Neuromedin B
An endogenous 10-amino-acid neuropeptide of the bombesin family that acts through its own receptor across breathing, itch, appetite, hormones and cancer growth — studied in the lab, not a drug
Neuromedin B (NMB) is a small human neuropeptide, first isolated from spinal cord in 1983. It is one of two mammalian members of the bombesin family — the other is gastrin-releasing peptide — and it works through its own receptor, the neuromedin B receptor (NMBR). For a tiny ten-amino-acid peptide it touches a remarkable range of systems: it helps set body temperature, tunes appetite and the release of thyroid-stimulating hormone, signals itch in the skin’s sensory nerves, and marks the brainstem neurons that drive breathing in response to carbon dioxide. It is also an autocrine growth signal that several cancers — lung, cervical and others — switch on for their own benefit. Neuromedin B is an endogenous peptide studied as a research tool and a drug target (usually to block it); 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
Neuromedin B is an endogenous human neuropeptide that has never been given to people as a treatment. It is studied as a signal and, mostly, as a drug target to BLOCK (with neuromedin B receptor antagonists in animals and cells), not to administer; human research is on patient tissue and blood.
Work out syringe units → · New to syringes? · All dosing data ↓ · Dose and vial tracker · Is this vial OK?
What is it?
Neuromedin B belongs to the bombesin-like peptide family, named after bombesin, a peptide first found in frog skin. Mammals make two of these peptides — neuromedin B and gastrin-releasing peptide (GRP) — and each has its own receptor: NMB acts mainly through the neuromedin B receptor (NMBR, also called BB1), while GRP acts through the GRP receptor (BB2). A third family receptor, BRS-3, has no known natural ligand. This receptor selectivity is what gives NMB a set of jobs distinct from its sister peptide.
NMB is widely distributed in the brain, spinal cord and gut, and its classic physiology reads like a tour of the neuroendocrine system: it lowers body temperature, influences feeding, triggers the release of thyroid-stimulating hormone, and contracts smooth muscle. Much of this was mapped in the pharmacology of the bombesin receptors; NMB is the ligand that reports specifically on NMBR biology.
Two of its most striking modern roles are in sensation and in breathing. In the skin’s sensory nerves, NMB can set off itch — injected into skin it makes mice and monkeys scratch — marking it as one of the peptides the body uses to signal the urge to scratch, separate from the GRP itch pathway. In the brainstem, neurons that express neuromedin B sit in the retrotrapezoid nucleus, the region that senses carbon dioxide and drives the depth of breathing; losing those neurons in mice causes unstable, insufficient breathing, placing NMB-marked cells at the centre of respiratory control.
NMB also acts on metabolism and the body’s tissues. Blocking or deleting its receptor in mice and in cultured cells impairs the making of new fat cells and leaves female mice partly resistant to diet-induced obesity, and in blood-vessel cells NMB signalling worsens the calcium build-up (vascular calcification) that stiffens arteries in kidney disease — both findings pointing to NMB blockade as a possible lever rather than something to give.
In cancer, NMB is an autocrine growth factor: tumour cells make it and respond to it. In lung cancer it switches on the EGF-receptor pathway, and in cervical cancer tumour-made NMB was shown to reprogram the nerve-supporting Schwann cells and drive the tumour’s invasion along nerves, with blood levels of NMB proposed as a marker of that spread. In Cushing’s disease, the pituitary tumours that oversecrete ACTH carry high levels of the NMB receptor, and blocking it shrank tumour activity in human-derived cells and in mice — an experimental therapeutic idea, not an approved treatment.
Neuromedin B is an endogenous human neuropeptide and a research and drug-target tool, not a medicine. No published study has given neuromedin B to people as a treatment, it is approved nowhere, and material sold online as ‘neuromedin B’ 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
Neuromedin B is a bombesin-family peptide that works through one receptor, NMBR. Through it, NMB reaches across breathing, itch, appetite and hormones, the blood vessels and tumour growth — which is why most of the therapeutic interest is in blocking it.
Neuromedin B receptor (NMBR / BB1)
NMB binds selectively to its own receptor, NMBR, with far higher affinity than to the sister GRP receptor — so it reports specifically on NMBR biology, distinct from gastrin-releasing peptide (PMID 37642928). NMBR antagonists such as PD168368 are the main research tools.
Broad neuroendocrine and sensory signalling
Through NMBR, neuromedin B acts across the brain, spinal cord and gut: marking the brainstem neurons that drive CO2-sensitive breathing (PMID 37290937) and signalling itch in skin sensory nerves (PMID 30734045), alongside classic roles in temperature, feeding and hormone release.
