khavinson is an author on 497 PubMed records, 65 percent of them Russian-language, with 42 percent in just two journals ^[7].

That institute developed the compound, and its director is among the four named inventors on the US patent claiming it ^[19]. It also supplies the material, and the later primate paper names it as the source of the peptide tested ^[4]. Two of the papers cited on this page nonetheless carry the declaration that their authors have no conflict of interest ^[2][5]. None of the Pancragen literature should be described as independent.

One transfer error is worth heading off: the large lifespan and mortality figures circulated for "Khavinson peptides" belong to Epithalamin and Thymalin ^[8], both of them crude animal-tissue extracts. The FDA has stated that Epithalamin and the synthetic tetrapeptide modeled on it are different substances ^[8], and neither extract is Pancragen, so those numbers do not carry across.

Cell and tissue findings

Pancragen was one of four peptides applied to organotypic explant cultures from young and aged rats, and the report describes stimulation of explant growth ^[9]. This is an ex vivo assay used in-house by the originating institute ^[9].

A cell culture study reported changes in pancreatic differentiation markers including Pdx1, Ptf1a, Pax6 and Foxa2 ^[10]. That paper's own conclusion, that the peptide is a treatment tool for diabetes and pancreatitis, is not supported by its in vitro design ^[10].

An in vitro methylation study reported that promoter methylation at PDX1, PAX6 and NGN3 changed with age and was altered by the peptide ^[11]. The same paper also reported dissociations, with methylation at PAX4 and FOXA1 unchanged even though expression did change ^[11].

For this compound the DNA-binding mechanism is computational: a docking study predicted that KEDW can reach the major groove, and named GGCAG as a putative binding site ^[12]. That paper ran no experiment. An earlier rat study framed the same promoter mechanism explicitly as a presumption, and the two papers name different candidate motifs ^[12]. Separately, an in vitro study from the same network reported these peptides binding wheat histones, which is a different mechanism from direct sequence recognition ^[13].

Animal and human reports

The animal evidence is a small primate series. In old female rhesus monkeys, Pancragen was reported to increase the glucose disappearance rate and to normalize insulin and C-peptide dynamics after a glucose load ^[3]. A later report compared Pancragen against glimepiride in nine old macaque females, five of which received the peptide and four the comparator drug ^[4]. That paper concludes that Pancragen is "effective and safe" for age-related pancreatic imbalance, a conclusion five treated animals cannot support for either property ^[4]. Both reports are Russian-language, small, and unreplicated outside the originating network ^[3][4].

Two human reports exist, and neither is a controlled trial. The first examined 33 elderly people with type 2 diabetes alongside 30 healthy elderly people ^[14]. That healthy group is the reference for a melatonin comparison, not a comparator arm for the peptide ^[14]. The Pancragen comparison sits inside the diabetic group, where treated patients showed reductions in fasting glucose, glucose on tolerance testing, plasma insulin and an insulin resistance index ^[14]. Patients in that group receiving no Pancragen showed no change in carbohydrate metabolism indices ^[14]. That makes it a quasi-controlled clinical observation, describing no randomization, blinding or placebo, and giving no effect sizes or p-values ^[14]. The second report is uncontrolled outright, giving Pankragen-forte to 12 elderly people with impaired glucose tolerance over four weeks ^[15]. A response was reported in half of them, which is six people, and the abstract does not state the route of administration ^[15].

Both report surrogate metabolic markers only, neither reports a clinical outcome, and neither supports a treatment claim.

What has not been established

No pharmacokinetic study of Pancragen in humans has been published ^[20], and no lifespan or longevity study of Pancragen exists in any species ^[16]. No trial of Pancragen is registered on ClinicalTrials.gov ^[17], and no toxicology has been published for it either ^[20]. A search crossing this compound with toxicity, genotoxicity, carcinogenicity, mutagenicity and adverse events returns nothing at all ^[20].

That silence is not evidence of safety. It is the reason the primate paper's "effective and safe" wording cannot be carried forward ^[4]. A reader should weigh that absence against any safety impression this page might otherwise leave. Pancragen is a tetrapeptide, and two general reviews of peptide-transporter physiology, neither of which tested any Khavinson peptide, establish that the intestinal transporter PepT1 carries di- and tripeptides only ^[18]. No carrier-mediated intestinal route is therefore known for it, and the originating group's own work on transport of this peptide is computational rather than measured ^[2]. That is not proof it cannot cross the gut wall, but no study has measured systemic exposure by any route.

