Pancragen

updated

Pancragen is the Khavinson group's synthetic tetrapeptide Lys-Glu-Asp-Trp, sold as a pancreas bioregulator for glucose handling. It has rat, monkey and pancreatic cell culture studies and two small human reports from the originating group: one has no control group, and neither describes randomization or blinding. No regulator record exists, no pharmacokinetics or adverse events are reported, and the group prints the end group both as an amide and as a free acid.

Synthetic tetrapeptide bioregulator

  • A PubChem name search on 10 October 2026 for pancragen, KEDW and Lys-Glu-Asp-Trp-NH2 returned no record. The free-acid tetrapeptide H-Lys-Glu-Asp-Trp-OH is CID 68452877, C26H36N6O9, molecular weight 576.6.
  • The originating group writes the sequence both as an amide (Lys-Glu-Asp-Trp-NH2) and with no amide. PubChem holds only the free acid, so a vial labeled Pancragen cannot be assumed to match any given paper.
  • In old female rhesus monkeys, 50 micrograms per animal per day intramuscularly for 10 days raised the rate of glucose disappearance and normalized insulin and C-peptide responses to a glucose load.
  • A 2011 report in 33 older patients with type 2 diabetes found lower fasting glucose and insulin resistance index with pancragen. The abstract does not state the treated-arm size, dose, route, duration or design.
  • A PubMed search on 10 October 2026 for pancragen returned 9 records, 8 with Khavinson as an author. Adding clinical trial or randomized controlled trial publication types returned 0.
  • On 10 October 2026, openFDA Drugs@FDA returned no match for pancragen, DailyMed returned no label, and ClinicalTrials.gov returned no record.

What is Pancragen, and is it an approved drug?

Pancragen is the synthetic tetrapeptide Lys-Glu-Asp-Trp (KEDW) from the Khavinson group. PubChem has no record under the name, and its free-acid record is CID 68452877. On 10 October 2026, FDA, DailyMed and ClinicalTrials.gov searches returned nothing under the name, so no approval was found.

A PubChem name search on 10 October 2026 for pancragen, for KEDW and for Lys-Glu-Asp-Trp-NH2 returned no record. The free-acid tetrapeptide H-Lys-Glu-Asp-Trp-OH is CID 68452877, C26H36N6O9, molecular weight 576.6, with one vendor-style synonym (SCHEMBL2946041) and no CAS number listed. That record does not carry the name Pancragen, so the trade name is tied to the sequence only by the originating group's own papers.

The group's papers give the sequence as Lys-Glu-Asp-Trp (KEDW): lysine, glutamic acid, aspartic acid, tryptophan. A 2007 rat paper and a 2010 paper write it as Lys-Glu-Asp-Trp-NH2, and a 2012 paper on human pancreatic cells writes H-Lys-Glu-Asp-Trp-NH2. A 2012 differentiation paper and a 2014 monkey paper write Lys-Glu-Asp-Trp with no amide. A C-terminal amide and a free acid are different molecules, and PubChem holds only the free acid, so a vendor vial labeled Pancragen cannot be assumed to match the end group of any given paper. The sequence is also not the tripeptide Lys-Glu-Asp (Vesugen, which has its own page on this site), which the 2012 differentiation paper names separately. The 2010 abstract describes the amidated tetrapeptide as natural and endogenous and reports no result.

On 10 October 2026, an openFDA Drugs@FDA query for pancragen returned no match, a DailyMed search for the drug name pancragen returned no label, and ClinicalTrials.gov returned no record for pancragen or for the Lys-Glu-Asp-Trp tetrapeptide. No FDA record was found in these sources, so Pancragen is not an FDA-approved drug or a labeled product. This says nothing about other regulators.

PubChem: free-acid KEDW tetrapeptide, no record under the name Pancragen

Chemical identity record

National Library of Medicine. PubChem compound record CID 68452877 (H-Lys-Glu-Asp-Trp-OH). PubChem name searches run 10 October 2026.

A PubChem name search on 2026-10-10 for pancragen, for KEDW and for Lys-Glu-Asp-Trp-NH2 returned no record. The free-acid tetrapeptide H-Lys-Glu-Asp-Trp-OH is CID 68452877, C26H36N6O9, molecular weight 576.6, with one vendor-style synonym (SCHEMBL2946041) and no CAS number listed. That record does not carry the name Pancragen, so the trade name is tied to the sequence only by the originating group's own papers.

Participants / model
Chemical identity, not a clinical population
Treatment
Defined synthetic tetrapeptide, free acid
Follow-up
Not applicable
Study design
NLM chemical record
Funding
not stated in the source

PubChem holds only the free acid, not the amidated form that some papers write.

Read the original source
2010 paper: amidated Lys-Glu-Asp-Trp-NH2, no result reported

Chemical identity record

Khavinson VKh et al. Bull Exp Biol Med. 2010;149(3):351-3. PMID 21246099.

The group's papers give the sequence as Lys-Glu-Asp-Trp (KEDW). A 2007 rat paper (PMID 18642713) and this 2010 paper write it as Lys-Glu-Asp-Trp-NH2, and a 2012 paper on human pancreatic cells writes H-Lys-Glu-Asp-Trp-NH2 (PMID 23734516). A 2012 differentiation paper (PMID 22808515) and a 2014 monkey paper (PMID 25946840) write Lys-Glu-Asp-Trp with no amide. A C-terminal amide and a free acid are different molecules and PubChem holds only the free acid. The sequence is also not the tripeptide Lys-Glu-Asp (Vesugen), which the 2012 differentiation paper names separately. The 2010 abstract describes the amidated tetrapeptide as natural and endogenous and reports no result.

Participants / model
Chemical identity, not a clinical population
Treatment
Synthetic tetrapeptide, amidated and free-acid forms in print
Follow-up
Not applicable
Study design
Original reports
Funding
not stated in the source

A vendor vial labeled Pancragen cannot be assumed to match the end group of any given paper.

Read the original source
FDA, DailyMed and registry: no pancragen record, 10 October 2026

Regulatory record

U.S. Food and Drug Administration, openFDA Drugs@FDA query for pancragen; DailyMed search for the drug name pancragen; ClinicalTrials.gov queries for pancragen and Lys-Glu-Asp-Trp tetrapeptide, all run on 10 October 2026.

An openFDA Drugs@FDA query for pancragen returned no match, a DailyMed search for the drug name pancragen returned no label, and ClinicalTrials.gov returned no record for pancragen or for the Lys-Glu-Asp-Trp tetrapeptide. No FDA record was found in these sources, so Pancragen is not an FDA-approved drug or a labeled product.

Participants / model
Not a clinical population
Treatment
Not applicable
Follow-up
Searches run on 2026-10-10
Study design
Official FDA, NLM and registry records
Funding
not stated in the source

This says nothing about other regulators.

Read the original source

What have the human reports found?

Two small reports from the originating group exist, and neither describes randomization or blinding. A 2011 report in 33 older patients with type 2 diabetes found lower fasting glucose and insulin resistance index with pancragen. A 2013 report of 12 older people with impaired glucose tolerance, given a product called pankragen forte, had no control group.

