Neuromedin S
A short peptide named for the brain's master clock, related to neuromedin U, studied for appetite, hormones and daily rhythms in animals and only measured in people
Neuromedin S is a 33-residue human neuropeptide, named for the suprachiasmatic nucleus, the brain's master clock, where its gene is most active. It shares its active tail and its two receptors with neuromedin U. Injected into the brains of rats and mice it reduces eating, releases vasopressin and oxytocin, shifts reproductive and stress hormones and speeds the heart. In people it has only been found in heart, placenta and brain tissue, and it has never been given to anyone.
No established human dose Details ↓
Recommended Dosing
No established human dose
Neuromedin S has not been given to people in any study on this page. The human evidence is measurement in tissue only: the peptide identified in heart muscle and tested on donated vein rings, found in term placenta and in decidua from preterm births, and its gene mapped in the human brain's clock.
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What is it?
Neuromedin S is a short neuropeptide that was found in 2005, in rat brain, while researchers were looking for natural partners of two receptors already known to respond to neuromedin U. It was named for the suprachiasmatic nucleus, the small cluster of hypothalamic neurons that acts as the body's master clock, because that is where its gene is most active inside the brain. The rat peptide has 36 amino acids. The human form, cut from a 153-residue precursor, has 33, ends in an amidated asparagine and shares its last seven residues with neuromedin U.
That shared tail is what both peptides need to switch on their receptors, NMUR1 and NMUR2. NMUR1 sits mostly in peripheral tissues and NMUR2 mostly in the brain, and injected into the brain neuromedin S works almost entirely through NMUR2. Neuromedin S is often the stronger of the two in rodent tests: it cut rats' eating for longer than the same amount of neuromedin U, and neuromedin U needed about ten times as much to match its effect on urine output. Neuromedin U has its own entry; this page covers neuromedin S only.
In the brain its gene is largely confined to the core of the suprachiasmatic nucleus, though rats carry the peptide itself down into the midbrain and brainstem. Outside the brain the gene is active in the testis and spleen, and the peptide has been found in human heart muscle, in human placenta at term and in the testis of goats. In mice, repeated morphine switches the gene on in a group of dopamine neurons in the ventral tegmental area.
Almost everything known about what neuromedin S does comes from injecting it into the brains of rats, mice, pigs and cattle. Given that way it reduces eating and slows the stomach, releases vasopressin and reduces urine, releases oxytocin and helps milk let-down, shifts luteinising hormone up or down depending on the reproductive state, raises stress hormones and anxious behaviour, speeds the heart through the sympathetic nerves and warms the body. In cell cultures from goats it increases testosterone and oestrogen production. Each of these is a single-species finding, and none has been tested in people.
Its link to the body clock turned out to be subtler than its name suggests. The suprachiasmatic neurons that make neuromedin S are essential pacemakers in mice: change their molecular clock and the whole animal's rhythm changes. Yet mice lacking both the neuromedin S and neuromedin U genes keep their daily rhythms, so what the clock needs is these neurons and their signalling, not the peptide itself. Researchers now use the gene mainly as a label for that group of cells. In 2026 a human brain atlas linked a vasopressin and neuromedin S neuron type in the human clock to being a morning person.
Human evidence is thin and consists only of measurement. Neuromedin S has been identified in human heart tissue, where it constricted vein rings less than neuromedin U did, and in human placenta, where infection raised it and women who delivered early with signs of infection had more of it in the decidua. It has never been given to a person, it is not a medicine anywhere, and ClinicalTrials.gov lists no study of it. The abbreviation NMS causes confusion in searches: in medicine it usually means neuroleptic malignant syndrome, a reaction to antipsychotic drugs that has nothing to do with this peptide.
Mechanism of Action
Neuromedin S acts on the same two receptors as neuromedin U, and in the brain almost entirely on NMUR2. Through it, rodent studies show effects on eating, the stomach, water balance, reproductive and stress hormones, heart rate and body heat; none has been tested in people.
NMUR2 receptor
Its amidated tail, shared with neuromedin U, switches on NMUR2 in the brain and NMUR1 elsewhere; mice without NMUR2 do not eat less after a brain dose.
Vasopressin and oxytocin
It releases vasopressin, reducing urine output, and oxytocin, supporting milk let-down in nursing rats.