Frequently Asked Questions

Is there human evidence for Pancragen?

There are two human reports, and neither is a controlled trial ^[14][15]. Both report surrogate metabolic markers only, and neither reports a clinical outcome ^[14][15]. The larger of the two describes no randomization, blinding or placebo, and gives no effect sizes or p-values ^[14]. Its untreated comparison sits inside the diabetic group rather than in a separate arm ^[14], and no trial of Pancragen is registered on ClinicalTrials.gov ^[17].

Is Pancragen the free acid or the amide?

The NLM and PubChem records describe the amidated form, KEDW-NH2 ^[1], as does the originating group's 2023 transporter-docking paper ^[2]. A US patent naming four of the group's members as inventors claims the same amide ^[19]. Several primary papers, however, write the free acid Lys-Glu-Asp-Trp ^[3][5]. Which form a given batch holds cannot be read off the product name, only from a certificate of analysis.

Has any independent group replicated this work?

No, and the reason is structural: a title-and-abstract search of the product name returns seven PubMed records, all seven from the originating group or its collaborators ^[7]. The further compound-specific papers that fall outside that query are in-network too ^[7]. That same institute developed the compound, supplied the peptide used in the later primate study ^[4], and its director is among the named inventors on the patent claiming it ^[19].

Does Pancragen have a CAS number?

No, because the PubChem record matching the amidated form, CID 68451868, carries no depositor-supplied name or synonym beyond an internal SCHEMBL identifier, and no CAS registry number ^[1]. There is no authoritative CAS number for Pancragen ^[1].

References

1. 1

   NLM MeSH supplementary concept record C531938, "lysyl-glutamyl-aspartyl-tryptophanamide"; PubChem CID 68451868 (C26H37N7O8, MW 575.6). Both records retrieved 27 August 2026.
2. 2

   Khavinson VK, et al. (2023). Biomolecules 13(3):552. PMID 36979488.; DOI 10.3390/biom13030552. Molecular modelling and computer-assisted docking of 26 ultrashort peptides against LAT and PEPT family transporters; no transport assay is reported. Carries the declaration "the authors declare no conflict of interest".
3. 3

   Goncharova ND, et al. (2014). Advances in Gerontology (Uspekhi Gerontologii) 27(4):662-667. PMID 25946840. Russian, English abstract only.
4. 4

   Goncharova ND, et al. (2015). Advances in Gerontology (Uspekhi Gerontologii). PMID 28509500. Russian.
5. 5

   Khavinson V, et al. (2022). International Journal of Molecular Sciences. PMID 35887081. Table 2 lists the family's named compounds with their sequences. Carries the declaration "the authors declare no conflict of interest". Sequence relationship corroborated by Khavinson VKh, et al. (2012). Bulletin of Experimental Biology and Medicine 153(1):148-151. PMID 22808515.; DOI 10.1007/s10517-012-1664-1, which names pancragen and vesugen in a single abstract and writes the free acid, "pancragen (Lys-Glu-Asp-Trp)".
6. 6

   Kuznik BI, et al. (2008). Advances in Gerontology (Uspekhi Gerontologii) 21(3):372-381. PMID 19432169. Russian, English abstract only.
7. 7

   PubMed E-utilities bibliometric analysis, run 27 August 2026: pancragen[tiab] returns 7 records (PMIDs 28509500, 25946840, 23486591, 22808515, 22448364, 18642713, 17152728), 7 of 7 intersecting the Khavinson author and institute set; author-name query returns 497 records, 322 Russian-language, with 132 in Bulletin of Experimental Biology and Medicine and 76 in Advances in Gerontology. Scope note: the count is query-bound. pankragen[tiab] returns a further record, PMID 28976155. (reference 15 here), and PMIDs 25761685, 24770759, 16671579 and 23581987 are compound-specific but name only the KEDW sequence in title and abstract. Each was checked individually and each is in-network.
8. 8

   US Food and Drug Administration, Center for Drug Evaluation and Research (2026). Briefing document, Pharmacy Compounding Advisory Committee, July 2026. https://www.fda.gov/media/193345/download - FDA found that of 26 articles submitted as evidence for a synthetic tetrapeptide, seven concerned Epithalamin, which it stated is a different substance (footnotes 26 and 27). The mortality ratios themselves are from Khavinson VKh, Morozov VG (2003). Neuroendocrinology Letters 24(3-4):233-240. PMID 14523363., in which subjects received Thymalin and/or Epithalamin.
9. 9

