Neuromedin U
The gut and brain peptide that squeezes smooth muscle, cuts feeding in animals, and turns out to be a messenger between nerves and immune cells
Neuromedin U is a neuropeptide, 25 amino acids long in people, whose capped C-terminal end carries its activity. It was isolated from pig spinal cord in the 1980s for its ability to contract uterine muscle, and the same end of the molecule contracts human colon, gallbladder and vein. Given into the brains of rodents it sharply reduces food intake, which made it an obesity drug target, and it raises stress hormones and blood pressure. It also activates mast cells and type 2 immune cells, so it has become a peptide of interest in asthma and allergy. In people it has been measured, not given.
No established human dose Details ↓
Recommended Dosing
No established human dose
No dose exists for neuromedin U. In the human studies here it is measured in serum, airways and gut biopsies, or applied to donated human cells and tissue in the laboratory; every study that gave it to a living body used mice or rats, and one used a modified analogue rather than the peptide.
What is it?
Neuromedin U is one of the most strongly conserved neuropeptides across species, which usually means it matters. The 2004 review that remains its reference account describes it as isolated first from pig spinal cord, named for contracting the uterus, and present at the highest levels in the gut and pituitary. Its activity sits at the C-terminal end, and the amide cap on the last amino acid is essential. Two receptors were found in 2000: NMUR1 mostly in peripheral tissues and NMUR2 mostly in the brain.
The appetite story began the same year. Neuromedin U was found in the rat ventromedial hypothalamus, its levels dropped with fasting, and injecting it into the brain markedly cut food intake. Later work showed mice bred without the peptide overeat and become obese, while mice making extra stay lean. Part of the anorectic effect is mechanical: a long-acting lipid-modified version slowed stomach emptying in mice, which blunted food intake and improved blood sugar, though the effect faded after a week of twice-daily dosing and was weak in rats. Species differences run through this literature.
In human tissue the smooth-muscle actions are clear. Neuromedin U-25 contracted strips of human ascending colon, gallbladder and long saphenous vein in organ baths, and both receptors were present in those tissues. The peptide and its receptor also sit in human heart and coronary artery, where it constricted coronary and mammary artery and saphenous vein; its precursor's gene expression was higher in failing and ischaemic hearts. One natural variant of the peptide linked to childhood obesity had no contracting effect at all.
The newer thread is immunity. Neuromedin U degranulates mast cells in mice, and in human cells it drives type 2 immune responses: its receptor is carried by most human immune cells and more by type 2 cells, and the human peptide made those cells produce type 2 cytokines and migrate. In people with mild asthma, sputum immune cells carrying the receptor rose within seven hours of an inhaled allergen challenge, and dexamethasone blocked the peptide's effect in the dish. It also activates immune cells in the nasal lining in allergic rhinitis.
Human measurement studies are mixed. Serum neuromedin U was the same in newly diagnosed type 2 diabetes as in healthy people and did not follow insulin during a glucose load, and a duodenal biopsy study found no support for it as a human 'decretin' that suppresses insulin. Another comparison found no difference between people with diabetes and controls, but an inverse relationship with body mass index in the healthy group. In heart failure it was higher than in healthy donors and tracked right atrial pressure. Gene variants have been linked to obesity and body fat in European children and adults. Nothing read gave the peptide to a person; obesity work has moved to modified analogues, which are separate molecules.
Mechanism of Action
Neuromedin U acts through two receptors with different homes: NMUR2 in the brain, where it curbs feeding and raises stress hormones, and NMUR1 in peripheral tissues and immune cells, where it contracts smooth muscle and drives type 2 inflammation.
Appetite in the brain
Through NMUR2 in hypothalamic feeding nuclei it suppresses food intake in rodents; animals without the peptide overeat (PMIDs 10894543, 37517560).
Smooth muscle
Its amidated C-terminal end contracts human colon, gallbladder, saphenous vein and arteries (PMIDs 16782214, 18987052).
Type 2 immunity
Through NMUR1 on mast cells, type 2 lymphocytes and eosinophils it triggers degranulation, cytokine release and cell migration (PMIDs 16009716, 35810259).
Cut by thrombin
Thrombin cleaves within the active core in human serum, which limits how long the peptide survives in blood (PMID 26567043).
Published Research
These are studies of neuromedin U itself read from their PubMed abstracts: its receptors and structure, contraction studies on human tissue, immune studies in human cells and in people with asthma and rhinitis, measurements in human blood and gut, gene-variant studies of the peptide's own gene, animal feeding and inflammation experiments, and three reviews. Work on modified neuromedin U analogues and on neuromedin S is listed under References only.