Reproductive and stress hormones
It raises or lowers LH depending on the reproductive state, raises ACTH and corticosterone through CRH1 receptors, and increases steroid output in goat testis and ovary cells.
Body clock and arousal
The suprachiasmatic neurons that make it are essential pacemakers in mice, though the peptide itself is not needed for rhythms; brain doses speed the heart through the sympathetic nerves and warm the body.
Published Research
These are studies of neuromedin S and its gene, read from their PubMed abstracts: the discovery paper, rat, mouse, pig and cattle studies that injected it into the brain, gene-knockout mice, goat cell cultures, receptor and laboratory-method papers, three studies that found it in human heart, placenta or brain tissue, and two reviews. No study gave neuromedin S to a person.
Named for the body clock
Searching rat brain for the natural partner of a receptor already known to respond to neuromedin U, the team isolated a new 36-residue peptide and named it neuromedin S after the suprachiasmatic nucleus, the clock centre where its gene was active. Its tail end matched neuromedin U's. Within the brain the gene was confined to the core of that nucleus and peaked at one point of the day under light and dark, though not in constant darkness, and injecting the peptide into rat brain ventricles excited clock neurons and moved the timing of the animals' daily running.
Rats eat less, for longer than with neuromedin U
Injected into the brain ventricles of rats, neuromedin S cut what they ate over the twelve dark hours, and the drop was deeper and lasted longer than with the same amount of neuromedin U. It also blunted the extra eating normally set off by neuropeptide Y, ghrelin and agouti-related protein. The peptide raised POMC gene activity in the arcuate nucleus and CRH gene activity in the paraventricular nucleus, and blocking either the melanocortin or the CRH receptor weakened its effect on 24-hour intake.
Luteinising hormone, depending on the cycle
In female rats the hypothalamic genes for neuromedin S and its brain receptor, NMU2R, rose and fell with age and across the oestrous cycle, were highest at proestrus, dropped after the ovaries were removed and climbed again with progesterone. Brain injections gave small LH rises in young and dioestrous females and much larger bursts at oestrus or after a short fast, but lowered the already high LH of ovariectomised rats, so the response turned on the animal's reproductive state.
Which rat glands make it
Measuring gene activity across rat tissues, the authors found neuromedin S ahead of neuromedin U in the hypothalamus and testis, while neuromedin U led in the anterior pituitary and thyroid and was the only one found in pancreatic islets. The brain receptor NMUR2 far outweighed NMUR1 in the hypothalamus, whereas the ovary, testis and other glands leaned towards NMUR1, so the two peptides may serve different glands.
Less urine, through vasopressin
A brain injection of neuromedin S raised rats' blood vasopressin in step with the dose and was followed by less urine overnight. The neurons it activated in the paraventricular and supraoptic nuclei were vasopressin cells. Neuromedin U, which uses the same receptor, needed about ten times the amount to reduce urine output by the same margin.
Stress hormones, grooming and anxious behaviour
Given into the brain ventricles of rats, neuromedin S raised ACTH and corticosterone in a dose-related way, and the CRH1 receptor blocker antalarmin prevented the rise. The rats groomed more and kept out of the open arms of an elevated maze, a sign of anxiety; haloperidol and antalarmin abolished the grooming. In slices of amygdala the peptide increased dopamine release, which the authors link to the behaviour.
Milk let-down through oxytocin
Brain injections of neuromedin S switched on oxytocin neurons in the paraventricular and supraoptic nuclei of rats, raised blood oxytocin with dose and increased milk output in nursing mothers. When the researchers instead injected an antiserum that soaks up the rat's own neuromedin S, suckling pups triggered a much weaker milk-ejection response, which suggests the natural peptide helps run that reflex.
Found in human heart tissue
In samples of human heart and blood vessel, chromatography picked out neuromedin S, as well as neuromedin U-25, in the left ventricle. The study centred on neuromedin U, which tightened isolated human arteries and veins strongly; neuromedin S also constricted rings of human saphenous vein, but its maximum effect there was clearly smaller. The work used donated tissue in organ baths, and no person was given either peptide.
The brain receptor carries the effect
Mice bred without NMUR2 resisted diet-induced obesity a little, partly because they ate less. A single brain dose of neuromedin S reduced food intake in normal mice but not in the knockouts, and repeated brain dosing lowered body weight and kept intake down in normal mice while the knockouts were largely spared. The authors conclude that NMUR2 carries most of the peptide's weight-lowering action in the brain.
