Gastrin-releasing peptide
The nerve peptide that tells the stomach to release gastrin, infused into volunteers since the 1980s and now known for its role in itch
Gastrin-releasing peptide (GRP) is a 27-amino-acid peptide made by nerves in the gut, pancreas, brain and spinal cord. It is the mammalian counterpart of bombesin, a peptide first found in frog skin. Infused into people, it releases gastrin, cholecystokinin and other gut hormones, and in one trial it made healthy men eat fewer calories. In animals it carries itch signals in the spinal cord and helps reset the body clock. It has never become a medicine; drugs aimed at its receptor are separate molecules.
Used in human trials: 10, 40 or 160 pmol/kg/h, Continuous infusion, Intravenous (Study: food intake in healthy men) Details ↓
Recommended Dosing
Used in human trials
No manufacturer dose exists for this use: these are amounts given in published trials, not recommendations.
What is it?
Gastrin-releasing peptide was named for the first thing it was seen to do: make the stomach lining release gastrin, the hormone that drives acid secretion. It belongs to the same family as bombesin, a peptide from frog skin, and shares its last few amino acids, which is the part that binds the receptor. In people and other mammals it is made mainly by nerve cells, including nerves in the wall of the stomach and gut, the pancreas, the brain and the spinal cord. All forms come from one precursor of 125 amino acids, proGRP, which is cut into the 27-residue peptide, a shorter 10-residue form (GRP 18-27, also called neuromedin C) and other fragments.
Most of what is known about GRP in people comes from research infusions in the 1980s and 1990s. When it was dripped into a vein, plasma gastrin rose quickly, peaking about 15 minutes in, in one study of ulcer patients, along with cholecystokinin, pancreatic polypeptide and, in some studies, neurotensin; it also boosted insulin release when blood glucose was raised. One group found it as potent as bombesin on acid output, pancreatic enzymes and gallbladder contraction. Another found the two peptides behaved differently once atropine blocked the vagal nerve signal, so they are related but not interchangeable.
Surgeons used GRP as a probe. Infusions in patients who had lost the lower stomach or the duodenum showed where gastrin comes from: most from the antrum and the first part of the duodenum, a little from the rest of the duodenum, and essentially none after a Whipple operation. Cutting the vagus nerve to the acid-secreting part of the stomach made the gastrin response larger, pointing to a nerve brake on gastrin release. In people infected with Helicobacter pylori the gastrin response to GRP was exaggerated, which helped explain the high acid output linked to duodenal ulcers. A 1995 review described GRP as a useful test because it switches on many control systems at once.
Two studies tried GRP as something closer to a treatment. In healthy men, intravenous GRP for a meal-time period cut calorie intake and made them feel less hungry and fuller before the meal, without obvious side effects. In a small crossover trial in ten boys with autism, four days of GRP infusions lowered behaviour scores, but so did placebo, and the difference between them was not statistically significant. Neither led anywhere, and GRP has not been developed as a medicine.
Animal work has given GRP a second identity as an itch and stress signal. In mice, a small group of spinal cord nerve cells that make GRP relays itch but not pain, and itch only gets through when these cells fire in sustained bursts. In the brain's master clock, GRP mimics the resetting effect of light, and in rats an injection of GRP right after a fear memory was recalled weakened that memory. A study in rats showed GRP's effect on meal size depends on vagal and splanchnic nerves from the gut.
GRP's receptor is also overproduced by several cancers, including prostate, breast, lung and gut tumours, and GRP acts as a growth signal for small-cell lung cancer cells in culture. That is why imaging agents and radioactive drugs aimed at the receptor, such as RM2, are in clinical trials. Those are different molecules with their own entries; their results are not GRP's. The precursor fragment proGRP 31-98 is measured in blood as a marker of small-cell lung cancer, which is a separate use of the gene's products and is listed under References.