Structure, receptors and roles
This review traces neuromedin U from its isolation in pig spinal cord through sequencing in several species, noting how little the sequence varies and that the C-terminal end with its amide cap is required for activity. Levels are highest in the gut and pituitary, and reported roles include smooth-muscle contraction, blood pressure and local blood flow, gut ion transport, stress responses, stomach acid, pain and feeding; its two receptors have different distributions.
Receptors found, and feeding suppressed
Two orphan receptors, renamed NMU1R and NMU2R, were shown to be neuromedin U's receptors, the first abundant in peripheral tissues and the second in specific brain regions. The peptide was found in the rat ventromedial hypothalamus, its level dropped after fasting, and injection into the brain ventricles markedly suppressed food intake.
Contracts human gut and vein
In organ baths, neuromedin U-25 produced sustained, concentration-dependent contraction of human ascending colon, gallbladder and long saphenous vein, with the colon the most sensitive. Both receptor transcripts were found in all tissues tested, with NMUR1 predominating in sigmoid colon and vein.
In the human heart and arteries
Radiolabelled neuromedin U-25 bound human left ventricle and coronary artery with high affinity, mostly through NMUR1, and the peptide was detected in plasma, heart, coronary artery, vein and epicardial fat. It constricted human coronary and mammary artery and saphenous vein, its precursor's gene was more active in dilated cardiomyopathy and ischaemic heart disease, and the obesity-linked Arg165Trp variant had no effect.
Thrombin cuts it in human serum
Short peptide agonists derived from neuromedin U, and the human peptide itself, were quickly cut in serum at a bond inside their shared C-terminal core. Thrombin inhibitors prevented it and the cutting did not happen in citrated plasma, where thrombin stays inactive, identifying thrombin as the enzyme responsible.
Drives human type 2 immune responses
Human neuromedin U-25 was detected in blood and, at higher concentrations, in the airways. Its receptor NMUR1 was carried by most human immune cells and more by type 2 cells including type 2 helper T cells, group-2 innate lymphoid cells and eosinophils. The peptide made those cells release type 2 cytokines and migrate, and it amplified their response to other stimuli.
Allergen challenge in mild asthma
Eight people with mild asthma underwent allergen and diluent inhalation challenges. Sputum group-2 innate lymphoid cells carrying the neuromedin U receptor rose significantly seven hours after allergen, and most of them made IL-5 or IL-13. Counts were higher in mild than in moderate to severe asthma, and the peptide's effect on cells in the dish was blocked by dexamethasone.
Immune cells in allergic rhinitis
In 15 patients with persistent allergic rhinitis and 8 healthy controls, circulating group-2 innate lymphoid cells were more numerous in the patients and tracked symptom severity. Neuromedin U made the patients' blood cells release more IL-5 and IL-13 than IL-33 did, and blocking the ERK pathway prevented the activation.
No link to insulin in type 2 diabetes
Serum neuromedin U was the same in 57 people with newly diagnosed type 2 diabetes and 50 matched healthy controls, and it neither changed nor tracked insulin during a glucose tolerance test in either group. The authors conclude it is not a human decretin hormone.
Duodenal cells in obesity
In duodenal biopsies from 34 people with obesity and 6 controls, cells making GLP-1, serotonin and chromogranin A were more numerous with obesity, but neuromedin U, found in the lamina propria, did not differ between groups. It showed a weak association with the insulin response, and again no support for a decretin role in people.
Blood levels and body mass index
Serum neuromedin U in 45 people with type 1 diabetes, 49 with type 2 diabetes and 40 healthy controls did not differ between the groups. In the healthy group alone it fell as body mass index rose, which the authors read as a possible role in metabolic regulation rather than as a diabetes marker.
Higher in heart failure
Serum neuromedin U measured by a selective assay was 8.5 ng/mL in 24 patients in stage II and III heart failure against 5.4 ng/mL in healthy donors, with no difference between the two stages. Of the measures taken, only mean right atrial pressure correlated with it.
Peptide gene variants and obesity
Sequencing the coding region of the NMU gene in 289 obese Czech children and 84 obese Danish adults found a rare Arg165Trp change that tracked childhood obesity through one family. In 5,851 Danish adults, carrying two copies of the Glu19 variant was about 2.5 times more common among overweight and obese people than lean people.
A protective haplotype in European children
In 4,528 children aged 2 to 10 from a European cohort, all three tagged variants of the NMU gene were associated with body mass index. One haplotype carrying the minor alleles, held by 22% of the children, went with lower body mass index, less fat mass and smaller skinfolds and a lower risk of overweight, repeated two years later; in girls the link was strongest between ages 7 and 9.
Appetite through slower stomach emptying
A lipid-modified neuromedin U analogue sharply slowed gastric emptying and food intake and improved glucose control in mice after the first dose, but all effects were gone after seven days of twice-daily dosing, and in rats the effect on food intake was small. The peptide's gene was found throughout the gut's nervous system and the brain receptor mainly in two hypothalamic nuclei.
