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Evidence: LowPeptideResearch ChemicalEndogenous neuropeptideHunger signalResearch compound

Agouti-Related Peptide (AgRP)

The brain's built-in hunger signal: a peptide released by a small group of hypothalamic neurons that blocks the body's satiety switch and powerfully drives eating. A research molecule, never a drug

Deep in the hypothalamus, a tiny cluster of neurons controls the drive to eat. When the body senses it is short of energy, these neurons release agouti-related peptide (AgRP), which blocks the melanocortin-4 receptor — the same satiety switch that the weight-loss drug setmelanotide turns on. Where the satiety peptide alpha-MSH presses that switch to say ‘stop eating,’ AgRP releases it to say ‘keep eating.’ In animals, switching these AgRP neurons on triggers immediate, voracious feeding; switching them off suppresses it. AgRP is one of the most intensively studied molecules in the neuroscience of appetite and obesity, and it sits directly opposite the melanocortin pathway that modern anti-obesity medicines act on. It is an endogenous signalling peptide studied as a research compound — it is not an approved medicine and has not been given to people as a treatment in a published trial.

No established human dose Details ↓

Overview

What is it?

The body keeps a running account of its energy, and much of the bookkeeping happens in the arcuate nucleus of the hypothalamus. Two opposing sets of neurons sit there. One makes pro-opiomelanocortin (POMC), from which comes alpha-MSH, a peptide that presses the melanocortin-4 receptor to signal fullness and curb eating. The other makes agouti-related peptide together with neuropeptide Y (the AgRP/NPY neurons), and it does the reverse: AgRP is the hunger signal.

AgRP works by blocking the same receptor alpha-MSH activates. It is an antagonist and, unusually, an inverse agonist at the melanocortin-3 and -4 receptors — meaning it does not merely get in alpha-MSH’s way but actively turns the receptor's resting signal down, releasing the brake on appetite. Its companions matter too: the same neurons release neuropeptide Y, another orexigenic signal, and the inhibitory transmitter GABA, so when they fire they drive feeding through several routes at once.

How powerful that drive is became clear when researchers learned to switch the neurons on and off at will. In a landmark 2011 study, briefly activating AgRP neurons in mice caused rapid, voracious eating and, over time, weight gain; silencing them in hungry mice suppressed feeding. Later work showed AgRP neurons sense the body's energy state — they are switched on by the hunger hormone ghrelin and by fasting, and turned down by the fat hormone leptin and by insulin — and that they coordinate with the POMC neurons so that feeding is set by the two systems together. AgRP neurons reach well beyond simple intake, shaping food-seeking motivation, energy expenditure, blood-sugar handling and even liver metabolism during a fast.

In people the evidence is mostly indirect. Circulating AgRP can be measured, and levels have been compared across conditions — for example in children with the genetic obesity syndromes Prader-Willi and Bardet-Biedl, and in obesity and anorexia more broadly — while rare human mutations in the melanocortin pathway AgRP acts on cause severe inherited obesity. The clearest clinical link is through that pathway's other side: the melanocortin-4-receptor agonist setmelanotide is approved for several forms of genetic obesity, acting on the very receptor AgRP blocks.

AgRP itself is an endogenous signalling peptide and a laboratory research tool, not a medicine. No published study has given AgRP to people as a treatment, it is approved nowhere, and material sold online as ‘AgRP’ is an unregulated research chemical. Nothing here is a dose or a therapy; this page records what the published science says about one of the brain's core hunger signals.

MC3R/MC4R
What it blocks
the melanocortin satiety receptors · PMID 34798121
Arcuate
Where it is made
AgRP/NPY neurons of the hypothalamus · PMID 34798121
0
Published trials giving it to people
human studies measure its levels only · PMID 35098494
Science

Mechanism of Action

AgRP is the hunger half of a two-sided switch. It is released by hypothalamic neurons that sense low energy and acts on the melanocortin receptors to release the brake on appetite, opposing the satiety peptide alpha-MSH.

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Releasing the melanocortin brake

AgRP is an antagonist and inverse agonist at the melanocortin-3 and -4 receptors (MC3R/MC4R), the receptors alpha-MSH activates to signal fullness. By blocking and actively turning down their signal, AgRP removes the brake on appetite (PMID 34798121) — the receptor setmelanotide turns on from the other side.

🍽️

AgRP/NPY neurons drive feeding

AgRP is co-released with neuropeptide Y and GABA from arcuate-nucleus neurons; switching those neurons on in mice triggers rapid, voracious eating and lowers energy expenditure, and switching them off suppresses feeding (PMIDs 21364278, 38378998).