Tested in cattle
Rat neuromedin S injected into the brain ventricles of steers raised blood cortisol in step with the dose, as neuromedin U did. Only neuromedin U clearly raised rectal temperature, and at the highest dose the steers tended to spend less time lying down and to shake their heads more, which the authors read as behavioural arousal.
Slower stomach emptying in mice
A brain injection of neuromedin S reduced eating in both fasted and freely fed mice and slowed how fast the stomach emptied. Pressure recordings in awake, fasted mice showed that it broke up the normal contractions of the antrum and duodenum, the first evidence that the peptide reaches gut movement as well as appetite.
Part of leptin's effect on appetite
Both neuromedins reduced rats' food intake early in the night, more with higher doses. When rats first received an antibody against neuromedin S into the brain, leptin, whether injected into the brain or the abdomen, no longer curbed their eating; an antibody against neuromedin U left leptin's effect intact. In arcuate tissue neuromedin S released alpha-MSH more strongly than neuromedin U did.
LH falls in ovariectomised pigs
In ovariectomised pigs an injection of neuromedin S lowered serum LH from about 12 to 60 minutes later, with the low point at 24 minutes, and reduced GnRH and LH gene activity. Pretreatment with SHU9119, a drug that blocks melanocortin receptors, removed the fall, so the authors propose that MSH neurons in the hypothalamus relay the effect.
Heart rate through the sympathetic nerves
Brain injections of neuromedin S raised the heart rate of mice in proportion to the dose, and the beta-blocker timolol prevented the rise. Mice born without the gene had slower hearts with longer PR and QRS intervals on the ECG and slowed less with timolol. Neither the peptide nor its receptor was made in the heart, so the authors place the effect in the brain's drive to the sympathetic nerves.
More peptide in the brainstem than the gene suggested
With a new radioimmunoassay, whole rat brain held about 68 fmol of neuromedin S per gram, while spleen and testis, where the gene is active, held almost none. The peptide was plentiful in the hypothalamus, midbrain, pons and medulla, but its gene was active mainly in the hypothalamus, which suggests hypothalamic neurons carry it down into the brainstem, where the NMUR2 receptor is also common.
The clock cells that carry it
In mice, the subset of suprachiasmatic neurons that make neuromedin S proved necessary for normal daily rhythms: slowing the molecular clock in just these cells slowed the animal's whole rhythm, and removing their clock left behaviour without a coherent daily pattern. Mice lacking both the neuromedin S and neuromedin U genes kept their rhythms, though, so the clock depends on these neurons' synaptic signalling rather than on the peptide itself.
Body heat and energy use
Brain injections of neuromedin S warmed the skin of rats' backs by day and by night, an effect blocked by a beta-3 adrenergic blocker and by indomethacin; it also raised prostaglandin-making enzymes in the hypothalamus and the heat-producing uncoupling protein in brown fat. Mice lacking neuromedin S, alone or with neuromedin U, ran cooler during their active phase and in the cold than mice lacking only neuromedin U, and all the knockouts used less energy at night.
Placenta, infection and preterm labour
Neuromedin S and neuromedin U contracted mouse uterus in the dish and brought on labour in pregnant mice through NMU-R2. In human placenta at term the peptide sat mainly in cytotrophoblast cells, bacterial endotoxin raised it sharply in cultured human cytotrophoblasts, and decidua from women with signs of infection who delivered early held more of it than decidua from women without infection. Knocking the receptor down in mice prevented endotoxin-triggered preterm birth.
Same receptor, different after-effects
In cell lines made to carry human NMU2, neuromedin S and neuromedin U gave the same immediate calcium signal, and each was pulled into the cell together with the receptor. After that they diverged: the receptor recovered more slowly after neuromedin S, and its ERK and p38 signalling ran longer, differences the authors tie to how endothelin-converting enzyme-1 inside the cell handles each peptide.
Goat ovarian cells make more oestrogen
Added to cultured goat granulosa cells, neuromedin S raised oestrogen output and the steroid-making enzymes STAR, CYP11A1, 3BHSD and CYP19A1, and it supported mitochondrial fusion, membrane potential and ATP production. Silencing NMUR2 cancelled these effects; the authors trace them through the YAP1 and PPARGC1A pathway.