Mast cells and inflammation
Mice lacking neuromedin U did not develop the mast cell degranulation, swelling and neutrophil influx that adjuvant injection normally causes, and injecting the peptide into the paw of normal mice produced those early inflammatory changes but not in mast-cell-deficient mice. Its receptor NMUR1 was abundant on mast cells, where the peptide mobilised calcium and triggered degranulation.
Human skin mast cells
This short report finds that neuromedin U directly degranulates mast cells from human skin, probably through the receptor MRGPRX2 rather than its own receptors. Only the summary line was available, so no numbers are stated here.
Immunity and inflammation reviewed
This review gathers the evidence that neuromedin U acts as a pro-inflammatory signal, activating immune cells and triggering cytokine release either through nerves or directly. It notes effects in worm infection, sepsis, autoimmune arthritis and allergy models and considers what they could mean for inflammatory disease in people.
Obesity and binge eating
This review describes neuromedin U as made in gut and brain, acting through NMUR1 in the periphery and NMUR2 in the brain, with the latter concentrated in the hypothalamic feeding centres. Direct administration and gene-deletion experiments show a strong appetite-suppressing effect, deleting the gene produces obesity, and the authors argue receptor-2 agonists are worth developing, including for binge eating.
No Established Human Dose
No dose exists for neuromedin U. In the human studies here it is measured in serum, airways and gut biopsies, or applied to donated human cells and tissue in the laboratory; every study that gave it to a living body used mice or rats, and one used a modified analogue rather than the peptide. No trial in people was found, and no product is approved.
What this rests on: PMID 31004673, PMID 38581170, PMID 35810259.
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 Neuromedin U 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 Neuromedin U 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 Neuromedin U, 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 Neuromedin U stays intact once mixed.
How it is taken
Unknown: with no established human dose, there is no established way of taking Neuromedin U. What the human studies gave and how is set out under No Established Human Dose.
What to expect, and when
Unknown: no cited half-life and no label or trial duration on this page says how long Neuromedin U lasts or how long it was given. Results reported in the studies are under Published Research.
Side effects, and when to stop or get help
From the Side Effects section: Contracts human gut, gallbladder, vein and artery tissue in the laboratory, which is why effects on blood pressure and gut motility are expected (PMIDs 16782214, 18987052); Triggers mast cell degranulation and swelling in mice and in human skin mast cells, a pro-allergic effect (PMIDs 16009716, 29987892); Drives the type 2 cytokine response linked to asthma and allergic inflammation in human cells and in people with mild asthma (PMIDs 35810259, 38598774); The appetite effect of an analogue wore off within a week in mice (PMID 25895852); No safety data in people. Full list and cautions ↓
When to stop or get help: unknown; no label or trial on file sets rules for stopping Neuromedin U. Treat a severe or unexpected reaction as a reason to stop and see a doctor.
Source: the Side Effects section below (“Neuromedin U has not been given to people, so these come from animal and cell studies”).
Interactions
Unknown: a PubMed search for human interaction studies of Neuromedin U (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 Neuromedin U 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 Neuromedin U's expected mass, 3,080.4 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: no approval and no human treatment trial 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
Neuromedin U has not been given to people, so these come from animal and cell studies.
Contraindications & Cautions
There is no product label. These cautions follow from the evidence.
Legal Status
Neuromedin U is a research peptide; it is not approved as a medicine anywhere in the sources read.
Frequently Asked Questions
?What is neuromedin U?
A neuropeptide 25 amino acids long in people, made mostly in the gut and pituitary, that acts on two receptors: NMUR1 in peripheral tissues and immune cells and NMUR2 in the brain. It was named for contracting uterine muscle.
?Does it reduce appetite?
Strongly, in rodents given it into the brain, and mice bred without it become obese. No study has tested the peptide for appetite in people, and the effect of one long-acting analogue faded within a week in mice.
?Why is it studied in asthma and allergy?
It activates mast cells and type 2 immune cells. In people with mild asthma, airway cells carrying its receptor rose within hours of an allergen challenge, and in human cells the peptide made type 2 lymphocytes release cytokines and migrate.
?Is blood neuromedin U a useful marker?
Not for diabetes: two studies found no difference from healthy controls and no link with insulin. In heart failure it was higher than in healthy donors and tracked right atrial pressure, which the authors call a lead rather than a validated marker.
?Has neuromedin U been given to people?
No. Human research measures it or tests it on donated cells and tissue; the drug work uses modified analogues, which are separate molecules.
?What is its half-life?
No human figure was found in the sources read. In human serum thrombin cuts it inside its active core, so it does not last long in blood.