⚖️

Reading the body's energy state

AgRP neurons are switched on by the hunger hormone ghrelin and by fasting and turned down by the fat hormone leptin and by insulin, and they act reciprocally with POMC neurons so that feeding, glucose handling and energy use are set by the two systems together (PMID 38378998).

Evidence

Published Research

These are studies of agouti-related peptide read from their PubMed abstracts on November 5, 2026. The mechanistic record is in animals — switching AgRP neurons on and off to drive or suppress feeding, their reciprocal action with POMC neurons, and AgRP's effect in a self-starvation model — with a human study measuring circulating AGRP in genetic obesity syndromes and a review of the circuit as an obesity target. AgRP has not been given to people as a treatment in any published study.

Animal2011

Switching AgRP neurons on drives feeding

Using DREADD chemogenetics to turn AgRP neurons on and off in mice, acute activation rapidly and dramatically induced feeding, cut energy expenditure and increased fat stores, all reversing when stimulation stopped; inhibiting the neurons in hungry mice reduced intake. The landmark demonstration that AgRP-neuron activity is both necessary and sufficient for feeding, and that it drives food-seeking and motivation, not just eating.

PMID: 21364278
Animal2024

AgRP and POMC neurons act reciprocally

By expressing opposing chemogenetic receptors in both populations at once, this study showed that food intake is set by the sum of AgRP-neuron activation and POMC-neuron inhibition, while insulin sensitivity and glucose production are modulated differently by the two. It mapped a circuit in which activated AgRP and inhibited POMC neurons cooperate to drive eating, refining how the hunger and satiety arms combine.

PMID: 38378998
Animal2003

AgRP prevents self-starvation in rats

In a rat model of activity-based anorexia — food restriction with running wheels that drives paradoxical hyperactivity and self-starvation — central infusion of AgRP suppressed melanocortin-receptor activity and increased survival by countering the hyperactivity, the suppressed intake and the deranged body temperature, implicating the melanocortin system in anorexia-like behaviour.

PMID: 12610657
Animal2003

Appetite versus reward

AgRP injected into the rat paraventricular hypothalamus increased intake of ordinary chow but not of a palatable sucrose solution, unlike opioid agonists, suggesting its primary effect is to drive eating to meet energy need rather than for reward, though with some opioid-like features from melanocortin-opioid interactions.

PMID: 12851315
Human2022

Serum AGRP in genetic obesity syndromes

In children with Prader-Willi (12) or Bardet-Biedl (12) syndromes versus obese and lean controls, serum alpha-MSH was significantly lower and BDNF higher in the syndrome groups, consistent with a disrupted leptin-melanocortin pathway; serum AGRP did not differ from obese controls. An observational levels study bearing on the pathway AgRP works in, not a trial of giving AgRP.

PMID: 35098494
Review2021

The AgRP/NPY and POMC circuit as an obesity target

A review of the arcuate-nucleus microcircuit: AgRP/NPY neurons signal hunger and stimulate feeding while POMC neurons signal satiety, with the two integrating leptin, ghrelin and insulin to set energy balance. It surveys the proteins, genes and candidate drugs acting through this circuit as potential obesity therapies.

PMID: 34798121
Dosing

No Established Human Dose

Agouti-related peptide is an endogenous brain signal that has never been given to people as a treatment. The human study carded here only measured circulating AGRP in children with genetic obesity syndromes, not what happens when it is administered, and no regulator has approved any dose. Animal studies delivered it directly into the brain (intracerebroventricular or intrahypothalamic infusion) at amounts that do not carry over to people, so no amount is printed here.

What this rests on: PMID 35098494, PMID 21364278, PMID 12610657, PMID 12851315.

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.

For Buyers

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 Agouti-Related Peptide (AgRP) 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 Agouti-Related Peptide (AgRP) 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 Agouti-Related Peptide (AgRP), 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 Agouti-Related Peptide (AgRP) stays intact once mixed.

How it is taken

Unknown: with no established human dose, there is no established way of taking Agouti-Related Peptide (AgRP). 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 central signalling peptide. After about five half-lives almost none is left.

When effects appear: unknown; no source on this page gives a time to effect for Agouti-Related Peptide (AgRP). Results reported in the studies are under Published Research.

Source: half-life: PMID 34798121.

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 AgRP to people; Human research measures its circulating levels only (PMID 35098494); In animals it is a powerful orexigenic signal — brain infusion drives overeating and weight gain (PMID 21364278); Material sold online as ‘AgRP’ 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 Agouti-Related Peptide (AgRP). Treat a severe or unexpected reaction as a reason to stop and see a doctor.