A 2011 paper examined 30 healthy older persons and 33 older patients with type 2 diabetes. Nocturnal melatonin production was reduced by 70% in the patients with diabetes compared with the healthy group. In the patients with diabetes, pancragen significantly lowered fasting glucose and glucose in a standard glucose tolerance test and reduced plasma insulin and the insulin resistance index, while in patients not receiving pancragen no changes in carbohydrate metabolism indices were observed. The abstract does not state how many patients received pancragen, the dose, route or duration, how patients were assigned, or whether anyone was blinded, so it cannot be read as a randomized trial. Khavinson is a co-author.

A 2013 Russian-language study of pankragen forte screened 150 healthy people (39 aged 20 to 39, 42 aged 40 to 59, 69 aged 60 and over) and gave 500 micrograms twice a day for 4 weeks to 12 older people with impaired glucose tolerance. In 50 percent of those 12, plasma glucose during a standard oral glucose tolerance test fell significantly, and the authors link this to better serum lipids, endothelial function and platelet aggregation. The abstract describes no control group, and the composition of forte is not stated, so it cannot be treated as the same product as plain pancragen. Khavinson is a co-author.

A PubMed search on 10 October 2026 for pancragen returned 9 records. Eight have Khavinson as an author, and the exception is a 2006 explant report by other authors. A search for pancragen with clinical trial or randomized controlled trial publication types returned 0 records. A wider search for pancragen, pankragen or Lys-Glu-Asp-Trp with patients, humans, elderly or diabetes returned 10 records, all among the papers described here, and the only two studies that gave the peptide to people are the 2011 and 2013 reports. In the records reviewed there is no randomized placebo-controlled trial, no independent replication, no human pharmacokinetics, no reported adverse events and no pancreatitis study.

2011 human report: 30 healthy older persons and 33 patients with type 2 diabetes

Human study

Korkushko OV et al. Bull Exp Biol Med. 2011;151(4):454-6. PMID 22448364.

A 2011 paper examined 30 healthy older persons and 33 older patients with type 2 diabetes. Nocturnal melatonin production was reduced by 70% in the patients with diabetes compared with the healthy group. In the patients with diabetes, pancragen significantly lowered fasting glucose and glucose in a standard glucose tolerance test and reduced plasma insulin and the insulin resistance index, while in patients not receiving pancragen no changes in carbohydrate metabolism indices were observed.

Participants / model
30 healthy older persons and 33 older patients with type 2 diabetes
Treatment
Pancragen; dose and route not stated in the abstract
Follow-up
not stated in the source
Study design
Original clinical study; assignment and blinding not stated
Funding
not stated in the source

The abstract does not state how many patients received pancragen, the dose, route, duration, how patients were assigned, or whether anyone was blinded, so it cannot be read as a randomized trial. Khavinson is a co-author.

Read the original source
2013 pankragen forte report: 12 older people, 4 weeks, no control group

Human study

Korkushko OV et al. Adv Gerontol. 2013;26(2):297-308. PMID 28976155.

A 2013 Russian-language study of pankragen forte screened 150 healthy people (39 aged 20 to 39, 42 aged 40 to 59, 69 aged 60 and over) and gave 500 micrograms twice a day for 4 weeks to 12 older people with impaired glucose tolerance. In 50 percent of those 12, plasma glucose during a standard oral glucose tolerance test fell significantly, and the authors link this to better serum lipids, endothelial function and platelet aggregation.

Participants / model
12 older people with impaired glucose tolerance, selected from 69 older adults
Treatment
Pankragen forte 500 micrograms twice a day for 4 weeks; route not stated in the abstract
Follow-up
4 weeks
Study design
Original clinical study, no control group described
Funding
not stated in the source

The abstract describes no control group, and the composition of forte is not stated, so it cannot be treated as the same product as plain pancragen. Khavinson is a co-author. The abstract is the publisher's Russian text with an English translation in PubMed.

Read the original source
Searches, 10 October 2026: 9 records, 0 controlled trials

PubMed search record

PubMed search run on 10 October 2026: pancragen, 9 records. Related PubMed searches run the same day.

A PubMed search for pancragen returned 9 records. Eight have Khavinson as an author, and the exception is the 2006 explant report by other authors. A search for pancragen AND (clinical trial[pt] OR randomized controlled trial[pt]) returned 0 records. A wider search for (pancragen OR pankragen OR Lys-Glu-Asp-Trp) AND (patients OR humans OR elderly OR diabetes) returned 10 records, all among the papers already described, and the only two studies that gave the peptide to people are the 2011 and 2013 reports. In the records reviewed there is no randomized placebo-controlled trial, no independent replication, no human pharmacokinetics, no reported adverse events and no pancreatitis study.

Participants / model
Records returned, not a population
Treatment
Not applicable
Follow-up
Searches run on 2026-10-10
Study design
Literature searches
Funding
not stated in the source

A search result shows what the databases returned on that date. It is not proof that no unindexed study exists.

Read the original source

What did the rat and monkey studies find?

In diabetic Wistar rats, oral pancragen produced a pronounced hypoglycemic effect during treatment. In old female rhesus monkeys, 50 micrograms per animal per day intramuscularly for 10 days raised the rate of glucose disappearance and normalized insulin and C-peptide responses to a glucose load. Khavinson co-authored both monkey reports, and the groups were very small.

A 2006 Russian-language report used synthetic cardiogen, bronchogen, prostamax and pancragen on organotypic explants of heart, lung, prostate and pancreas from 3-week-old and 18-month-old rats. At 0.05 ng/ml the peptide stimulated growth in its matching tissue culture compared with control explants in all groups. The abstract reports no endocrine, glucose or function endpoint, and the authors' statement that these peptides can be used in clinical practice is a conclusion the abstract's data do not reach.

In Wistar rats with streptozotocin-induced diabetes, oral pancragen (written Lys-Glu-Asp-Trp-NH2) produced a pronounced hypoglycemic effect during treatment, and intramuscular pancragen normalized the adhesion of mesenteric capillary endothelium but did not change capillary permeability. The authors read this as homeostatic and endothelioprotective effects in the early period of diabetes. This is a chemically induced model, and the abstract states no dose, group size or duration.

In old female rhesus monkeys, pancragen at 50 micrograms per animal per day intramuscularly for 10 days raised the rate of glucose disappearance and normalized plasma insulin and C-peptide responses to a glucose load, and the effect partly remained 3 weeks after the course. A second report in 9 old (20 to 25 years) clinically healthy females compared 5 given pancragen (0.05 mg per animal per day for 10 days, intramuscular) with 4 given glimepiride (4 mg per animal per day, oral). Both lowered basal glucose, pancragen also normalized insulin and C-peptide, and glimepiride had a stronger, delayed glucose effect and raised C-peptide without a significant effect on insulin. The authors call pancragen effective and safe, but the abstract lists no safety endpoint, and the groups are very small. Khavinson is a co-author of both.

2006 explant report: pancreas explants from 3-week and 18-month-old rats

Cell study

Zakutskiĭ AN et al. Adv Gerontol. 2006;19:93-6. PMID 17152728.

A 2006 Russian-language report used synthetic cardiogen, bronchogen, prostamax and pancragen on organotypic explants of heart, lung, prostate and pancreas from 3-week-old and 18-month-old rats. At 0.05 ng/ml the peptide stimulated growth in its matching tissue culture compared with control explants in all groups. The abstract reports no endocrine, glucose or function endpoint.

