Pancreastatin
An endogenous peptide cut from chromogranin A that opposes insulin — raising blood sugar from the liver and blunting insulin release; raised in diabetes, and a target to block, not a drug
Pancreastatin is a peptide the body makes by cutting up a larger granule protein, chromogranin A (the same parent that gives rise to catestatin). Its name comes from its first-known job: it tells the pancreas to release less insulin. More broadly it behaves as a counter-regulatory, ‘dysglycemic’ signal — the opposite of insulin’s metabolic effects. It prompts the liver to release glucose (glycogenolysis), drives fat breakdown (lipolysis), and blunts the uptake of glucose into cells. When it was infused into the arm of healthy volunteers, it cut the forearm’s glucose uptake by about half — a direct metabolic effect in people. Pancreastatin runs high in type 2 diabetes, insulin resistance, gestational diabetes and high blood pressure, and a common gene variant that makes it more potent raises the risk of cardiometabolic disease. Because of all this, the therapeutic interest is in blocking pancreastatin, not giving it. It is an endogenous peptide studied as a research tool and drug target; it is not an approved medicine and has not been given to people as a treatment.
No established human dose Details ↓
Recommended Dosing
No established human dose
Pancreastatin has been infused into people only briefly, as a research probe of metabolism (a local brachial-artery infusion of about 200 nM over roughly 15 minutes), never as a treatment — and because it is elevated and harmful in metabolic disease, the therapeutic aim is to block it, not to give it. No regulator has approved any dose, and those experimental infusion concentrations are not a therapeutic dose, so no amount is printed here.
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What is it?
Chromogranin A is a large protein stored in the secretory granules of neuroendocrine cells. The body cuts it into several active peptides, and pancreastatin is one of them — the sister of catestatin, which comes from a different part of the same parent. Pancreastatin was named for its first-described action: it inhibits glucose-stimulated insulin secretion from the pancreatic beta cells.
Its wider role is as a counter-regulatory, or ‘dysglycemic’, peptide — broadly opposing what insulin does to metabolism. It triggers the liver to break down glycogen and release glucose, it drives fat cells to release fatty acids, and it reduces the uptake of glucose into muscle and fat. It does this through a receptor coupled to the Gq–phospholipase-C–calcium–PKC pathway, and recent work points to an interaction with the chaperone GRP78.
Unusually for an endogenous research peptide, pancreastatin has been studied directly in people. When synthetic human pancreastatin was infused into the brachial artery of healthy men, it reduced the forearm’s glucose uptake by roughly half, with no change in blood flow — showing the effect is metabolic, not circulatory. Interestingly, the same studies found that pancreastatin did not block insulin’s own action, so it is not a simple insulin antagonist but a parallel, independent dysglycemic signal.
The disease link is consistent. Plasma pancreastatin is elevated in type 2 diabetes, insulin resistance, gestational diabetes and essential hypertension, and it tracks with catecholamine (adrenaline-type) levels, appearing to amplify their metabolic effects when the sympathetic nervous system is active. A naturally occurring variant of the peptide, Gly297Ser, is more potent at inhibiting glucose uptake, and in large population studies the 297Ser version carries a modestly higher risk of type 2 diabetes, high blood pressure and coronary artery disease. Pancreastatin also has immune effects, acting on macrophages and inflammation.
That biology points to blocking pancreastatin, not supplementing it. A designed inhibitor peptide, PSTi8 (pancreastatin inhibitor peptide-8), improved insulin sensitivity and glucose handling and eased fatty liver in rodent models of diabetes, acting through the GRP78–AMPK pathway. This is preclinical, and PSTi8 is a laboratory tool, not a medicine.
Pancreastatin is an endogenous human peptide and a research and drug-target tool, not a medicine. No published study has given pancreastatin to people as a treatment — the human studies infused it briefly to probe metabolism — it is approved nowhere, and material sold online as ‘pancreastatin’ is an unregulated research chemical. Nothing here is a dose or a therapy; this page records what the published science says about the peptide.
Mechanism of Action
Pancreastatin is a chromogranin A fragment that opposes insulin: it raises glucose from the liver, drives fat breakdown and blunts insulin release and glucose uptake. In metabolic disease it runs too high — which is why the therapeutic idea is to block it.