References
- [other] UniProt P48645 (NMU_HUMAN), peptide residues 142-166 with C-terminal asparagine amide, neuromedin-U-25; read October 28, 2026. https://www.uniprot.org/uniprotkb/P48645/entry
- [review] Brighton PJ, et al. "Neuromedin U and its receptors: structure, function, and physiological roles." Pharmacol Rev, 2004;56(2):231-48. PMID: 15169928.
- [pubmed] Howard AD, et al. "Identification of receptors for neuromedin U and its role in feeding." Nature, 2000;406(6791):70-4. PMID: 10894543.
- [pubmed] Jones NA, et al. "Neuromedin U stimulates contraction of human long saphenous vein and gastrointestinal smooth muscle in vitro." Regul Pept, 2006;136(1-3):109-16. PMID: 16782214.
- [pubmed] Mitchell JD, et al. "Expression and vasoconstrictor function of anorexigenic peptides neuromedin U-25 and S in the human cardiovascular system." Cardiovasc Res, 2009;81(2):353-61. PMID: 18987052.
- [pubmed] Takayama K, et al. "Identification of a degrading enzyme in human serum that hydrolyzes a C-terminal core sequence of neuromedin U." Biopolymers, 2016;106(4):440-5. PMID: 26567043.
- [pubmed] Ye Y, et al. "Neuromedin U promotes human type 2 immune responses." Mucosal Immunol, 2022;15(5):990-999. PMID: 35810259.
- [clinical-trial] Ju X, et al. "Neuromedin-U Mediates Rapid Activation of Airway Group 2 Innate Lymphoid Cells in Mild Asthma." Am J Respir Crit Care Med, 2024;210(6):755-765. PMID: 38598774.
- [clinical-trial] Qi X, et al. "Neuromedin U Induces Activation of Peripheral Group 2 Innate Lymphoid Cells through the ERK Pathway in Allergic Rhinitis Patients." Int Arch Allergy Immunol, 2023;184(1):1-11. PMID: 36244335.
- [clinical-trial] Han M, et al. "Circulating neuromedin U levels are similar in subjects with NGT and newly diagnosed T2DM and do not correlate with insulin secretion." Diabetes Res Clin Pract, 2019;151:163-168. PMID: 31004673.
- [clinical-trial] Bur H, et al. "Duodenal neuroendocrine cells and neuromedin U in subjects with obesity: Relationship with type 2 diabetes and glucose homeostasis." Physiol Rep, 2025;13(15):e70489. PMID: 40790227.
- [clinical-trial] Çalışkan Y, et al. "Neuromedin U and BMI correlation in T1DM and T2DM vs healthy controls: A comparative study." Endocrinol Diabetes Nutr (Engl Ed), 2025;72(8):501631. PMID: 41067800.
- [clinical-trial] Healy V, et al. "The peptide neuromedin U (NMU) is elevated in NYHA II and III heart failure." ESC Heart Fail, 2024;11(4):2113-2119. PMID: 38581170.
- [clinical-trial] Hainerová I, et al. "Association between neuromedin U gene variants and overweight and obesity." J Clin Endocrinol Metab, 2006;91(12):5057-63. PMID: 16984985.
- [clinical-trial] Gianfagna F, et al. "The role of neuromedin U in adiposity regulation. Haplotype analysis in European children from the IDEFICS Cohort." PLoS One, 2017;12(2):e0172698. PMID: 28235053.
- [pubmed] Dalbøge LS, et al. "Neuromedin U inhibits food intake partly by inhibiting gastric emptying." Peptides, 2015;69:56-65. PMID: 25895852.
- [pubmed] Moriyama M, et al. "The neuropeptide neuromedin U promotes inflammation by direct activation of mast cells." J Exp Med, 2005;202(2):217-24. PMID: 16009716.
- [clinical-trial] Matsuo Y, et al. "Neuromedin U directly induces degranulation of skin mast cells, presumably via MRGPRX2." Allergy, 2018;73(11):2256-2260. PMID: 29987892.
- [review] Ye Y, et al. "Neuromedin U: potential roles in immunity and inflammation." Immunology, 2021;162(1):17-29. PMID: 32888314.
- [review] Botticelli L, et al. "The neuromedin U system: Pharmacological implications for the treatment of obesity and binge eating behavior." Pharmacol Res, 2023;195:106875. PMID: 37517560.
- [pubmed] De Prins A, et al. "Neuromedin U and Structural Analogs: An Overview of their Structure, Function and Selectivity." Curr Med Chem, 2020;27(39):6744-6768. PMID: 31526341.
Sources & Citations
Every study on this page was read from its PubMed record on October 29, 2026. Status comes from Drugs@FDA (openFDA), the EMA medicines list and ClinicalTrials.gov, searched October 28, 2026. 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.