Participants / model
Pancreas explants from young (3-week) and aged (18-month) rats, among other tissues
Treatment
Peptide in culture medium at 0.05 ng/ml
Follow-up
not stated in the source
Study design
Original preclinical explant study
Funding
not stated in the source

The authors' statement that these peptides can be used in clinical practice is a conclusion the abstract's data do not reach. This is the one pancragen paper without Khavinson as an author.

Read the original source
Diabetic rats: oral pancragen lowered glucose; intramuscular normalized capillary adhesion

Animal study

Khavinson VKh et al. Bull Exp Biol Med. 2007;144(4):559-62. PMID 18642713.

In Wistar rats with streptozotocin-induced diabetes, oral pancragen produced a pronounced hypoglycemic effect during treatment, and intramuscular pancragen normalized the adhesion of mesenteric capillary endothelium but did not change capillary permeability. The authors read this as homeostatic and endothelioprotective effects in the early period of diabetes.

Participants / model
Wistar rats with streptozotocin-induced diabetes
Treatment
Oral and intramuscular pancragen (Lys-Glu-Asp-Trp-NH2)
Follow-up
not stated in the source
Study design
Original preclinical study
Funding
not stated in the source

This is a chemically induced model, and the abstract states no dose, group size or duration.

Read the original source
Old rhesus monkeys: glucose disappearance rate and insulin and C-peptide responses

Animal study

Goncharova ND et al. Adv Gerontol. 2014;27(4):662-7. PMID 25946840.

In old female rhesus monkeys, pancragen at 50 micrograms per animal per day intramuscularly for 10 days raised the rate of glucose disappearance and normalized plasma insulin and C-peptide responses to a glucose load, and the effect partly remained 3 weeks after the course. A second report in 9 old (20 to 25 years) clinically healthy females compared 5 given pancragen (0.05 mg per animal per day for 10 days, intramuscular) with 4 given glimepiride (4 mg per animal per day, oral). Both lowered basal glucose, pancragen also normalized insulin and C-peptide, and glimepiride had a stronger, delayed glucose effect and raised C-peptide without a significant effect on insulin (PMID 28509500).

Participants / model
Old female rhesus monkeys (5 on pancragen and 4 on glimepiride in the second report)
Treatment
Intramuscular pancragen 50 micrograms or 0.05 mg per animal per day for 10 days
Follow-up
10 days of treatment; effect partly present 3 weeks later
Study design
Original preclinical studies
Funding
not stated in the source

The authors call pancragen effective and safe, but the abstract lists no safety endpoint, and the groups are very small. Khavinson is a co-author of both reports. The second report (PMID 28509500) is described from the same source record and is not a separate page source.

Read the original source

What do the pancreatic cell culture studies show?

In cultures of aging pancreatic cells, pancragen raised expression of acinar and islet differentiation factors, including Pdx1, Pax6, Pax4, Foxa2 and Nkx2.2. None of these abstracts measures insulin secretion, glucose or an inflammatory marker.

In cultures of aging pancreatic cells, pancragen stimulated expression of differentiation factors of acinar cells and of islet cells, including Pdx1, Pax6, Pax4, Foxa2 and Nkx2.2, in young and aged cultures. A 2012 report on aged human pancreatic cell cultures found raised expression of MMP2, MMP9, serotonin, CD79alpha, Mcl1, PCNA and Ki67 and lowered p53 with the amidated tetrapeptide (PMID 23734516), and a 2012 differentiation paper reports higher CXCL12 and Hoxa3 in human embryonic pancreatic cultures (PMID 22808515). Doses are not stated in the abstracts.

The authors call the differentiation effect a possible mechanism for anti-diabetic and anti-inflammatory effects, but none of these abstracts measures insulin secretion, glucose or an inflammatory marker.

Pancreatic cell cultures: acinar and islet differentiation factors raised

Cell study

Khavinson VKh et al. Bull Exp Biol Med. 2013;154(4):501-4. PMID 23486591.

In cultures of aging pancreatic cells, pancragen stimulated expression of differentiation factors of acinar cells and of islet cells (including Pdx1, Pax6, Pax4, Foxa2 and Nkx2.2) in young and aged cultures. A 2012 report on aged human pancreatic cell cultures found raised expression of MMP2, MMP9, serotonin, CD79alpha, Mcl1, PCNA and Ki67 and lowered p53 with the amidated tetrapeptide (PMID 23734516), and the 2012 differentiation paper reports higher CXCL12 and Hoxa3 in human embryonic pancreatic cultures (PMID 22808515).

Participants / model
Cultured pancreatic cells (the 2012 papers say human); young and aged late-passage cultures
Treatment
Peptide in culture medium; doses not stated in the abstracts
Follow-up
not stated in the source
Study design
Original preclinical studies
Funding
not stated in the source

The authors call the differentiation effect a possible mechanism for anti-diabetic and anti-inflammatory effects, but none of these abstracts measures insulin secretion, glucose or an inflammatory marker.

Read the original source

Does Pancragen support pancreatic function and glucose handling?

Glucose handling has animal support and two small human reports from the originating group with improved glucose-tolerance measures. Pancreatic function is supported only as marker expression in cell cultures and hormone responses in old monkeys, with no pancreatic disease endpoint in people.

Sellers describe Pancragen, a Khavinson pancreas bioregulator tetrapeptide, as supporting pancreatic function and healthy glucose handling, especially with age. The glucose claim has support in diabetic rats and old rhesus monkeys and in two small human reports with improved glucose-tolerance measures. Eight of the 9 PubMed records for pancragen have Khavinson as an author, including both human reports and both monkey reports, and neither human report describes randomization or blinding.

The pancreatic function claim is supported as marker expression in pancreatic cell cultures and as hormone responses in old monkeys. No record measures a pancreatic disease endpoint in people, and no record concerns pancreatitis treatment by title. A vendor vial labeled Pancragen cannot be assumed to match the end group of any given paper.

Old rhesus monkeys: glucose disappearance rate and insulin and C-peptide responses

Animal study

Goncharova ND et al. Adv Gerontol. 2014;27(4):662-7. PMID 25946840.

In old female rhesus monkeys, pancragen at 50 micrograms per animal per day intramuscularly for 10 days raised the rate of glucose disappearance and normalized plasma insulin and C-peptide responses to a glucose load, and the effect partly remained 3 weeks after the course. A second report in 9 old (20 to 25 years) clinically healthy females compared 5 given pancragen (0.05 mg per animal per day for 10 days, intramuscular) with 4 given glimepiride (4 mg per animal per day, oral). Both lowered basal glucose, pancragen also normalized insulin and C-peptide, and glimepiride had a stronger, delayed glucose effect and raised C-peptide without a significant effect on insulin (PMID 28509500).

Participants / model
Old female rhesus monkeys (5 on pancragen and 4 on glimepiride in the second report)
Treatment
Intramuscular pancragen 50 micrograms or 0.05 mg per animal per day for 10 days
Follow-up
10 days of treatment; effect partly present 3 weeks later
Study design
Original preclinical studies
Funding
not stated in the source

The authors call pancragen effective and safe, but the abstract lists no safety endpoint, and the groups are very small. Khavinson is a co-author of both reports. The second report (PMID 28509500) is described from the same source record and is not a separate page source.