   Zakutskii AN, et al. (2006). Advances in Gerontology (Uspekhi Gerontologii) 19:93-96. PMID 17152728. Russian, English abstract only.
10. 10

    Khavinson VKh, et al. (2013). Bulletin of Experimental Biology and Medicine. PMID 23486591.; DOI 10.1007/s10517-013-1987-6.
11. 11

    Ashapkin VV, et al. (2015). Biochemistry (Moscow). PMID 25761685.; DOI 10.1134/S0006297915030062.
12. 12

    Tarnovskaya SI, et al. (2014). Bulletin of Experimental Biology and Medicine. PMID 24770759.; DOI 10.1007/s10517-014-2426-z. Earlier companion, single-authored: Khavinson VK (2005). Bulletin of Experimental Biology and Medicine 140(4):452-454. PMID 16671579.; DOI 10.1007/s10517-005-0517-6.
13. 13

    Fedoreyeva LI, et al. (2013). Biochemistry (Moscow). PMID 23581987.; DOI 10.1134/S0006297913020053.
14. 14

    Korkushko OV, et al. (2011). Bulletin of Experimental Biology and Medicine 151(4):454-456. PMID 22448364.; DOI 10.1007/s10517-011-1354-4.
15. 15

    Korkushko OV, et al. (2013). Advances in Gerontology (Uspekhi Gerontologii). PMID 28976155. Russian, no DOI assigned.
16. 16

    PubMed E-utilities searches, run 27 August 2026: per-compound and per-sequence queries for pancragen and KEDW crossed with lifespan, longevity, survival and mortality returned no survival study. Scope note: that cross is not a zero-record query. It returns one record, PMID 33280436., a cost-effectiveness paper on catheter ablation in heart failure that matches the string KEDW incidentally and concerns no peptide.
17. 17

    ClinicalTrials.gov (US National Library of Medicine), API v2 query run 27 August 2026: zero registered studies for pancragen.
18. 18

    Spanier B, Rohm F (2018). Comprehensive Physiology 8:843-869. PMID 29687907.; DOI 10.1002/cphy.c170038. Terada T, Inui K (2012). Current Topics in Membranes. PMID 23177989.; DOI 10.1016/B978-0-12-394316-3.00008-9. Both are general reviews of peptide-transporter physiology, and neither tests any Khavinson peptide. Both state the positive substrate range; neither prints an explicit exclusion of tetrapeptides.
19. 19

    US Patent 7,491,703 B2, "Tetrapeptide regulating blood glucose level in diabetes mellitus" (application 10/580,957; published as US 2007/0142298 A1; granted 17 February 2009; 8 claims). Four named inventors: Vladimir Khatskelevich Khavinson, Vladimir Viktorovich Malinin, Evgeny Iosifovich Grigoriev and Galina Anatolievna Ryzhak. Granted claim 1 reads in full: "Tetrapeptide Lys-Glu-Asp-Trp-NH2 [SEQ ID NO:1]". The longer form, "Tetrapeptide lysyl-glutamyl-aspartyl-tryptophane amide of the general formula Lys-Glu-Asp-Trp-NH2 [SEQ ID NO:1]", is claim 1 of the published application, not of the grant. The assignment chain runs from the four inventors to the St Petersburg Institute of Bioregulation and Gerontology on 26 September 2006, to "Access Bioscience" CJSC on 2 November 2007, and to "Peptid Products" LLC on 14 May 2018. Access Bioscience CJSC was therefore the assignee at grant. The patent lapsed in 2021 for non-payment of maintenance fees. Retrieved from the Google Patents and USPTO records, 27 August 2026.
20. 20

    PubMed E-utilities search, run 27 August 2026 and independently re-run the same day: (pancragen OR pankragen OR "Lys-Glu-Asp-Trp" OR KEDW) crossed with toxicity, toxicology, genotoxicity, carcinogenicity, mutagenicity, adverse events and teratogenicity returns 0 records. The same compound set crossed with pharmacokinetics and bioavailability also returns 0. For scale, the compound set alone returns 18 records, so both zeros are real absences and not a dead query.