Asprosin
A hormone released by body fat during fasting that tells the liver to release sugar and the brain to feel hungry; raised in obesity and diabetes, and a research target for blocking — not a drug
Asprosin is a protein hormone discovered in 2016. When the body fasts, white fat cuts it from the tail end of a large structural protein, profibrillin, and releases it into the blood. It does two things that make sense for a fast: it travels to the liver and tells it to release glucose, keeping blood sugar up, and it crosses into the brain and switches on the hunger neurons (the AgRP neurons) to drive appetite. In people with obesity, type 2 diabetes and metabolic syndrome, asprosin runs pathologically high, and in rare people who genetically lack it, appetite is low and they are very lean. Because of this, the therapeutic interest is in blocking asprosin — with neutralizing antibodies in animal studies — rather than giving it. Asprosin itself is an endogenous hormone studied as a research compound; 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
Asprosin is an endogenous fasting hormone that has never been given to people as a treatment, and because it is elevated and harmful in metabolic disease, the therapeutic aim is to block it (with neutralizing antibodies in animal studies), not to administer it. Human studies only measured circulating asprosin.
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What is it?
Most hormones that control blood sugar and appetite were known for decades; asprosin is a newcomer, identified only in 2016. Researchers studying a rare genetic condition traced a signalling molecule to an unexpected source: the very end of profibrillin, the precursor of fibrillin-1, a large protein best known as a structural fibre in connective tissue. An enzyme clips off that C-terminal tail, and the released fragment turned out to be an active hormone they named asprosin.
Asprosin is a fasting hormone. White fat releases it when food is scarce, it circulates at nanomolar levels, and it is recruited to the liver, where it switches on the G-protein-cAMP-PKA pathway and prompts the liver to release glucose into the blood — exactly what is needed to keep the brain fuelled between meals. The olfactory receptor OLFR734 was later identified as a liver receptor that carries this glucose-raising effect.
Its second job is in the brain. Circulating asprosin crosses the blood-brain barrier and directly activates the orexigenic AgRP neurons of the hypothalamus through a cAMP pathway, while indirectly quietening the appetite-suppressing POMC neurons. The result is increased appetite and a drive to store fat. This places asprosin alongside the classic hunger signals, upstream of the same AgRP/POMC switch that other appetite hormones converge on.
The disease link is consistent and striking. People and mice with insulin resistance, obesity or type 2 diabetes have pathologically high asprosin; one human study across the whole spectrum of glucose handling found circulating asprosin stepwise higher in obesity and dysglycemia and correlated with insulin resistance, blood lipids and even carotid artery thickness. At the opposite extreme, people with a genetic deficiency of asprosin (a form of neonatal progeroid syndrome) have low appetite and extreme leanness — a natural experiment showing what asprosin normally does.
That biology points to blocking asprosin, not supplementing it. In mice, monoclonal antibodies that neutralize asprosin lowered appetite, body weight and blood glucose, acting on two pillars of metabolic syndrome at once, and the authors framed this as a path toward human trials. Exercise also appears to modulate asprosin, adding a lifestyle dimension to its regulation.
Asprosin is an endogenous hormone and a research target, not a medicine. No published study has given asprosin to people as a treatment, it is approved nowhere, and material sold online as ‘asprosin’ is an unregulated research chemical. Nothing here is a dose or a therapy; this page records what the published science says about a recently discovered fasting hormone.
Mechanism of Action
Asprosin is a fasting signal cut from a structural protein. It raises blood sugar from the liver and raises appetite from the brain, and in metabolic disease both run too high — which is why the therapeutic idea is to block it.
Appetite via AgRP neurons
Circulating asprosin crosses the blood-brain barrier and directly activates the orexigenic AgRP neurons while inhibiting anorexigenic POMC neurons, stimulating appetite and fat accumulation (PMID 29106398) — linking it to the central hunger circuit.