Mechanism of Action
Gastrin-releasing peptide is released from nerve endings and acts on the GRP receptor, a G protein-coupled receptor on gut, pancreatic, brain and spinal cord cells.
Gut hormone release
On the stomach and intestine it releases gastrin, cholecystokinin, pancreatic polypeptide and somatostatin, raising acid and pancreatic secretion and contracting the gallbladder.
Brain and spinal cord signalling
In animals it relays itch from the skin through spinal neurons, helps reset the brain's clock, and affects fear memory and meal size.
Growth signal in some cancers
Tumour cells that overproduce its receptor can use GRP as a growth signal, which is why receptor-targeted tracers are tested for cancer imaging.
Published Research
These are studies of gastrin-releasing peptide itself, read from their PubMed abstracts: research infusions in healthy volunteers and surgical patients, two small treatment trials, animal studies of itch, body clock, appetite and fear memory, and three reviews. Trials of receptor-targeted tracers and of a receptor blocker are listed under References, not carded.
First infusions in people: gut hormones rise
Intravenous GRP at two rates raised plasma gastrin, cholecystokinin-like immunoreactivity and neurotensin, and enhanced insulin secretion driven by glucose. The authors noted GRP sits in nerve fibres of the upper gut and pancreas and suggested it works as a regulatory nerve peptide.
Fewer calories eaten during GRP infusion
Healthy men received GRP at three infusion rates or saline. GRP reduced calorie intake significantly, while the 19% drop in the amount of food eaten did not reach significance; drinking was unchanged. Volunteers felt less hungry and fuller before the meal, and no clear side effects were seen.
As potent as bombesin in volunteers
Graded infusions in healthy volunteers raised gastric acid and pancreatic secretion, contracted the gallbladder and released gastrin, CCK and pancreatic polypeptide in a dose-dependent way. Molecule for molecule, human GRP matched synthetic bombesin on each of these measures.
GRP and bombesin differ under atropine
Hour-long infusions of GRP and bombesin released gastrin about equally, but GRP raised pancreatic polypeptide more and did not raise neurotensin. Atropine increased GRP's gastrin effect and blocked its pancreatic polypeptide release, so the two related peptides acted differently in people at the rate tested.
Where the released gastrin comes from
In healthy people the top infusion rate gave maximal gastrin release. After complete removal of the antrum and duodenal bulb the response was small, and after a Whipple pancreaticoduodenectomy it disappeared, showing GRP releases gastrin mainly from the antrum and duodenal bulb with a little from the rest of the duodenum.
The duodenum also answers GRP
In 28 patients after different stomach operations, antrectomy patients still released gastrin when given GRP, while Whipple patients did not. Excluding the duodenum from food passage did not change the response, but cutting its vagal nerve supply nearly abolished it.
GRP releases cholecystokinin from the small bowel
GRP infusion caused a prompt, substantial rise in cholecystokinin. The response survived removal of the duodenum, antrum or vagal supply, which places most CCK release below the duodenum, in the upper jejunum.
A nerve brake on GRP-driven gastrin
In patients with duodenal ulcer disease, gastrin rose sharply within 15 minutes of starting GRP. Cutting the vagal nerves to the acid-producing stomach, or giving an anticholinergic drug, made the GRP-driven gastrin response larger, pointing to a vagal reflex that normally holds it back.
Only a small somatostatin response
Stepwise GRP infusions caused a small but significant rise in somatostatin, most clearly when the stomach was perfused with acid. Vagotomy and cholinergic blockade did not change this response, unlike their effect on gastrin.
Helicobacter pylori and the gastrin response
In patients without ulcers, plasma gastrin rose more after GRP in those infected with H. pylori. In uninfected patients GRP lowered antral gastrin messenger RNA, but in infected patients it raised it, a failure of inhibition the authors linked to low somatostatin.
Autism trial: no significant benefit
In a randomised, double-blind crossover trial in ten boys aged 4 to 9 with autism, four days of GRP lowered behaviour checklist scores, but placebo did too; the difference was not significant (five responders on GRP, two on placebo). No adverse effects, vital-sign changes or laboratory abnormalities were linked to GRP.