Counter-regulatory metabolic signal
Through a Gq-PLCβ-calcium-PKC-coupled receptor, pancreastatin inhibits glucose-induced insulin secretion, drives hepatic glycogenolysis and fat-cell lipolysis, and reduces cellular glucose uptake — broadly opposing insulin (PMID 20184923), as shown directly in human forearm infusions (PMID 15956083).
Raised in metabolic disease
Plasma pancreastatin is elevated in type 2 diabetes, insulin resistance, gestational diabetes and hypertension and tracks with catecholamines (PMID 12438174); the more-potent Gly297Ser variant raises cardiometabolic risk (PMID 34862200).
A target to block, via GRP78
Because high pancreastatin worsens metabolism, the therapeutic strategy is to block it: the inhibitor peptide PSTi8 improved insulin sensitivity in diabetic rodents through the GRP78–AMPK pathway (PMID 29880906). Pancreastatin also has immunomodulatory effects (PMID 36244579).
Published Research
These are studies of pancreastatin read from their PubMed abstracts on November 6, 2026. They include two human forearm-infusion studies that gave synthetic pancreastatin and measured its effect on glucose metabolism, reviews of its metabolic and immune actions, a human population study of its potency-raising Gly297Ser variant, and the discovery of an inhibitor peptide (PSTi8) in diabetic rodents. Pancreastatin has not been given to people as a treatment in any published study; the human work is short metabolic infusions and genetics, and the therapeutic direction is to block it.
Pancreastatin cuts human glucose uptake in vivo
Synthetic human pancreastatin (CgA273-301-amide, ~200 nM) infused into the brachial artery of healthy men reduced forearm glucose uptake by about 48-50% with no change in blood flow — a metabolic, not circulatory, effect. It did not antagonize insulin’s own glucose action, so it acts as an independent dysglycemic signal. Plasma pancreastatin was about 3.7-fold higher in diabetes, and the naturally occurring Gly297Ser variant was more potent at inhibiting glucose uptake.
Human forearm model of pancreastatin
In six healthy men, pancreastatin (CgA273-301-amide, ~200 nM) infused into the brachial artery over 15 minutes significantly reduced forearm glucose uptake (about 54%) without changing blood flow, and infusing it together with insulin did not diminish insulin’s own effect. The authors concluded pancreastatin may contribute to the dysglycemia of type 2 diabetes and essential hypertension, in which its plasma levels are elevated.
Metabolic effects and mechanism of pancreastatin
A review of pancreastatin as a chromogranin A-derived peptide with a general counter-regulatory effect to insulin: it induces glycogenolysis in liver and lipolysis in fat, and its effects are confirmed in humans. It signals through a seven-transmembrane Gq-PLCβ-calcium-PKC receptor system, runs high in insulin-resistant states alongside catecholamines, and potentiates their metabolic effects — a physiological and pathophysiological role in insulin resistance.
Immunomodulatory functions of pancreastatin
A review of pancreastatin’s inflammatory and immune actions. Beyond its metabolic role as a glycogenolytic peptide that inhibits glucose-induced insulin secretion, pancreastatin has emerging immunomodulatory properties — acting on macrophages and inflammation — and the authors frame it as a possible therapeutic target in inflammatory diseases, linking it to inflammatory bowel disease, diabetes and cancer.
The Gly297Ser variant as a cardiometabolic risk factor
In Indian populations (about 4,300 people), a functional pancreastatin variant (Gly297Ser) was associated with higher blood glucose, HbA1c, blood pressure and catecholamines, and a roughly 1.3-1.6-fold increased risk of type 2 diabetes, hypertension, coronary artery disease and metabolic syndrome. The variant peptide was more potent in cellular assays and bound GRP78 and the insulin receptor more tightly — a mechanistic basis for its gain of function.
A pancreastatin inhibitor (PSTi8) for insulin resistance
Because pancreastatin is elevated and harmful in type 2 diabetes, researchers developed an inhibitor peptide, PSTi8, to oppose it. PSTi8 rescued pancreastatin-induced insulin resistance in cells, improved insulin sensitivity and glucose handling in several diabetic mouse models (comparable to metformin), and acted through the GRP78–AMPK pathway — a preclinical proof of the ‘block pancreastatin’ strategy.