Raised in metabolic disease
Asprosin is pathologically elevated in obesity, type 2 diabetes and metabolic syndrome (PMID 36773601), while its genetic deficiency causes leanness — so neutralizing asprosin lowered appetite, weight and glucose in mice (PMID 33904407), the basis of its therapeutic interest.
Published Research
These are studies of asprosin read from their PubMed abstracts on November 5, 2026. They run from its 2016 discovery as a fasting glucogenic hormone, through its orexigenic action on AgRP neurons and the identification of its liver receptor OLFR734, to a preclinical antibody therapy and a human study of its blood levels in obesity and dysglycemia, with a review of its link to exercise. Asprosin has not been given to people as a treatment in any published study.
Discovery of a fasting glucogenic hormone
The paper that identified asprosin: the C-terminal cleavage product of profibrillin, secreted by white fat, circulating at nanomolar levels, and recruited to the liver where it activates the G protein-cAMP-PKA pathway to release glucose. Humans and mice with insulin resistance had pathologically elevated asprosin, and blocking it (immunologically or genetically) profoundly lowered glucose and insulin by reducing hepatic glucose release.
A centrally acting appetite hormone
Asprosin in the circulation was shown to cross the blood-brain barrier and directly activate the orexigenic AgRP neurons via cAMP, inhibiting the anorexigenic POMC neurons and stimulating appetite and weight gain. Humans genetically deficient in asprosin had low appetite and extreme leanness, phenocopied in mice and rescued by asprosin; obese humans and mice had high asprosin, and neutralizing it reduced appetite, weight and blood glucose.
OLFR734 is a receptor for asprosin
A search for asprosin's receptor identified the olfactory receptor OLFR734 on liver cells as the G-protein-coupled receptor mediating its glucose-raising effect. Mice lacking Olfr734 had a blunted response to asprosin — lower cAMP and hepatic glucose production and improved insulin sensitivity — and losing it attenuated both fasting and high-fat-diet glucose production, placing OLFR734 at the centre of asprosin's glucose control.
Anti-asprosin antibodies in metabolic syndrome
Three monoclonal antibodies against distinct asprosin epitopes were tested in three mouse models of metabolic syndrome. Each lowered appetite, body weight and blood glucose in a dose-dependent way, with a half-life over three days, targeting two pillars of metabolic syndrome — over-nutrition and hyperglycemia — at once. The authors positioned anti-asprosin antibodies as a candidate therapy heading toward human trials (a preclinical result).
Circulating asprosin across the glucose spectrum
In 153 people spanning healthy, obese, prediabetic and newly diagnosed type 2 diabetic groups, serum asprosin was significantly higher in those with obesity and dysglycemia than in controls and correlated with anthropometric measures, liver enzymes, glucose and insulin, lipids and carotid intima-media thickness. The authors suggested circulating asprosin as a predictive marker for early carbohydrate disorders — an observational levels study.
Asprosin and exercise in metabolic disease
A review of asprosin's metabolism, its OLFR734 receptor signalling, and growing evidence that exercise regulates asprosin. It frames asprosin — made from the FBN1 profibrillin and released from fat during fasting to raise liver glucose — as a potential lever in diabetes and obesity, including through exercise intervention.
No Established Human Dose
Asprosin is an endogenous fasting hormone that has never been given to people as a treatment, and because it is elevated and harmful in metabolic disease, the therapeutic aim is to block it (with neutralizing antibodies in animal studies), not to administer it. Human studies only measured circulating asprosin. No regulator has approved any dose, and animal mechanistic studies used recombinant asprosin at experimental amounts that do not carry over to people, so no amount is printed here.
What this rests on: PMID 36773601, PMID 27087445, PMID 29106398, PMID 33904407.
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 Asprosin 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 Asprosin 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 Asprosin, 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 Asprosin stays intact once mixed.
How it is taken
Unknown: with no established human dose, there is no established way of taking Asprosin. 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 circulating hormone. After about five half-lives almost none is left.
When effects appear: unknown; no source on this page gives a time to effect for Asprosin. Results reported in the studies are under Published Research.
Source: half-life: PMID 27087445.