Source: the Side Effects section below (“AgRP 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 Agouti-Related Peptide (AgRP) (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 Agouti-Related Peptide (AgRP) 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 agouti-related peptide (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.

Safety

Side Effects & Contraindications

Reported Side Effects

AgRP 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.

● No human adverse-event data exist: no published study has administered AgRP to people
● Human research measures its circulating levels only (PMID 35098494)
● In animals it is a powerful orexigenic signal — brain infusion drives overeating and weight gain (PMID 21364278)
● Material sold online as ‘AgRP’ is an unregulated research chemical of unverified content

Contraindications & Cautions

AgRP has no approved use and no label. These points reflect its endogenous, research status.

● Not a medicine: no FDA application or label, and no approval anywhere
● No human dosing, interaction, pregnancy or long-term safety data exist
● It is a laboratory research peptide, not a treatment — and as a hunger signal it would be expected to increase, not reduce, body weight
● Altered levels in disease are associations, not evidence that taking AgRP helps
Questions

Frequently Asked Questions

?What is agouti-related peptide?

A hunger signal the brain makes. AgRP is released by a group of hypothalamic neurons and blocks the melanocortin-4 receptor — the satiety switch — so it powerfully drives eating. It is the opposite number of the satiety peptide alpha-MSH.

?What does it do?

In animals, activating the neurons that release AgRP triggers rapid, voracious feeding and lowers energy use; silencing them suppresses eating (PMID 21364278). AgRP senses the body's energy state via ghrelin, leptin and insulin and works reciprocally with POMC neurons (PMID 38378998).

?Has it been tested in people?

Not as a treatment. Human studies measure circulating AGRP — for example in children with Prader-Willi and Bardet-Biedl syndromes (PMID 35098494) — and the melanocortin pathway it acts on is targeted by the approved drug setmelanotide. No published study has given AgRP to people.

?Is it approved or available to buy?

No. AgRP is not a medicine, has no FDA application or label, and is approved nowhere. As a hunger signal it would be expected to increase body weight, not reduce it. Material sold online as AgRP is an unregulated research chemical. Grey Peptides lists no sellers and recommends no source.

Bibliography

References

  1. [animal] Krashes MJ, et al. "Rapid, reversible activation of AgRP neurons drives feeding behavior in mice." J Clin Invest, 2011;121(4):1424-8. PMID: 21364278.
  2. [animal] De Solis AJ, et al. "Reciprocal activity of AgRP and POMC neurons governs coordinated control of feeding and metabolism." Nat Metab, 2024;6(3):473-493. PMID: 38378998.
  3. [animal] Kas MJ, et al. "Agouti-related protein prevents self-starvation." Mol Psychiatry, 2003;8(2):235-40. PMID: 12610657.
  4. [animal] Olszewski P, et al. "Agouti-related protein: appetite or reward?." Ann N Y Acad Sci, 2003;994:187-91. PMID: 12851315.
  5. [clinical-trial] Turkkahraman D, et al. "Serum alpha-melanocyte-stimulating hormone (a-MSH), brain-derived neurotrophic factor (BDNF), and agouti-related protein (AGRP) levels in children with Prader-Willi or Bardet-Biedl syndromes." J Endocrinol Invest, 2022;45(5):1031-1037. PMID: 35098494.
  6. [review] Vohra MS, et al. "AgRP/NPY and POMC neurons in the arcuate nucleus and their potential role in treatment of obesity." Eur J Pharmacol, 2022;915:174611. PMID: 34798121.
  7. [other] UniProt O00253 (AGRP_HUMAN), read November 5, 2026: agouti-related protein, a 132-amino-acid protein (gene AGRP); its active C-terminal fragment AgRP(83-132) carries the melanocortin-receptor activity. https://www.uniprot.org/uniprotkb/O00253/entry
  8. [other] Agouti-related peptide is the product of the AGRP gene, expressed in AgRP/NPY neurons of the hypothalamic arcuate nucleus; it is an endogenous antagonist and inverse agonist at the melanocortin-3 and -4 receptors (MC3R/MC4R), as summarised in the review carded on this page (read November 5, 2026).
  9. [other] US FDA, Drugs@FDA and the drug label endpoint (openFDA), searched November 5, 2026: no application and no label record for agouti-related peptide. It is an endogenous human protein, 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 (O00253, gene AGRP); AgRP's role as a melanocortin-receptor antagonist and inverse agonist and its place in the arcuate circuit are from the review 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.

Last reviewed: 2026-11-05