Read the original source
2011 human report: 30 healthy older persons and 33 patients with type 2 diabetes

Human study

Korkushko OV et al. Bull Exp Biol Med. 2011;151(4):454-6. PMID 22448364.

A 2011 paper examined 30 healthy older persons and 33 older patients with type 2 diabetes. Nocturnal melatonin production was reduced by 70% in the patients with diabetes compared with the healthy group. In the patients with diabetes, pancragen significantly lowered fasting glucose and glucose in a standard glucose tolerance test and reduced plasma insulin and the insulin resistance index, while in patients not receiving pancragen no changes in carbohydrate metabolism indices were observed.

Participants / model
30 healthy older persons and 33 older patients with type 2 diabetes
Treatment
Pancragen; dose and route not stated in the abstract
Follow-up
not stated in the source
Study design
Original clinical study; assignment and blinding not stated
Funding
not stated in the source

The abstract does not state how many patients received pancragen, the dose, route, duration, how patients were assigned, or whether anyone was blinded, so it cannot be read as a randomized trial. Khavinson is a co-author.

Read the original source
2013 pankragen forte report: 12 older people, 4 weeks, no control group

Human study

Korkushko OV et al. Adv Gerontol. 2013;26(2):297-308. PMID 28976155.

A 2013 Russian-language study of pankragen forte screened 150 healthy people (39 aged 20 to 39, 42 aged 40 to 59, 69 aged 60 and over) and gave 500 micrograms twice a day for 4 weeks to 12 older people with impaired glucose tolerance. In 50 percent of those 12, plasma glucose during a standard oral glucose tolerance test fell significantly, and the authors link this to better serum lipids, endothelial function and platelet aggregation.

Participants / model
12 older people with impaired glucose tolerance, selected from 69 older adults
Treatment
Pankragen forte 500 micrograms twice a day for 4 weeks; route not stated in the abstract
Follow-up
4 weeks
Study design
Original clinical study, no control group described
Funding
not stated in the source

The abstract describes no control group, and the composition of forte is not stated, so it cannot be treated as the same product as plain pancragen. Khavinson is a co-author. The abstract is the publisher's Russian text with an English translation in PubMed.

Read the original source
Pancreatic cell cultures: acinar and islet differentiation factors raised

Cell study

Khavinson VKh et al. Bull Exp Biol Med. 2013;154(4):501-4. PMID 23486591.

In cultures of aging pancreatic cells, pancragen stimulated expression of differentiation factors of acinar cells and of islet cells (including Pdx1, Pax6, Pax4, Foxa2 and Nkx2.2) in young and aged cultures. A 2012 report on aged human pancreatic cell cultures found raised expression of MMP2, MMP9, serotonin, CD79alpha, Mcl1, PCNA and Ki67 and lowered p53 with the amidated tetrapeptide (PMID 23734516), and the 2012 differentiation paper reports higher CXCL12 and Hoxa3 in human embryonic pancreatic cultures (PMID 22808515).

Participants / model
Cultured pancreatic cells (the 2012 papers say human); young and aged late-passage cultures
Treatment
Peptide in culture medium; doses not stated in the abstracts
Follow-up
not stated in the source
Study design
Original preclinical studies
Funding
not stated in the source

The authors call the differentiation effect a possible mechanism for anti-diabetic and anti-inflammatory effects, but none of these abstracts measures insulin secretion, glucose or an inflammatory marker.

Read the original source
Searches, 10 October 2026: 9 records, 0 controlled trials

PubMed search record

PubMed search run on 10 October 2026: pancragen, 9 records. Related PubMed searches run the same day.

A PubMed search for pancragen returned 9 records. Eight have Khavinson as an author, and the exception is the 2006 explant report by other authors. A search for pancragen AND (clinical trial[pt] OR randomized controlled trial[pt]) returned 0 records. A wider search for (pancragen OR pankragen OR Lys-Glu-Asp-Trp) AND (patients OR humans OR elderly OR diabetes) returned 10 records, all among the papers already described, and the only two studies that gave the peptide to people are the 2011 and 2013 reports. In the records reviewed there is no randomized placebo-controlled trial, no independent replication, no human pharmacokinetics, no reported adverse events and no pancreatitis study.

Participants / model
Records returned, not a population
Treatment
Not applicable
Follow-up
Searches run on 2026-10-10
Study design
Literature searches
Funding
not stated in the source

A search result shows what the databases returned on that date. It is not proof that no unindexed study exists.

Read the original source

How is Pancragen thought to work?

The originating group's possible mechanism is a differentiation effect on pancreatic cells: in aging pancreatic cell cultures, pancragen raised expression of acinar and islet differentiation factors. None of those abstracts measures insulin secretion or glucose, so the link to the animal and human glucose results is not shown.

In cultures of aging pancreatic cells, pancragen raised expression of differentiation factors of acinar cells and islet cells, and the authors call this a possible mechanism for anti-diabetic and anti-inflammatory effects. None of those abstracts measures insulin secretion, glucose or an inflammatory marker.

The glucose findings come from other systems. In old rhesus monkeys, insulin and C-peptide responses to a glucose load were normalized. In diabetic rats, oral pancragen produced a hypoglycemic effect and intramuscular pancragen normalized capillary endothelium adhesion. The 2011 report found lower fasting glucose, glucose tolerance test values and insulin resistance index in older patients with type 2 diabetes, whose nocturnal melatonin production was 70% lower than in healthy older people. The records reviewed do not show how these relate to the differentiation signal in cultures.

Pancreatic cell cultures: acinar and islet differentiation factors raised

Cell study

Khavinson VKh et al. Bull Exp Biol Med. 2013;154(4):501-4. PMID 23486591.

In cultures of aging pancreatic cells, pancragen stimulated expression of differentiation factors of acinar cells and of islet cells (including Pdx1, Pax6, Pax4, Foxa2 and Nkx2.2) in young and aged cultures. A 2012 report on aged human pancreatic cell cultures found raised expression of MMP2, MMP9, serotonin, CD79alpha, Mcl1, PCNA and Ki67 and lowered p53 with the amidated tetrapeptide (PMID 23734516), and the 2012 differentiation paper reports higher CXCL12 and Hoxa3 in human embryonic pancreatic cultures (PMID 22808515).

Participants / model
Cultured pancreatic cells (the 2012 papers say human); young and aged late-passage cultures
Treatment
Peptide in culture medium; doses not stated in the abstracts
Follow-up
not stated in the source
Study design
Original preclinical studies
Funding
not stated in the source

The authors call the differentiation effect a possible mechanism for anti-diabetic and anti-inflammatory effects, but none of these abstracts measures insulin secretion, glucose or an inflammatory marker.

Read the original source
Old rhesus monkeys: glucose disappearance rate and insulin and C-peptide responses

Animal study

Goncharova ND et al. Adv Gerontol. 2014;27(4):662-7. PMID 25946840.

