Gastrin is a peptide hormone produced by G cells in the gastric antrum and proximal duodenum in response to food, gastric distension, and vagal stimulation. The primary physiological role of gastrin is to stimulate parietal cell HCl secretion via CCK2 receptors, acting through histamine intermediacy via ECL cells.

What is the recommended dose of Gastrin?

The typical research dose of Gastrin is Diagnostic (pentagastrin): 6 mcg/kg SC, administered Diagnostic single dose; endogenous meal-regulated via Endogenous (antral G cells); pentagastrin SC/IV for diagnostic. Use the ASCEND calculator for exact syringe draw volumes based on your vial size.

How is Gastrin administered?

Gastrin is typically administered Endogenous (antral G cells); pentagastrin SC/IV for diagnostic, Diagnostic single dose; endogenous meal-regulated, in research cycles of Diagnostic single use; endogenous continuous. Approximate half-life: 2-3 minutes (G-17); 7-10 minutes (G-34).

What is the research status of Gastrin?

Gastrin is at the Endogenous / Diagnostic / Research stage of research. FDA status: Pentagastrin previously approved for diagnostic use (discontinued); gastrin itself not approved as drug. WADA status: Not listed.

Gastrin: Mechanism, Dosing & Research Data

Storage Stability

Lyophilized

1-2 years (-20°C)

Reconstituted

~30 days (2-8°C)

Room temp

Avoid

Mechanism of Action

CCK2 Receptor Signaling

Gastrin binds CCK2 receptors (identical to brain CCK-B receptors) on enterochromaffin-like (ECL) cells, stimulating histamine release, which then acts on H2 receptors on parietal cells to drive HCl secretion. Direct CCK2 receptor activation on parietal cells contributes approximately 30% of acid stimulation. Gastrin also directly activates chief cells for pepsinogen secretion and is a major trophic factor for the gastric mucosa.

Gastrinoma and Hypergastrinemia

Zollinger-Ellison syndrome results from gastrin-secreting tumors (gastrinomas) causing massive acid hypersecretion and refractory peptic ulcers. Understanding gastrin physiology underpins proton pump inhibitor therapy (PPIs). By reducing luminal acid, PPIs remove the normal acid-inhibition feedback, causing compensatory hypergastrinemia with chronic PPI use. Elevated gastrin may drive gastric carcinoid formation over time.

Research Summary

Diagnostic Applications

Historical/Current

Pentagastrin stimulation test historically used to measure maximal acid output (gastric physiology, ulcer diagnosis). Pentagastrin was more recently used to stimulate calcitonin release for screening and follow-up of medullary thyroid carcinoma (MTC). The pentagastrin stimulation test for MTC has been largely replaced by calcium gluconate stimulation or ultrasensitive calcitonin assays.

Cancer and Anti-Gastrin Therapy

Active Research

CCK2 receptors are overexpressed in many gastrointestinal and pancreatic cancers. Anti-gastrin immunotherapy (Gastrimmune/polyclonal antibody approach) and gastrin receptor antagonists (netazepide) are in clinical trials for gastric cancer, Barrett esophagus, and type 1 gastric carcinoids. Gastrin-stimulated trophic effects may promote carcinogenesis in chronic hypergastrinemia.

Research Protocols

Goal	Dose	Frequency	Route
Gastric acid secretion testing (historical)	Pentagastrin 6 mcg/kg SC; measure gastric acid output at 15-60 min	Single diagnostic dose	Subcutaneous
MTC calcitonin stimulation (historical)	Pentagastrin 0.5 mcg/kg IV over 5 seconds; measure calcitonin at 0, 1, 2, 5 min	Single diagnostic dose	Intravenous

Pentagastrin has been discontinued in many countries. Calcium gluconate stimulation test has replaced pentagastrin for calcitonin testing in most centers.

Interactions

Feedback loop

Proton pump inhibitors

PPIs reduce gastric acid, removing negative feedback, causing compensatory hypergastrinemia; long-term concern for gastric ECL hyperplasia

Reduce gastrin response

Antacids/H2 blockers

Reduce gastrin stimulation by neutralizing luminal acid cues; therapeutic use in acid-related disease

Safety Profile

Pentagastrin SC/IV causes nausea, abdominal pain, urgency, dizziness, and flushing. Similar to CCK. Hypotension and tachycardia at higher doses. Contraindicated in active gastrointestinal bleeding and acute pancreatitis. Endogenous gastrin does not cause adverse effects at physiological levels; pathological hypergastrinemia (Zollinger-Ellison) causes symptoms via excessive acid production rather than direct hormone toxicity. Pentagastrin manufacture has been discontinued in major markets; alternatives are now standard of care for former indications.

References

[1]Gregory RA, Tracy HJ. The constitution and properties of two gastrins extracted from hog antral mucosa. Gut. 1964;5:103-117.
[2]Dockray GJ. Gastrin and gastric acid secretion. Physiol Rev. 2009;89(4):1459-1496.

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Categories: GI Hormone Gastric Acid Endogenous Diagnostic Digestive

Evidence	D · Preclinical
AA count	17 or 34 (main biologically active forms)
Mol. weight	2098 Da (G-17)
Half-life	2-3 minutes (G-17); 7-10 minutes (G-34)
Peak time	20-40 minutes post-meal
Route(s)	Endogenous (antral G cells); pentagastrin SC/IV for diagnostic
Typical dose	Diagnostic (pentagastrin): 6 mcg/kg SC
Frequency	Diagnostic single dose; endogenous meal-regulated
Cycle	Diagnostic single use; endogenous continuous
Storage	-20C lyophilized
WADA	Not listed Not on WADA Prohibited List; no anti-doping restrictions as of 2026
FDA	Pentagastrin previously approved for diagnostic use (discontinued); gastrin itself not approved as drug No approved indication in the US; research use only (RUO)
Research	Endogenous / Diagnostic / Research

Gastrin