Metabolism, vessels and tumour growth
NMB-receptor signalling supports fat-cell formation (PMID 31067509) and worsens vascular calcification (PMID 34674793), while tumours use NMB as an autocrine growth and invasion signal (PMID 39214988) — so the therapeutic idea across these settings is to block NMB, not give it.
Published Research
These are studies of neuromedin B read from their PubMed abstracts on November 6, 2026. They range across its roles in CO2-driven breathing, skin itch, fat-cell formation and obesity, vascular calcification, and its autocrine action in cancer — from cervical-cancer nerve invasion to the neuromedin B receptor as a target in Cushing’s disease. Neuromedin B has not been given to people as a treatment in any published study; the human work is on patient tissue and blood, and the interventional studies are in animals and cells.
Neuromedin B neurons regulate CO2-driven breathing
Neurons expressing neuromedin B in the retrotrapezoid nucleus of the brainstem were shown, in a new transgenic mouse, to be central to respiratory homeostasis. Ablating about 95% of them caused chronic under-breathing, profound breathing instability and sleep-disordered breathing, and abolished the ventilatory response to carbon dioxide — identifying NMB-marked neurons as a core part of the CO2-sensing drive to breathe.
Neuromedin B induces acute itch
Injected into the skin, neuromedin B produced scratching in mice and monkeys, acting through peripheral sensory (dorsal root ganglion) neurons rather than through mast cells. The authors concluded that NMB is a peripheral pruritogen and a possible therapeutic target for itch at the level of the sensory nerves — a preclinical result.
Blocking the NMB receptor impairs fat-cell formation
Female mice lacking the neuromedin B receptor were partly resistant to diet-induced obesity, and their fat stem cells accumulated less lipid when pushed to become fat cells. In cultured pre-adipocytes a neuromedin B receptor antagonist cut cell proliferation and lipid accumulation and lowered the master fat-cell genes, suggesting NMB-receptor signalling supports adipogenesis (a preclinical finding).
Neuromedin B and vascular calcification
Neuromedin B and its receptor were raised when vascular smooth-muscle cells were driven to calcify by phosphate. Silencing NMB or blocking its receptor (with PD168368) curbed the bone-like change in the cells, and the antagonist reduced arterial calcification in cultured aortic rings and in a rat model of chronic kidney disease — positioning the NMB–receptor axis as a candidate target in vascular calcification.
Tumour-made neuromedin B drives cervical-cancer nerve invasion
In cervical cancer, neuromedin B produced by the tumour cells reprogrammed the nerve-supporting Schwann cells — changing their shape and gene expression and driving their proliferation and migration — to initiate perineural invasion, the spread of cancer along nerves. The signal ran through the NMB receptor on Schwann cells, and the authors proposed combined serum neuromedin B and CCL2 as a way to predict nerve invasion before nerve-sparing surgery.
NMB receptor as a target in Cushing's disease
Pituitary tumours that cause Cushing’s disease (corticotroph adenomas) carried higher levels of the neuromedin B receptor than other pituitary tumours. Blocking the receptor with PD168368 lowered ACTH output and tumour growth in mouse corticotroph cells, in tumour-bearing mice, and in several patient-derived adenoma cultures, suggesting the NMB receptor as a potential target in a disease where current drug options are limited — an experimental, preclinical result.
No Established Human Dose
Neuromedin B is an endogenous human neuropeptide that has never been given to people as a treatment. It is studied as a signal and, mostly, as a drug target to BLOCK (with neuromedin B receptor antagonists in animals and cells), not to administer; human research is on patient tissue and blood. No regulator has approved any dose, and the animal and cell studies used neuromedin B or its antagonists at experimental amounts that do not carry over to people, so no amount is printed here.
What this rests on: PMID 39214988, PMID 37642928, PMID 30734045.
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 B 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 B 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 B, 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 B stays intact once mixed.
How it is taken
Unknown: with no established human dose, there is no established way of taking Neuromedin B. 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; an endogenous, locally acting neuropeptide. After about five half-lives almost none is left.
When effects appear: unknown; no source on this page gives a time to effect for Neuromedin B. Results reported in the studies are under Published Research.
Source: half-life: PMID 39214988.