In old female rhesus monkeys, pancragen at 50 micrograms per animal per day intramuscularly for 10 days raised the rate of glucose disappearance and normalized plasma insulin and C-peptide responses to a glucose load, and the effect partly remained 3 weeks after the course. A second report in 9 old (20 to 25 years) clinically healthy females compared 5 given pancragen (0.05 mg per animal per day for 10 days, intramuscular) with 4 given glimepiride (4 mg per animal per day, oral). Both lowered basal glucose, pancragen also normalized insulin and C-peptide, and glimepiride had a stronger, delayed glucose effect and raised C-peptide without a significant effect on insulin (PMID 28509500).

Participants / model
Old female rhesus monkeys (5 on pancragen and 4 on glimepiride in the second report)
Treatment
Intramuscular pancragen 50 micrograms or 0.05 mg per animal per day for 10 days
Follow-up
10 days of treatment; effect partly present 3 weeks later
Study design
Original preclinical studies
Funding
not stated in the source

The authors call pancragen effective and safe, but the abstract lists no safety endpoint, and the groups are very small. Khavinson is a co-author of both reports. The second report (PMID 28509500) is described from the same source record and is not a separate page source.

Read the original source
Diabetic rats: oral pancragen lowered glucose; intramuscular normalized capillary adhesion

Animal study

Khavinson VKh et al. Bull Exp Biol Med. 2007;144(4):559-62. PMID 18642713.

In Wistar rats with streptozotocin-induced diabetes, oral pancragen produced a pronounced hypoglycemic effect during treatment, and intramuscular pancragen normalized the adhesion of mesenteric capillary endothelium but did not change capillary permeability. The authors read this as homeostatic and endothelioprotective effects in the early period of diabetes.

Participants / model
Wistar rats with streptozotocin-induced diabetes
Treatment
Oral and intramuscular pancragen (Lys-Glu-Asp-Trp-NH2)
Follow-up
not stated in the source
Study design
Original preclinical study
Funding
not stated in the source

This is a chemically induced model, and the abstract states no dose, group size or duration.

Read the original source
2011 human report: 30 healthy older persons and 33 patients with type 2 diabetes

Human study

Korkushko OV et al. Bull Exp Biol Med. 2011;151(4):454-6. PMID 22448364.

A 2011 paper examined 30 healthy older persons and 33 older patients with type 2 diabetes. Nocturnal melatonin production was reduced by 70% in the patients with diabetes compared with the healthy group. In the patients with diabetes, pancragen significantly lowered fasting glucose and glucose in a standard glucose tolerance test and reduced plasma insulin and the insulin resistance index, while in patients not receiving pancragen no changes in carbohydrate metabolism indices were observed.

Participants / model
30 healthy older persons and 33 older patients with type 2 diabetes
Treatment
Pancragen; dose and route not stated in the abstract
Follow-up
not stated in the source
Study design
Original clinical study; assignment and blinding not stated
Funding
not stated in the source

The abstract does not state how many patients received pancragen, the dose, route, duration, how patients were assigned, or whether anyone was blinded, so it cannot be read as a randomized trial. Khavinson is a co-author.

Read the original source

What is known about the safety of Pancragen?

No safety endpoint or adverse event is reported in the records reviewed. The monkey authors call pancragen effective and safe, but the abstract lists no safety endpoint and the groups were very small. No human pharmacokinetics or pancreatitis study was found.

None of the human or monkey abstracts reports an adverse event or a safety endpoint. The 2011 report does not state the treated-arm size, dose, route or duration, and the 2013 report treated 12 older people with no control group.

A PubMed search on 10 October 2026 found no human pharmacokinetics, no independent replication and no pancreatitis study. The end group is also unsettled: the group writes Lys-Glu-Asp-Trp both as an amide and with no amide, PubChem holds only the free acid, and a vial labeled Pancragen cannot be assumed to match any given paper. Pankragen forte, studied in 2013, has no stated composition and is not shown to be the same product.

Old rhesus monkeys: glucose disappearance rate and insulin and C-peptide responses

Animal study

Goncharova ND et al. Adv Gerontol. 2014;27(4):662-7. PMID 25946840.

In old female rhesus monkeys, pancragen at 50 micrograms per animal per day intramuscularly for 10 days raised the rate of glucose disappearance and normalized plasma insulin and C-peptide responses to a glucose load, and the effect partly remained 3 weeks after the course. A second report in 9 old (20 to 25 years) clinically healthy females compared 5 given pancragen (0.05 mg per animal per day for 10 days, intramuscular) with 4 given glimepiride (4 mg per animal per day, oral). Both lowered basal glucose, pancragen also normalized insulin and C-peptide, and glimepiride had a stronger, delayed glucose effect and raised C-peptide without a significant effect on insulin (PMID 28509500).

Participants / model
Old female rhesus monkeys (5 on pancragen and 4 on glimepiride in the second report)
Treatment
Intramuscular pancragen 50 micrograms or 0.05 mg per animal per day for 10 days
Follow-up
10 days of treatment; effect partly present 3 weeks later
Study design
Original preclinical studies
Funding
not stated in the source

The authors call pancragen effective and safe, but the abstract lists no safety endpoint, and the groups are very small. Khavinson is a co-author of both reports. The second report (PMID 28509500) is described from the same source record and is not a separate page source.

Read the original source
2011 human report: 30 healthy older persons and 33 patients with type 2 diabetes

Human study

Korkushko OV et al. Bull Exp Biol Med. 2011;151(4):454-6. PMID 22448364.

A 2011 paper examined 30 healthy older persons and 33 older patients with type 2 diabetes. Nocturnal melatonin production was reduced by 70% in the patients with diabetes compared with the healthy group. In the patients with diabetes, pancragen significantly lowered fasting glucose and glucose in a standard glucose tolerance test and reduced plasma insulin and the insulin resistance index, while in patients not receiving pancragen no changes in carbohydrate metabolism indices were observed.

Participants / model
30 healthy older persons and 33 older patients with type 2 diabetes
Treatment
Pancragen; dose and route not stated in the abstract
Follow-up
not stated in the source
Study design
Original clinical study; assignment and blinding not stated
Funding
not stated in the source

The abstract does not state how many patients received pancragen, the dose, route, duration, how patients were assigned, or whether anyone was blinded, so it cannot be read as a randomized trial. Khavinson is a co-author.

Read the original source
2013 pankragen forte report: 12 older people, 4 weeks, no control group

Human study

Korkushko OV et al. Adv Gerontol. 2013;26(2):297-308. PMID 28976155.

A 2013 Russian-language study of pankragen forte screened 150 healthy people (39 aged 20 to 39, 42 aged 40 to 59, 69 aged 60 and over) and gave 500 micrograms twice a day for 4 weeks to 12 older people with impaired glucose tolerance. In 50 percent of those 12, plasma glucose during a standard oral glucose tolerance test fell significantly, and the authors link this to better serum lipids, endothelial function and platelet aggregation.

Participants / model
12 older people with impaired glucose tolerance, selected from 69 older adults
Treatment
Pankragen forte 500 micrograms twice a day for 4 weeks; route not stated in the abstract
Follow-up
4 weeks
Study design
Original clinical study, no control group described
Funding
not stated in the source

The abstract describes no control group, and the composition of forte is not stated, so it cannot be treated as the same product as plain pancragen. Khavinson is a co-author. The abstract is the publisher's Russian text with an English translation in PubMed.