Spinal GRP neurons carry itch, not pain
In transgenic mice, GRP-making nerve cells in the superficial dorsal horn received input from itch-sensing fibres. Destroying them reduced scratching to several itch triggers, and switching them on chemically caused itch-like behaviour, while pain responses stayed normal.
How GRP opens the spinal gate for itch
In mouse spinal cord slices and behaving mice, single signals from GRP neurons were too weak to excite the receptor-bearing neurons. Only sustained bursts of firing, which release GRP, drove them and produced itch-like behaviour; blocking the GRP receptor, but not glutamate receptors, prevented it.
GRP resets the body clock like light
Injected into the mouse suprachiasmatic nucleus late at night, GRP switched on the clock gene Per1 across the nucleus and raised firing of the activated neurons. Blocking Per1 or the CREB signalling pathway prevented GRP's shift of the clock rhythm.
Satiety from GRP needs gut nerves
In rats, GRP-29, the rat form of the peptide, reduced the size of the first meal and lengthened the gap before the next. Cutting the splanchnic nerves, the vagus, or the nerve layers of the duodenal wall weakened these effects.
GRP weakens a recalled fear memory
In rats given footshocks, GRP injected right after the fear memory was recalled reduced fear on re-testing a day and five days later; given 10 minutes or more after recall it did nothing. Flumazenil blocked the effect, pointing to a GABA-related mechanism.
GRP and cancer
The review sets out GRP as an autocrine growth factor for small-cell lung cancer, made from a 125-amino-acid prohormone and acting on receptors overproduced in lung, prostate, breast, stomach, pancreas and colon tumours, where it also affects blood-vessel growth and cell migration.
Different forms, different functions
All GRP forms come from proGRP 1-125. Besides the amidated peptides, non-amidated fragments are active, and GRP has been tied to circadian rhythm, spinal itch, inflammation, wound repair and psychiatric conditions. The fragment proGRP 31-98 is the most sensitive blood marker of small-cell lung cancer.
GRP as a test of stomach function
The review explains why GRP proved valuable for detecting disturbed acid control in duodenal ulcer disease and H. pylori infection: it switches on stimulatory and inhibitory controls at the same time, exposing a defect in any of them.
Dosing Data
Gastrin-releasing peptide is not approved anywhere as a medicine. These are research infusion amounts from the published human studies carded above, as their abstracts state them; none is a treatment dose.
Educational information, not medical advice. Each dose above is tagged with its source: an approved label, a published human study, animal data, or 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 Gastrin-releasing peptide is sold in. A vial's own label is a seller's claim, not a source.
Mixing a vial: a worked example
No worked example: none of the doses on this page is a fixed amount in mg or mcg injected under the skin or into a muscle (the routes given are: infusion, intravenous). There is no home-mixing step to show. The reconstitution calculator does the arithmetic for any vial.
Source: the route and amount of each dose row in Dosing Data below.
Storage before and after mixing
Unknown: no label or published stability study on file says how to store Gastrin-releasing peptide, 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 Gastrin-releasing peptide stays intact once mixed.
How it is taken
As it was given in human studies: Intravenous (Continuous infusion; Study: food intake in healthy men); Infusion (Once a day; Trial: boys with autism (crossover, 10 children)).
For injection technique, sites and needle disposal, see the mixing guide.
Source: Used in human trials: the route and frequency of each row in Dosing Data below.
What to expect, and when
How long it stays in the body: not established by a measurement cited on this entry.
How long the doses were given: Study: food intake in healthy men: Before and during a test meal; Study: gut hormone release in volunteers: Single study session; Study: graded doses compared with bombesin: Single study session.
When effects appear: unknown; no source on this page gives a time to effect for Gastrin-releasing peptide. Results reported in the studies are under Published Research.