No Established Human Dose
Pancreastatin has been infused into people only briefly, as a research probe of metabolism (a local brachial-artery infusion of about 200 nM over roughly 15 minutes), never as a treatment — and because it is elevated and harmful in metabolic disease, the therapeutic aim is to block it, not to give it. No regulator has approved any dose, and those experimental infusion concentrations are not a therapeutic dose, so no amount is printed here.
What this rests on: PMID 15956083, PMID 12438174, PMID 29880906.
Educational information, not medical advice. The doses on this page come from approved labels, published studies and, where no study exists, amounts reported by users. None is a recommendation for you. An unapproved compound has no established safe or effective human dose, and products sold for “research use only” are not made or tested for people. Talk to a doctor before acting on anything on this site, including before you start, stop or change any medicine or dose. Full medical disclaimer.
What a Buyer Needs to Know
What is sold, how it is mixed, stored and taken, and what is known about its safety, quality and legal status. Each part names its source. Where we have none, it says unknown.
What is sold
Unknown: we hold no label and no published test that says what forms or vial sizes Pancreastatin is sold in. A vial's own label is a seller's claim, not a source.
Mixing a vial: a worked example
Unknown: no human dose of Pancreastatin has been established (see No Established Human Dose below), so there is no amount to work out. The reconstitution calculator does the arithmetic for any vial, water and dose.
Storage before and after mixing
Unknown: no label or published stability study on file says how to store Pancreastatin, before or after mixing. The mixing guide sets out the general rules, with their sources: keep a mixed vial in the fridge, and use it promptly, as the bacteriostatic water label says of any drug dissolved in it. The 28 days often quoted is the limit for an opened multiple-dose vial from a manufacturer, an outer limit set for sterility, not a time a mixed solution has been shown to keep. Nobody has published how long Pancreastatin stays intact once mixed.
How it is taken
Unknown: with no established human dose, there is no established way of taking Pancreastatin. What the human studies gave and how is set out under No Established Human Dose.
What to expect, and when
How long it stays in the body: a half-life of not established for humans as a drug; an endogenous circulating peptide. After about five half-lives almost none is left.
When effects appear: unknown; no source on this page gives a time to effect for Pancreastatin. Results reported in the studies are under Published Research.
Source: half-life: PMID 15956083.
Side effects, and when to stop or get help
From the Side Effects section: No therapeutic human safety data exist: the human studies infused it briefly to measure metabolism (PMIDs 15956083, 12438174); Its physiological effect is to raise blood glucose and blunt insulin — harmful if sustained, which is why therapy aims to block it (PMID 20184923); High pancreastatin is associated with type 2 diabetes, insulin resistance and hypertension, and a gain-of-function variant raises cardiometabolic risk (PMID 34862200); Material sold online as ‘pancreastatin’ is an unregulated research chemical of unverified content. Full list and cautions ↓
When to stop or get help: unknown; no label or trial on file sets rules for stopping Pancreastatin. Treat a severe or unexpected reaction as a reason to stop and see a doctor.
Source: the Side Effects section below (“Pancreastatin has been given to people only as a short experimental infusion, not as a drug, so there is no treatment safety profile; the points below reflect that research status”).
Interactions
Unknown: a PubMed search for human interaction studies of Pancreastatin (reviewed 2026-11-06) found none. Unknown is not the same as safe to combine.
Every peptide's record, with its source: the interaction matrix.
Checking what you bought
Unknown: no published independent test of Pancreastatin products is in our lab-results database yet, so how products sold under this name measure up is not known.
To read a certificate of analysis, paste it into the COA decoder. Trust & Verification explains what independent testing can and cannot show.
Legal status
US: Research Chemical (Not a drug: Drugs@FDA and the openFDA label endpoint hold no record, and FDA GSRS and ChEMBL hold no substance record for pancreastatin (searched November 6, 2026)). Sport: Not on the 2026 List.
Country by country ↓ · Regulatory tracker
Source: this entry's approval status and the WADA Prohibited List, as in Legal Status below.
Side Effects & Contraindications
Reported Side Effects
Pancreastatin has been given to people only as a short experimental infusion, not as a drug, so there is no treatment safety profile; the points below reflect that research status.
Contraindications & Cautions
Pancreastatin has no approved use and no label. These points reflect its endogenous, research status.