Read the original source
Searches, 10 October 2026: 9 records, 0 controlled trials

PubMed search record

PubMed search run on 10 October 2026: pancragen, 9 records. Related PubMed searches run the same day.

A PubMed search for pancragen returned 9 records. Eight have Khavinson as an author, and the exception is the 2006 explant report by other authors. A search for pancragen AND (clinical trial[pt] OR randomized controlled trial[pt]) returned 0 records. A wider search for (pancragen OR pankragen OR Lys-Glu-Asp-Trp) AND (patients OR humans OR elderly OR diabetes) returned 10 records, all among the papers already described, and the only two studies that gave the peptide to people are the 2011 and 2013 reports. In the records reviewed there is no randomized placebo-controlled trial, no independent replication, no human pharmacokinetics, no reported adverse events and no pancreatitis study.

Participants / model
Records returned, not a population
Treatment
Not applicable
Follow-up
Searches run on 2026-10-10
Study design
Literature searches
Funding
not stated in the source

A search result shows what the databases returned on that date. It is not proof that no unindexed study exists.

Read the original source
2010 paper: amidated Lys-Glu-Asp-Trp-NH2, no result reported

Chemical identity record

Khavinson VKh et al. Bull Exp Biol Med. 2010;149(3):351-3. PMID 21246099.

The group's papers give the sequence as Lys-Glu-Asp-Trp (KEDW). A 2007 rat paper (PMID 18642713) and this 2010 paper write it as Lys-Glu-Asp-Trp-NH2, and a 2012 paper on human pancreatic cells writes H-Lys-Glu-Asp-Trp-NH2 (PMID 23734516). A 2012 differentiation paper (PMID 22808515) and a 2014 monkey paper (PMID 25946840) write Lys-Glu-Asp-Trp with no amide. A C-terminal amide and a free acid are different molecules and PubChem holds only the free acid. The sequence is also not the tripeptide Lys-Glu-Asp (Vesugen), which the 2012 differentiation paper names separately. The 2010 abstract describes the amidated tetrapeptide as natural and endogenous and reports no result.

Participants / model
Chemical identity, not a clinical population
Treatment
Synthetic tetrapeptide, amidated and free-acid forms in print
Follow-up
Not applicable
Study design
Original reports
Funding
not stated in the source

A vendor vial labeled Pancragen cannot be assumed to match the end group of any given paper.

Read the original source
PubChem: free-acid KEDW tetrapeptide, no record under the name Pancragen

Chemical identity record

National Library of Medicine. PubChem compound record CID 68452877 (H-Lys-Glu-Asp-Trp-OH). PubChem name searches run 10 October 2026.

A PubChem name search on 2026-10-10 for pancragen, for KEDW and for Lys-Glu-Asp-Trp-NH2 returned no record. The free-acid tetrapeptide H-Lys-Glu-Asp-Trp-OH is CID 68452877, C26H36N6O9, molecular weight 576.6, with one vendor-style synonym (SCHEMBL2946041) and no CAS number listed. That record does not carry the name Pancragen, so the trade name is tied to the sequence only by the originating group's own papers.

Participants / model
Chemical identity, not a clinical population
Treatment
Defined synthetic tetrapeptide, free acid
Follow-up
Not applicable
Study design
NLM chemical record
Funding
not stated in the source

PubChem holds only the free acid, not the amidated form that some papers write.

Read the original source

Why does Pancragen sit in C tier?

Pancragen is a defined tetrapeptide with a coherent preclinical profile and two small human reports. It stays at C because eight of the nine PubMed records have the originator as an author, the human reports describe no randomization or blinding, no regulator record exists, and the end group is not settled.

The preclinical profile covers rat pancreas explants, diabetic rats, aged pancreatic cell cultures and old rhesus monkeys. The human glucose reports are small and, as far as the abstracts show, uncontrolled, and one has 12 participants and no control group. There are human glucose reports and more than one paper, so it is not a single-study compound.

Epithalon and cartalax also sit in C on this site.

Old rhesus monkeys: glucose disappearance rate and insulin and C-peptide responses

Animal study

Goncharova ND et al. Adv Gerontol. 2014;27(4):662-7. PMID 25946840.

In old female rhesus monkeys, pancragen at 50 micrograms per animal per day intramuscularly for 10 days raised the rate of glucose disappearance and normalized plasma insulin and C-peptide responses to a glucose load, and the effect partly remained 3 weeks after the course. A second report in 9 old (20 to 25 years) clinically healthy females compared 5 given pancragen (0.05 mg per animal per day for 10 days, intramuscular) with 4 given glimepiride (4 mg per animal per day, oral). Both lowered basal glucose, pancragen also normalized insulin and C-peptide, and glimepiride had a stronger, delayed glucose effect and raised C-peptide without a significant effect on insulin (PMID 28509500).

Participants / model
Old female rhesus monkeys (5 on pancragen and 4 on glimepiride in the second report)
Treatment
Intramuscular pancragen 50 micrograms or 0.05 mg per animal per day for 10 days
Follow-up
10 days of treatment; effect partly present 3 weeks later
Study design
Original preclinical studies
Funding
not stated in the source

The authors call pancragen effective and safe, but the abstract lists no safety endpoint, and the groups are very small. Khavinson is a co-author of both reports. The second report (PMID 28509500) is described from the same source record and is not a separate page source.

Read the original source
Diabetic rats: oral pancragen lowered glucose; intramuscular normalized capillary adhesion

Animal study

Khavinson VKh et al. Bull Exp Biol Med. 2007;144(4):559-62. PMID 18642713.

In Wistar rats with streptozotocin-induced diabetes, oral pancragen produced a pronounced hypoglycemic effect during treatment, and intramuscular pancragen normalized the adhesion of mesenteric capillary endothelium but did not change capillary permeability. The authors read this as homeostatic and endothelioprotective effects in the early period of diabetes.

Participants / model
Wistar rats with streptozotocin-induced diabetes
Treatment
Oral and intramuscular pancragen (Lys-Glu-Asp-Trp-NH2)
Follow-up
not stated in the source
Study design
Original preclinical study
Funding
not stated in the source

This is a chemically induced model, and the abstract states no dose, group size or duration.

Read the original source
Pancreatic cell cultures: acinar and islet differentiation factors raised

Cell study

Khavinson VKh et al. Bull Exp Biol Med. 2013;154(4):501-4. PMID 23486591.

In cultures of aging pancreatic cells, pancragen stimulated expression of differentiation factors of acinar cells and of islet cells (including Pdx1, Pax6, Pax4, Foxa2 and Nkx2.2) in young and aged cultures. A 2012 report on aged human pancreatic cell cultures found raised expression of MMP2, MMP9, serotonin, CD79alpha, Mcl1, PCNA and Ki67 and lowered p53 with the amidated tetrapeptide (PMID 23734516), and the 2012 differentiation paper reports higher CXCL12 and Hoxa3 in human embryonic pancreatic cultures (PMID 22808515).

Participants / model
Cultured pancreatic cells (the 2012 papers say human); young and aged late-passage cultures
Treatment
Peptide in culture medium; doses not stated in the abstracts
Follow-up
not stated in the source
Study design
Original preclinical studies
Funding
not stated in the source

The authors call the differentiation effect a possible mechanism for anti-diabetic and anti-inflammatory effects, but none of these abstracts measures insulin secretion, glucose or an inflammatory marker.