Source: Used in human trials, the duration of each row in Dosing Data below.
Side effects, and when to stop or get help
From the Side Effects section: No clear side effects during infusions in healthy men; they felt less hungry and fuller (PMID 8174879); No adverse effects, vital-sign changes or laboratory abnormalities over four days in ten boys (PMID 28452904); Expected effects of the hormones it releases: more stomach acid, pancreatic secretion and gallbladder contraction (PMID 1811276). Full list and cautions ↓
When to stop or get help: unknown; no label or trial on file sets rules for stopping Gastrin-releasing peptide. Treat a severe or unexpected reaction as a reason to stop and see a doctor.
Source: the Side Effects section below (“From the short human studies above, which reported little on safety”).
Interactions
Unknown: a PubMed search for human interaction studies of Gastrin-releasing peptide (reviewed 2026-10-28) 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 Gastrin-releasing peptide 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; it checks the measured mass against Gastrin-releasing peptide's expected mass, 2,859.4 Da, from this entry's molecular data. Trust & Verification explains what independent testing can and cannot show.
Legal status
US: Research Chemical (Not a medicine anywhere in the sources read). Sport: Prohibited (S0 catch-all).
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
From the short human studies above, which reported little on safety.
Contraindications & Cautions
No product label exists. These cautions follow from the evidence.
Legal Status
Gastrin-releasing peptide is a research peptide; it is not approved as a medicine anywhere in the sources read.
Frequently Asked Questions
?What is gastrin-releasing peptide?
A 27-amino-acid peptide made by nerve cells in the gut, pancreas, brain and spinal cord. It is the mammalian counterpart of bombesin and makes the stomach release gastrin.
?What does GRP do in people?
In research infusions it raised gastrin, cholecystokinin and pancreatic polypeptide, increased stomach acid and pancreatic secretion, contracted the gallbladder and, in one trial, reduced the calories healthy men ate.
?Is gastrin-releasing peptide used as a treatment?
No. It has been given to people only in research studies. A small trial in boys with autism found no significant benefit over placebo.
?What is the link between GRP and itch?
In mice, spinal cord nerve cells that make GRP relay itch signals but not pain. This is animal research; no GRP-based itch treatment exists.
?Is GRP the same as the GRPR cancer scans?
No. Cancer imaging agents such as RM2 are separate molecules that bind the GRP receptor, which some tumours overproduce. Their results belong to those drugs, not to GRP.
?What is proGRP?
The precursor GRP is cut from. A fragment of it, proGRP 31-98, is measured in blood as a marker of small-cell lung cancer; that is a test, not a use of GRP itself.
References
- [clinical-trial] Wood SM, et al. "The effect of the mammalian neuropeptide, gastrin-releasing peptide (GRP), on gastrointestinal and pancreatic hormone secretion in man." Clin Sci (Lond), 1983;65(4):365-71. PMID: 6349902.
- [clinical-trial] Gutzwiller JP, et al. "Effect of intravenous human gastrin-releasing peptide on food intake in humans." Gastroenterology, 1994;106(5):1168-73. PMID: 8174879.
- [clinical-trial] Hildebrand P, et al. "Human gastrin-releasing peptide: biological potency in humans." Regul Pept, 1991;36(3):423-33. PMID: 1811276.
- [clinical-trial] Fletcher DR, et al. "The effect of atropine on bombesin and gastrin releasing peptide stimulated gastrin, pancreatic polypeptide and neurotensin release in man." Regul Pept, 1983;7(1):31-40. PMID: 6647889.
- [clinical-trial] Lundell L, et al. "Origin of gastrin liberated by gastrin releasing peptide in man." Gut, 1987;28(9):1128-33. PMID: 3678972.
- [clinical-trial] Sjövall M, et al. "Studies of the release of gastrin from the human duodenum induced by gastrin-releasing peptide." Scand J Gastroenterol, 1989;24(4):445-53. PMID: 2781240.