Legal Status
Pancreastatin is an endogenous human peptide studied as a research compound and drug target; it is not a drug and is not approved in any country.
Frequently Asked Questions
?What is pancreastatin?
An endogenous human peptide cut from chromogranin A (the sister fragment of catestatin). It is named for inhibiting insulin secretion, and it acts broadly as a counter-regulatory, ‘dysglycemic’ signal — the opposite of insulin’s metabolic effects.
?What does it do?
It blunts insulin release, drives the liver to release glucose and fat to break down, and reduces cellular glucose uptake (PMID 20184923). Infused into the arm of healthy men it cut forearm glucose uptake by about half (PMID 15956083). It is elevated in type 2 diabetes and hypertension.
?Could it be a treatment?
Not by giving it — the opposite. Pancreastatin raises blood sugar and is too high in metabolic disease, so the drug idea is to block it. An inhibitor peptide (PSTi8) improved insulin sensitivity in diabetic mice (PMID 29880906), but this is preclinical and no human trials are published.
?Is it approved or available to buy?
No. Pancreastatin is not a medicine, has no FDA application or label, and is approved nowhere. Material sold online as pancreastatin is an unregulated research chemical. Grey Peptides lists no sellers and recommends no source; this page records the published science.
References
- [clinical-trial] O'Connor DT, et al. "Pancreastatin: multiple actions on human intermediary metabolism in vivo, variation in disease, and naturally occurring functional genetic polymorphism." J Clin Endocrinol Metab, 2005;90(9):5414-25. PMID: 15956083.
- [clinical-trial] Cadman PE, et al. "Studies of the dysglycemic peptide, pancreastatin, using a human forearm model." Ann N Y Acad Sci, 2002;971:528-9. PMID: 12438174.
- [review] Sánchez-Margalet V, et al. "Metabolic effects and mechanism of action of the chromogranin A-derived peptide pancreastatin." Regul Pept, 2010;161(1-3):8-14. PMID: 20184923.
- [review] Ioannidis M, et al. "The immunomodulatory functions of chromogranin A-derived peptide pancreastatin." Peptides, 2022;158:170893. PMID: 36244579.
- [mechanism] Allu PKR, et al. "Functional Gly297Ser Variant of the Physiological Dysglycemic Peptide Pancreastatin Is a Novel Risk Factor for Cardiometabolic Disorders." Diabetes, 2022;71(3):538-553. PMID: 34862200.
- [animal] Hossain Z, et al. "Discovery of pancreastatin inhibitor PSTi8 for the treatment of insulin resistance and diabetes: studies in rodent models of diabetes mellitus." Sci Rep, 2018;8(1):8715. PMID: 29880906.
- [other] UniProt P10645 (CMGA_HUMAN, chromogranin A), read November 6, 2026: pancreastatin is a proteolytic fragment of chromogranin A (gene CHGA), the acidic protein of neuroendocrine secretory granules — the human peptide spanning CgA residues 250-301, whose amidated C-terminal form (CgA273-301-amide) carries the activity. https://www.uniprot.org/uniprotkb/P10645/entry
- [other] Pancreastatin was identified and named for its ability to inhibit insulin secretion from the pancreas; it is one of several bioactive peptides cut from chromogranin A (the sister fragment of catestatin), as set out in the metabolic and immunomodulatory reviews carded on this page (read November 6, 2026).
- [other] US FDA, Drugs@FDA and the drug label endpoint (openFDA), searched November 6, 2026: no application and no label record for pancreastatin. It is an endogenous human peptide, not a registered drug; FDA GSRS and ChEMBL hold no substance record for it, and the pancreastatin inhibitor PSTi8 in the research below is an experimental tool, not a medicine.
Sources & Citations
The six studies carded above were read from their PubMed records on November 6, 2026. Identity comes from UniProt (P10645, gene CHGA); pancreastatin’s origin as a chromogranin A fragment and its receptor signalling are from the reviews carded here; the human forearm-infusion data are from the two human studies; the absence of US approval and of a drug substance record from Drugs@FDA, openFDA, FDA GSRS and ChEMBL was checked the same day. Grey Peptides sells nothing and links to no vendor.
Medical Disclaimer: This content is for educational and informational purposes only. It is not medical advice, and nothing here is an instruction to obtain or use any compound. Talk to a licensed clinician about your own situation.