Goat testis cells make more testosterone
The peptide and its receptors were found mainly in the Leydig cells of goat testis, most strongly at three months of age. In culture, neuromedin S increased testosterone release, steroid-making enzymes and cell division, cut reactive oxygen species and supported mitochondrial function, and silencing NMUR2 suppressed all of this.
A labelled form for receptor work
Chemists attached tritium to synthetic human neuromedin S, a 33-residue peptide, through a propionyl tag on its first amino acid. Tagged versions bound NMUR2 and switched it on in cell assays as well as the untagged peptide did, and modelling put the tag positions outside the receptor's binding pocket, giving researchers a radioactive tracer for binding and metabolism studies.
Hard to measure because it sticks
Neuromedin S clings to the surfaces it touches during sample handling, so much of it can be lost before analysis. Adding a trace of plasma as a competitor stopped those losses; the authors then tuned the columns and column temperature, and adjusting two mass-spectrometer voltages alone raised its signal about sevenfold, bringing detection into the low picomolar range.
Switched on by morphine
Profiling dopamine neurons of the mouse ventral tegmental area after repeated morphine, the authors found the neuromedin S gene sharply increased. Activating the neurons that make it boosted morphine-driven movement, and silencing them reduced both that and the mice's preference for the place where they got morphine; cocaine neither raised the gene nor depended on these neurons.
Morning types in a human brain atlas
A spatial and single-cell gene atlas of the adult human suprachiasmatic nucleus sorted its neurons into seven types and found that the human clock's neuropeptide network has been reorganised compared with the mouse's. Combining the atlas with genome-wide association data pointed to a vasopressin and neuromedin S neuron type as a likely cellular basis for being a morning person. This measured gene activity in brain tissue; nobody was given the peptide.
From the clock to ovulation in mice
In female mice some neuromedin S neurons of the suprachiasmatic nucleus sent fibres to the kisspeptin neurons that help start the ovulation hormone surge. Stimulating those fibres released GABA onto about three quarters of the kisspeptin cells and silenced their firing, whereas neuromedin S added to the tissue changed calcium in only some cells and left firing unchanged.
Kidney injury in mice without both genes
In mice fed adenine to produce chronic kidney disease, animals lacking both neuromedin U and neuromedin S had lower serum creatinine and less early inflammation and scarring at four weeks than normal mice, but the difference had gone by six weeks. Because both genes were deleted, the study cannot say which peptide was responsible.
The discoverers' summary
Written by the group that found the peptide, this review sets out its structure, its two receptors, where it is made and what the first rat studies suggested it does, from the body clock to feeding.
Neuromedins U and S, an update
This overview of the two neuromedins notes that neuromedin S is made in a narrower range of tissues, mostly in the brain, and that each precursor also yields a second peptide (NURP and NSRP) that acts without NMUR1 or NMUR2, hinting at a receptor not yet found. The authors argue that selective blockers of each receptor are needed before either system can be developed into treatments.
No Established Human Dose
Neuromedin S has not been given to people in any study on this page. The human evidence is measurement in tissue only: the peptide identified in heart muscle and tested on donated vein rings, found in term placenta and in decidua from preterm births, and its gene mapped in the human brain's clock. There is no neuromedin S medicine and no amount for a person to state.
What this rests on: PMID 18987052, PMID 27512149, PMID 41720090.
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 S 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 S 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 S, 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 S stays intact once mixed.
How it is taken
Unknown: with no established human dose, there is no established way of taking Neuromedin S. 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 S 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: Reduced eating and slower stomach emptying in rats and mice (PMIDs 15976061, 20352600); Raised stress hormones, more grooming and anxiety-like behaviour in rats (PMID 17900576); Faster heart rate in mice through the sympathetic nerves (PMID 21356261); Raised vasopressin with less urine in rats (PMID 17645872); No study read gave neuromedin S to a person, so its human safety is unknown. Full list and cautions ↓
When to stop or get help: unknown; no label or trial on file sets rules for stopping Neuromedin S. Treat a severe or unexpected reaction as a reason to stop and see a doctor.
Source: the Side Effects section below (“Neuromedin S has never been given to people, so it has no recorded human side effects”).
Interactions
Unknown: a PubMed search for human interaction studies of Neuromedin S (reviewed 2026-11-03) 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 S 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 S's expected mass, 3,791.3 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: an endogenous neuropeptide studied in animals and found in human tissue). 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 S has never been given to people, so it has no recorded human side effects. These are the effects seen in animals given it into the brain.