Read the original source
2011 human report: 30 healthy older persons and 33 patients with type 2 diabetes

Human study

Korkushko OV et al. Bull Exp Biol Med. 2011;151(4):454-6. PMID 22448364.

A 2011 paper examined 30 healthy older persons and 33 older patients with type 2 diabetes. Nocturnal melatonin production was reduced by 70% in the patients with diabetes compared with the healthy group. In the patients with diabetes, pancragen significantly lowered fasting glucose and glucose in a standard glucose tolerance test and reduced plasma insulin and the insulin resistance index, while in patients not receiving pancragen no changes in carbohydrate metabolism indices were observed.

Participants / model
30 healthy older persons and 33 older patients with type 2 diabetes
Treatment
Pancragen; dose and route not stated in the abstract
Follow-up
not stated in the source
Study design
Original clinical study; assignment and blinding not stated
Funding
not stated in the source

The abstract does not state how many patients received pancragen, the dose, route, duration, how patients were assigned, or whether anyone was blinded, so it cannot be read as a randomized trial. Khavinson is a co-author.

Read the original source
2013 pankragen forte report: 12 older people, 4 weeks, no control group

Human study

Korkushko OV et al. Adv Gerontol. 2013;26(2):297-308. PMID 28976155.

A 2013 Russian-language study of pankragen forte screened 150 healthy people (39 aged 20 to 39, 42 aged 40 to 59, 69 aged 60 and over) and gave 500 micrograms twice a day for 4 weeks to 12 older people with impaired glucose tolerance. In 50 percent of those 12, plasma glucose during a standard oral glucose tolerance test fell significantly, and the authors link this to better serum lipids, endothelial function and platelet aggregation.

Participants / model
12 older people with impaired glucose tolerance, selected from 69 older adults
Treatment
Pankragen forte 500 micrograms twice a day for 4 weeks; route not stated in the abstract
Follow-up
4 weeks
Study design
Original clinical study, no control group described
Funding
not stated in the source

The abstract describes no control group, and the composition of forte is not stated, so it cannot be treated as the same product as plain pancragen. Khavinson is a co-author. The abstract is the publisher's Russian text with an English translation in PubMed.

Read the original source
FDA, DailyMed and registry: no pancragen record, 10 October 2026

Regulatory record

U.S. Food and Drug Administration, openFDA Drugs@FDA query for pancragen; DailyMed search for the drug name pancragen; ClinicalTrials.gov queries for pancragen and Lys-Glu-Asp-Trp tetrapeptide, all run on 10 October 2026.

An openFDA Drugs@FDA query for pancragen returned no match, a DailyMed search for the drug name pancragen returned no label, and ClinicalTrials.gov returned no record for pancragen or for the Lys-Glu-Asp-Trp tetrapeptide. No FDA record was found in these sources, so Pancragen is not an FDA-approved drug or a labeled product.

Participants / model
Not a clinical population
Treatment
Not applicable
Follow-up
Searches run on 2026-10-10
Study design
Official FDA, NLM and registry records
Funding
not stated in the source

This says nothing about other regulators.

Read the original source
2010 paper: amidated Lys-Glu-Asp-Trp-NH2, no result reported

Chemical identity record

Khavinson VKh et al. Bull Exp Biol Med. 2010;149(3):351-3. PMID 21246099.

The group's papers give the sequence as Lys-Glu-Asp-Trp (KEDW). A 2007 rat paper (PMID 18642713) and this 2010 paper write it as Lys-Glu-Asp-Trp-NH2, and a 2012 paper on human pancreatic cells writes H-Lys-Glu-Asp-Trp-NH2 (PMID 23734516). A 2012 differentiation paper (PMID 22808515) and a 2014 monkey paper (PMID 25946840) write Lys-Glu-Asp-Trp with no amide. A C-terminal amide and a free acid are different molecules and PubChem holds only the free acid. The sequence is also not the tripeptide Lys-Glu-Asp (Vesugen), which the 2012 differentiation paper names separately. The 2010 abstract describes the amidated tetrapeptide as natural and endogenous and reports no result.

Participants / model
Chemical identity, not a clinical population
Treatment
Synthetic tetrapeptide, amidated and free-acid forms in print
Follow-up
Not applicable
Study design
Original reports
Funding
not stated in the source

A vendor vial labeled Pancragen cannot be assumed to match the end group of any given paper.

Read the original source

Studies and sources

PubChem: free-acid KEDW tetrapeptide, no record under the name Pancragen

Chemical identity record

National Library of Medicine. PubChem compound record CID 68452877 (H-Lys-Glu-Asp-Trp-OH). PubChem name searches run 10 October 2026.

A PubChem name search on 2026-10-10 for pancragen, for KEDW and for Lys-Glu-Asp-Trp-NH2 returned no record. The free-acid tetrapeptide H-Lys-Glu-Asp-Trp-OH is CID 68452877, C26H36N6O9, molecular weight 576.6, with one vendor-style synonym (SCHEMBL2946041) and no CAS number listed. That record does not carry the name Pancragen, so the trade name is tied to the sequence only by the originating group's own papers.

Participants / model
Chemical identity, not a clinical population
Treatment
Defined synthetic tetrapeptide, free acid
Follow-up
Not applicable
Study design
NLM chemical record
Funding
not stated in the source

PubChem holds only the free acid, not the amidated form that some papers write.

Read the original source
2010 paper: amidated Lys-Glu-Asp-Trp-NH2, no result reported

Chemical identity record

Khavinson VKh et al. Bull Exp Biol Med. 2010;149(3):351-3. PMID 21246099.

The group's papers give the sequence as Lys-Glu-Asp-Trp (KEDW). A 2007 rat paper (PMID 18642713) and this 2010 paper write it as Lys-Glu-Asp-Trp-NH2, and a 2012 paper on human pancreatic cells writes H-Lys-Glu-Asp-Trp-NH2 (PMID 23734516). A 2012 differentiation paper (PMID 22808515) and a 2014 monkey paper (PMID 25946840) write Lys-Glu-Asp-Trp with no amide. A C-terminal amide and a free acid are different molecules and PubChem holds only the free acid. The sequence is also not the tripeptide Lys-Glu-Asp (Vesugen), which the 2012 differentiation paper names separately. The 2010 abstract describes the amidated tetrapeptide as natural and endogenous and reports no result.

Participants / model
Chemical identity, not a clinical population
Treatment
Synthetic tetrapeptide, amidated and free-acid forms in print
Follow-up
Not applicable
Study design
Original reports
Funding
not stated in the source

A vendor vial labeled Pancragen cannot be assumed to match the end group of any given paper.

Read the original source
2006 explant report: pancreas explants from 3-week and 18-month-old rats

Cell study

Zakutskiĭ AN et al. Adv Gerontol. 2006;19:93-6. PMID 17152728.

A 2006 Russian-language report used synthetic cardiogen, bronchogen, prostamax and pancragen on organotypic explants of heart, lung, prostate and pancreas from 3-week-old and 18-month-old rats. At 0.05 ng/ml the peptide stimulated growth in its matching tissue culture compared with control explants in all groups. The abstract reports no endocrine, glucose or function endpoint.