Side effects, and when to stop or get help
From the Side Effects section: No human adverse-event data exist: no published study has administered neuromedin B to people; In animals, neuromedin B in the skin provokes itch and scratching (PMID 30734045); Its signalling supports processes that are usually harmful in excess — fat-cell formation, vascular calcification and tumour growth — so therapeutic work aims to block it (PMIDs 31067509, 34674793, 39214988); Material sold online as ‘neuromedin B’ 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 Neuromedin B. Treat a severe or unexpected reaction as a reason to stop and see a doctor.
Source: the Side Effects section below (“Neuromedin B is an endogenous peptide that has not been given to people as a drug, so there is no human safety profile; the points below reflect that research status”).
Interactions
Unknown: a PubMed search for human interaction studies of Neuromedin B (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 Neuromedin B 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 neuromedin B (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
Neuromedin B is an endogenous peptide that has not been given to people as a drug, so there is no human safety profile; the points below reflect that research status.
Contraindications & Cautions
Neuromedin B has no approved use and no label. These points reflect its endogenous, research status.
Legal Status
Neuromedin B is an endogenous human neuropeptide 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 neuromedin B?
An endogenous human neuropeptide, isolated in 1983. It is a 10-amino-acid member of the bombesin-like peptide family (with gastrin-releasing peptide) and acts through its own receptor, the neuromedin B receptor (NMBR).
?What does it do?
For a small peptide, a lot: it helps regulate body temperature, feeding and thyroid-stimulating hormone, signals itch in sensory nerves (PMID 30734045), marks the brainstem neurons that drive CO2-sensitive breathing (PMID 37290937), and acts as a growth signal in some cancers (PMID 39214988).
?Is it a treatment for anything?
No. Neuromedin B is a research peptide and a drug target — usually one to block, since its signalling drives itch, fat-cell formation, vascular calcification and tumour growth. No human trial has given neuromedin B to people, and it is approved nowhere.
?Is it approved or available to buy?
No. Neuromedin B is not a medicine, has no FDA application or label, and is approved nowhere. Material sold online as neuromedin B is an unregulated research chemical. Grey Peptides lists no sellers and recommends no source; this page records the published science.
References
- [animal] Souza GMPR, et al. "Neuromedin B-Expressing Neurons in the Retrotrapezoid Nucleus Regulate Respiratory Homeostasis and Promote Stable Breathing in Adult Mice." J Neurosci, 2023;43(30):5501-5520. PMID: 37290937.
- [animal] Ehling S, et al. "Neuromedin B Induces Acute Itch in Mice via the Activation of Peripheral Sensory Neurons." Acta Derm Venereol, 2019;99(6):587-893. PMID: 30734045.
- [animal] de Paula GSM, et al. "Neuromedin B receptor disruption impairs adipogenesis in mice and 3T3-L1 cells." J Mol Endocrinol, 2019;63(1):93-102. PMID: 31067509.
- [animal] Park HJ, et al. "Neuromedin B modulates phosphate-induced vascular calcification." BMB Rep, 2021;54(11):569-574. PMID: 34674793.
- [mechanism] Gao X, et al. "Cervical cancer-produced neuromedin-B reprograms Schwann cells to initiate perineural invasion." Cell Death Dis, 2024;15(8):636. PMID: 39214988.
- [mechanism] Sekizaki T, et al. "Neuromedin B receptor as a potential therapeutic target for corticotroph adenomas." Pituitary, 2023;26(5):597-610. PMID: 37642928.
- [other] UniProt P08949 (NMB_HUMAN), read November 6, 2026: neuromedin B is the product of the NMB gene, a secreted, C-terminally amidated 10-amino-acid neuropeptide of the bombesin-like peptide family; it signals through the neuromedin B receptor (NMBR / BB1), a G-protein-coupled receptor. https://www.uniprot.org/uniprotkb/P08949/entry
- [other] Neuromedin B was isolated from porcine spinal cord and named in 1983, one of the mammalian counterparts of the amphibian peptide bombesin (with gastrin-releasing peptide); its receptor family and physiology are set out in the bombesin-receptor review by Jensen and colleagues (Pharmacological Reviews, 2007) and summarized in the studies 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 neuromedin B. It is an endogenous human neuropeptide, not a registered drug; FDA GSRS and ChEMBL hold no substance record for it, and the neuromedin B receptor antagonists used in the research below (such as PD168368) are laboratory tools, not medicines.
Sources & Citations
The six studies carded above were read from their PubMed records on November 6, 2026. Identity comes from UniProt (P08949, gene NMB); neuromedin B’s 1983 isolation and its receptor family are from the bombesin-receptor literature; 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.