Contraindications & Cautions
There is no neuromedin S medicine. These cautions concern the peptide as a research chemical and as a laboratory measurement.
Legal Status
Neuromedin S is an endogenous neuropeptide studied in animals; it is not approved as a medicine anywhere in the sources read.
Frequently Asked Questions
?What is neuromedin S?
A short neuropeptide, 33 amino acids long in humans, named for the suprachiasmatic nucleus, the brain's master clock, where its gene is most active. It is closely related to neuromedin U and uses the same two receptors.
?Is neuromedin S the same as neuromedin U?
No. They are separate genes and peptides that share the same last seven amino acids and the same receptors. Neuromedin U is made widely in the gut and pituitary, while neuromedin S is made mainly in the brain, and in several rat tests neuromedin S had the stronger effect.
?What does neuromedin S do?
In rats and mice given it into the brain, it reduces eating, releases vasopressin and oxytocin, changes reproductive and stress hormones, speeds the heart and raises body temperature. The neurons that make it are key cells of the body clock in mice.
?Does neuromedin S control the body clock?
The neurons that make it do, in mice. The peptide itself seems not to be needed: mice lacking both the neuromedin S and neuromedin U genes keep normal daily rhythms. A 2026 human brain atlas linked a vasopressin and neuromedin S neuron type to being a morning person.
?Does neuromedin S cause weight loss?
Brain injections reduced eating, and repeated brain dosing lowered weight, in rats and mice. It has never been tested in people, and an effect that depends on injection into the brain says little about any other route.
?Is NMS the same as neuroleptic malignant syndrome?
No. In medical writing NMS usually means neuroleptic malignant syndrome, a rare and serious reaction to antipsychotic drugs. Neuromedin S shares the abbreviation and nothing else.
?Can you take neuromedin S?
No. It has never been given to people in the studies read, there is no approved product, and no human dose exists.
References
- [other] UniProt Q5H8A3 (NMS_HUMAN), peptide residues 109-141 with C-terminal asparagine amide, neuromedin-S, from a 153-residue precursor; read November 3, 2026. Formula and mass computed from the 33-residue amidated sequence. https://www.uniprot.org/uniprotkb/Q5H8A3/entry
- [pubmed] Mori K, et al. "Identification of neuromedin S and its possible role in the mammalian circadian oscillator system." EMBO J, 2005;24(2):325-35. PMID: 15635449.
- [pubmed] Ida T, et al. "Neuromedin s is a novel anorexigenic hormone." Endocrinology, 2005;146(10):4217-23. PMID: 15976061.
- [pubmed] Vigo E, et al. "Neuromedin s as novel putative regulator of luteinizing hormone secretion." Endocrinology, 2007;148(2):813-23. PMID: 17110433.
- [pubmed] Rucinski M, et al. "Expression of neuromedins S and U and their receptors in the hypothalamus and endocrine glands of the rat." Int J Mol Med, 2007;20(2):255-9. PMID: 17611645.
- [pubmed] Sakamoto T, et al. "Neuromedin S exerts an antidiuretic action in rats." Biochem Biophys Res Commun, 2007;361(2):457-61. PMID: 17645872.
- [pubmed] Jászberényi M, et al. "Endocrine and behavioral effects of neuromedin S." Horm Behav, 2007;52(5):631-9. PMID: 17900576.
- [pubmed] Sakamoto T, et al. "Involvement of neuromedin S in the oxytocin release response to suckling stimulus." Biochem Biophys Res Commun, 2008;375(1):49-53. PMID: 18675786.
- [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] Peier A, et al. "The antiobesity effects of centrally administered neuromedin U and neuromedin S are mediated predominantly by the neuromedin U receptor 2 (NMUR2)." Endocrinology, 2009;150(7):3101-9. PMID: 19324999.
- [pubmed] Yayou K, et al. "Effects of intracerebroventricular administration of neuromedin U or neuromedin S in steers." Gen Comp Endocrinol, 2009;163(3):324-8. PMID: 19442664.
- [pubmed] Atsuchi K, et al. "Centrally administered neuromedin S inhibits feeding behavior and gastroduodenal motility in mice." Horm Metab Res, 2010;42(7):535-8. PMID: 20352600.