Participants / model
Pancreas explants from young (3-week) and aged (18-month) rats, among other tissues
Treatment
Peptide in culture medium at 0.05 ng/ml
Follow-up
not stated in the source
Study design
Original preclinical explant study
Funding
not stated in the source

The authors' statement that these peptides can be used in clinical practice is a conclusion the abstract's data do not reach. This is the one pancragen paper without Khavinson as an author.

Read the original source
Pancreatic cell cultures: acinar and islet differentiation factors raised

Cell study

Khavinson VKh et al. Bull Exp Biol Med. 2013;154(4):501-4. PMID 23486591.

In cultures of aging pancreatic cells, pancragen stimulated expression of differentiation factors of acinar cells and of islet cells (including Pdx1, Pax6, Pax4, Foxa2 and Nkx2.2) in young and aged cultures. A 2012 report on aged human pancreatic cell cultures found raised expression of MMP2, MMP9, serotonin, CD79alpha, Mcl1, PCNA and Ki67 and lowered p53 with the amidated tetrapeptide (PMID 23734516), and the 2012 differentiation paper reports higher CXCL12 and Hoxa3 in human embryonic pancreatic cultures (PMID 22808515).

Participants / model
Cultured pancreatic cells (the 2012 papers say human); young and aged late-passage cultures
Treatment
Peptide in culture medium; doses not stated in the abstracts
Follow-up
not stated in the source
Study design
Original preclinical studies
Funding
not stated in the source

The authors call the differentiation effect a possible mechanism for anti-diabetic and anti-inflammatory effects, but none of these abstracts measures insulin secretion, glucose or an inflammatory marker.

Read the original source
Diabetic rats: oral pancragen lowered glucose; intramuscular normalized capillary adhesion

Animal study

Khavinson VKh et al. Bull Exp Biol Med. 2007;144(4):559-62. PMID 18642713.

In Wistar rats with streptozotocin-induced diabetes, oral pancragen produced a pronounced hypoglycemic effect during treatment, and intramuscular pancragen normalized the adhesion of mesenteric capillary endothelium but did not change capillary permeability. The authors read this as homeostatic and endothelioprotective effects in the early period of diabetes.

Participants / model
Wistar rats with streptozotocin-induced diabetes
Treatment
Oral and intramuscular pancragen (Lys-Glu-Asp-Trp-NH2)
Follow-up
not stated in the source
Study design
Original preclinical study
Funding
not stated in the source

This is a chemically induced model, and the abstract states no dose, group size or duration.

Read the original source
Old rhesus monkeys: glucose disappearance rate and insulin and C-peptide responses

Animal study

Goncharova ND et al. Adv Gerontol. 2014;27(4):662-7. PMID 25946840.

In old female rhesus monkeys, pancragen at 50 micrograms per animal per day intramuscularly for 10 days raised the rate of glucose disappearance and normalized plasma insulin and C-peptide responses to a glucose load, and the effect partly remained 3 weeks after the course. A second report in 9 old (20 to 25 years) clinically healthy females compared 5 given pancragen (0.05 mg per animal per day for 10 days, intramuscular) with 4 given glimepiride (4 mg per animal per day, oral). Both lowered basal glucose, pancragen also normalized insulin and C-peptide, and glimepiride had a stronger, delayed glucose effect and raised C-peptide without a significant effect on insulin (PMID 28509500).

Participants / model
Old female rhesus monkeys (5 on pancragen and 4 on glimepiride in the second report)
Treatment
Intramuscular pancragen 50 micrograms or 0.05 mg per animal per day for 10 days
Follow-up
10 days of treatment; effect partly present 3 weeks later
Study design
Original preclinical studies
Funding
not stated in the source

The authors call pancragen effective and safe, but the abstract lists no safety endpoint, and the groups are very small. Khavinson is a co-author of both reports. The second report (PMID 28509500) is described from the same source record and is not a separate page source.

Read the original source
2011 human report: 30 healthy older persons and 33 patients with type 2 diabetes

Human study

Korkushko OV et al. Bull Exp Biol Med. 2011;151(4):454-6. PMID 22448364.

A 2011 paper examined 30 healthy older persons and 33 older patients with type 2 diabetes. Nocturnal melatonin production was reduced by 70% in the patients with diabetes compared with the healthy group. In the patients with diabetes, pancragen significantly lowered fasting glucose and glucose in a standard glucose tolerance test and reduced plasma insulin and the insulin resistance index, while in patients not receiving pancragen no changes in carbohydrate metabolism indices were observed.

Participants / model
30 healthy older persons and 33 older patients with type 2 diabetes
Treatment
Pancragen; dose and route not stated in the abstract
Follow-up
not stated in the source
Study design
Original clinical study; assignment and blinding not stated
Funding
not stated in the source

The abstract does not state how many patients received pancragen, the dose, route, duration, how patients were assigned, or whether anyone was blinded, so it cannot be read as a randomized trial. Khavinson is a co-author.

Read the original source
2013 pankragen forte report: 12 older people, 4 weeks, no control group

Human study

Korkushko OV et al. Adv Gerontol. 2013;26(2):297-308. PMID 28976155.

A 2013 Russian-language study of pankragen forte screened 150 healthy people (39 aged 20 to 39, 42 aged 40 to 59, 69 aged 60 and over) and gave 500 micrograms twice a day for 4 weeks to 12 older people with impaired glucose tolerance. In 50 percent of those 12, plasma glucose during a standard oral glucose tolerance test fell significantly, and the authors link this to better serum lipids, endothelial function and platelet aggregation.

Participants / model
12 older people with impaired glucose tolerance, selected from 69 older adults
Treatment
Pankragen forte 500 micrograms twice a day for 4 weeks; route not stated in the abstract
Follow-up
4 weeks
Study design
Original clinical study, no control group described
Funding
not stated in the source

The abstract describes no control group, and the composition of forte is not stated, so it cannot be treated as the same product as plain pancragen. Khavinson is a co-author. The abstract is the publisher's Russian text with an English translation in PubMed.

Read the original source
FDA, DailyMed and registry: no pancragen record, 10 October 2026

Regulatory record

U.S. Food and Drug Administration, openFDA Drugs@FDA query for pancragen; DailyMed search for the drug name pancragen; ClinicalTrials.gov queries for pancragen and Lys-Glu-Asp-Trp tetrapeptide, all run on 10 October 2026.

An openFDA Drugs@FDA query for pancragen returned no match, a DailyMed search for the drug name pancragen returned no label, and ClinicalTrials.gov returned no record for pancragen or for the Lys-Glu-Asp-Trp tetrapeptide. No FDA record was found in these sources, so Pancragen is not an FDA-approved drug or a labeled product.

Participants / model
Not a clinical population
Treatment
Not applicable
Follow-up
Searches run on 2026-10-10
Study design
Official FDA, NLM and registry records
Funding
not stated in the source

This says nothing about other regulators.

Read the original source

Why is Pancragen in C tier?

C fits a defined tetrapeptide with a coherent preclinical profile in rat pancreas explants and diabetic rats, aged pancreatic cell cultures and old rhesus monkeys, plus two small human reports. It stays at C because eight of the nine PubMed records have the originator as an author, the human reports describe no randomization or blinding, no regulator record exists, and the end group is not settled.