- [clinical-trial] Lundell L, et al. "Factors influencing the release of cholecystokinin induced by gastrin-releasing peptide in man." Scand J Gastroenterol, 1991;26(5):544-50. PMID: 1871546.
- [clinical-trial] Sjövall M, et al. "Effect of parietal cell vagotomy and cholinergic blockade on gastrin release in man induced by gastrin-releasing peptide." Digestion, 1990;46(2):114-20. PMID: 2253822.
- [clinical-trial] Sjövall M, et al. "Somatostatin release induced by gastrin-releasing peptide in man. Effect of proximal gastric vagotomy and cholinergic blockade." Regul Pept, 1990;29(2-3):133-41. PMID: 1977187.
- [clinical-trial] Gibbons AH, et al. "The effect of gastrin-releasing peptide on gastrin and somatostatin messenger RNAs in humans infected with Helicobacter pylori." Gastroenterology, 1997;112(6):1940-7. PMID: 9178686.
- [clinical-trial] Marchezan J, et al. "A Placebo-Controlled Crossover Trial of Gastrin-Releasing Peptide in Childhood Autism." Clin Neuropharmacol, 2017;40(3):108-112. PMID: 28452904.
- [pubmed] Albisetti GW, et al. "Dorsal Horn Gastrin-Releasing Peptide Expressing Neurons Transmit Spinal Itch But Not Pain Signals." J Neurosci, 2019;39(12):2238-2250. PMID: 30655357.
- [pubmed] Pagani M, et al. "How Gastrin-Releasing Peptide Opens the Spinal Gate for Itch." Neuron, 2019;103(1):102-117.e5. PMID: 31103358.
- [pubmed] Gamble KL, et al. "Gastrin-releasing peptide mediates light-like resetting of the suprachiasmatic nucleus circadian pacemaker through cAMP response element-binding protein and Per1 activation." J Neurosci, 2007;27(44):12078-87. PMID: 17978049.
- [pubmed] Wright SA, et al. "Gastrin releasing peptide-29 requires vagal and splanchnic neurons to evoke satiation and satiety." Peptides, 2012;33(1):125-31. PMID: 22210008.
- [pubmed] Murkar A, et al. "Gastrin-releasing peptide attenuates fear memory reconsolidation." Behav Brain Res, 2018;347:255-262. PMID: 29191578.
- [review] Patel O, et al. "Gastrin-releasing peptide and cancer." Biochim Biophys Acta, 2006;1766(1):23-41. PMID: 16490321.
- [review] Ischia J, et al. "Gastrin-releasing peptide: different forms, different functions." Biofactors, 2009;35(1):69-75. PMID: 19319848.
- [review] McColl KE, et al. "Review article: gastrin releasing peptide and its value in assessing gastric secretory function." Aliment Pharmacol Ther, 1995;9(4):341-7. PMID: 8527610.
- [clinical-trial] Hildebrand P, et al. "Regulation of gastric function by endogenous gastrin releasing peptide in humans: studies with a specific gastrin releasing peptide receptor antagonist." Gut, 2001;49(1):23-8. PMID: 11413106.
- [review] Tang JH, et al. "Diagnostic value of tumor marker pro-gastrin-releasing peptide in patients with small cell lung cancer: a systematic review." Chin Med J (Engl), 2011;124(10):1563-8. PMID: 21740817.
- [other] UniProt P07492: GRP_HUMAN, gastrin-releasing peptide; peptide 24-50 is gastrin-releasing peptide ending in a methionine amide, and peptide 41-50 is neuromedin-C. Read October 28, 2026. https://www.uniprot.org/uniprotkb/P07492/entry
Sources & Citations
Every study on this page was read from its PubMed record on October 28, 2026. Regulatory status comes from Drugs@FDA (openFDA) and the EMA medicines list, and trial status from ClinicalTrials.gov, read the same day. Grey Peptides sells nothing and links to no vendor.
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