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 asprosin to people; Pathologically high asprosin is associated with obesity, insulin resistance and type 2 diabetes (PMIDs 27087445, 36773601); Because high asprosin is harmful, therapeutic work aims to block it, not supplement it (PMID 33904407); Material sold online as ‘asprosin’ 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 Asprosin. Treat a severe or unexpected reaction as a reason to stop and see a doctor.
Source: the Side Effects section below (“Asprosin is an endogenous hormone 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 Asprosin (reviewed 2026-11-05) 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 Asprosin 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 asprosin (searched November 5, 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
Asprosin is an endogenous hormone 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
Asprosin has no approved use and no label. These points reflect its endogenous, research status.
Legal Status
Asprosin is an endogenous human protein hormone 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 asprosin?
A fasting hormone discovered in 2016. Body fat cuts it from the end of the protein profibrillin and releases it when you fast. It tells the liver to release glucose and the brain's AgRP neurons to drive appetite, so it raises both blood sugar and hunger.
?What does it do?
It raises blood glucose from the liver through the receptor OLFR734 (PMIDs 27087445, 31230984) and stimulates appetite by activating hypothalamic AgRP neurons (PMID 29106398). It is elevated in obesity and type 2 diabetes (PMID 36773601).
?Could it be a weight-loss drug?
Not by giving it — the opposite. Asprosin raises appetite and glucose and is too high in metabolic disease, so the drug idea is to block it. Anti-asprosin antibodies lowered appetite, weight and glucose in mice (PMID 33904407), but this is preclinical and no human trials are published.
?Is it approved or available to buy?
No. Asprosin is not a medicine, has no FDA application or label, and is approved nowhere. Material sold online as asprosin is an unregulated research chemical. Grey Peptides lists no sellers and recommends no source; this page records the published science.
References
- [mechanism] Romere C, et al. "Asprosin, a Fasting-Induced Glucogenic Protein Hormone." Cell, 2016;165(3):566-79. PMID: 27087445.
- [animal] Duerrschmid C, et al. "Asprosin is a centrally acting orexigenic hormone." Nat Med, 2017;23(12):1444-1453. PMID: 29106398.
- [animal] Li E, et al. "OLFR734 Mediates Glucose Metabolism as a Receptor of Asprosin." Cell Metab, 2019;30(2):319-328.e8. PMID: 31230984.
- [animal] Mishra I, et al. "Asprosin-neutralizing antibodies as a treatment for metabolic syndrome." Elife, 2021;10. PMID: 33904407.
- [clinical-trial] Nedeva IS, et al. "Circulating Asprosin Concentrations in Patients with Obesity and Carbohydrate Disturbances." Horm Metab Res, 2023;55(4):284-289. PMID: 36773601.
- [review] Liu L, et al. "The Effects of Asprosin on Exercise-Intervention in Metabolic Diseases." Front Physiol, 2022;13:907358. PMID: 35899030.
- [other] UniProt P35555 (FBN1_HUMAN), read November 5, 2026: asprosin is the C-terminal furin-cleavage fragment of profibrillin-1 (gene FBN1), a secreted protein hormone (adipokine) of about 140 amino acids. https://www.uniprot.org/uniprotkb/P35555/entry
- [other] Asprosin was discovered and named in 2016 as the C-terminal cleavage product of profibrillin; a genetic deficiency of it (in neonatal progeroid syndrome) causes low appetite and extreme leanness, as described in the discovery and orexigenic-hormone papers carded on this page (read November 5, 2026).
- [other] US FDA, Drugs@FDA and the drug label endpoint (openFDA), searched November 5, 2026: no application and no label record for asprosin. It is an endogenous human protein hormone, not a registered drug; FDA GSRS and ChEMBL hold no substance record for it.
Sources & Citations
The six studies carded above were read from their PubMed records on November 5, 2026. Identity comes from UniProt (P35555, gene FBN1); asprosin's 2016 discovery and the human genetic-deficiency phenotype are from the discovery and orexigenic-hormone papers carded here; 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.