- [pubmed] Nakahara K, et al. "Comparison of feeding suppression by the anorexigenic hormones neuromedin U and neuromedin S in rats." J Endocrinol, 2010;207(2):185-93. PMID: 20732934.
- [pubmed] Yang G, et al. "The regulatory mechanism of neuromedin S on luteinizing hormone in pigs." Anim Reprod Sci, 2010;122(3-4):367-74. PMID: 21071159.
- [pubmed] Sakamoto T, et al. "Neuromedin S regulates cardiovascular function through the sympathetic nervous system in mice." Peptides, 2011;32(5):1020-6. PMID: 21356261.
- [pubmed] Mori M, et al. "Different distribution of neuromedin S and its mRNA in the rat brain: NMS peptide is present not only in the hypothalamus as the mRNA, but also in the brainstem." Front Endocrinol (Lausanne), 2012;3:152. PMID: 23264767.
- [pubmed] Lee IT, et al. "Neuromedin s-producing neurons act as essential pacemakers in the suprachiasmatic nucleus to couple clock neurons and dictate circadian rhythms." Neuron, 2015;85(5):1086-102. PMID: 25741729.
- [pubmed] Nakahara K, et al. "Involvement of endogenous neuromedin U and neuromedin S in thermoregulation." Biochem Biophys Res Commun, 2016;470(4):930-5. PMID: 26826380.
- [pubmed] Nadeau-Vallée M, et al. "Uterotonic Neuromedin U Receptor 2 and Its Ligands Are Upregulated by Inflammation in Mice and Humans, and Elicit Preterm Birth." Biol Reprod, 2016;95(3):72. PMID: 27512149.
- [pubmed] Alhosaini K, et al. "Ligand-Specific Signaling Profiles and Resensitization Mechanisms of the Neuromedin U2 Receptor." Mol Pharmacol, 2018;94(1):674-688. PMID: 29724789.
- [pubmed] Sun X, et al. "Neuromedin S Regulates Steroidogenesis through Maintaining Mitochondrial Morphology and Function via NMUR2 in Goat Ovarian Granulosa Cells." Int J Mol Sci, 2022;23(21). PMID: 36362185.
- [pubmed] Sun X, et al. "Neuromedin S regulates steroidogenesis and proliferation in goat Leydig cells through modulating mitochondrial function." FASEB J, 2023;37(6):e22989. PMID: 37199674.
- [pubmed] Edelmann MR, et al. "Tritium Labeling of Neuromedin S by Conjugation with [(3)H]N-Succinimidyl Propionate." ACS Omega, 2023;8(2):2367-2376. PMID: 36687043.
- [pubmed] Bongaerts J, et al. "Improving the LC-MS/MS analysis of neuromedin U-8 and neuromedin S by minimizing their adsorption behavior and optimizing UHPLC and MS parameters." J Pharm Biomed Anal, 2023;228:115306. PMID: 36868028.
- [pubmed] Rivera Quiles C, et al. "Identification of a Novel Population of Neuromedin S Expressing Neurons in the Ventral Tegmental Area That Promote Morphine-Elicited Behavior." J Neurosci, 2025;45(13). PMID: 39929726.
- [pubmed] Yang Q, et al. "Spatial and single-cell transcriptomic atlas of human suprachiasmatic nucleus." Neuron, 2026;114(8):1362-1379.e10. PMID: 41720090.
- [pubmed] Abdulmajeed WI, et al. "Monosynaptic GABAergic projections from a subset of suprachiasmatic nucleus neuromedin S neurons suppress preoptic area kisspeptin neuron firing in female mice." J Neurosci, 2026. PMID: 42810967.
- [pubmed] Yoshida H, et al. "Genetic deletion of neuromedin U and neuromedin S confers transient reno-protection in adenine-induced chronic kidney disease." Peptides, 2026;196:171474. PMID: 41720195.
- [review] Mori K, et al. "Neuromedin S: discovery and functions." Results Probl Cell Differ, 2008;46:201-12. PMID: 18214396.
- [review] Malendowicz LK, et al. "Neuromedins NMU and NMS: An Updated Overview of Their Functions." Front Endocrinol (Lausanne), 2021;12:713961. PMID: 34276571.
Sources & Citations
Every study on this page was read from its PubMed record on November 3, 2026. Status comes from Drugs@FDA (openFDA) and ClinicalTrials.gov, read 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.