BRP peptide
A 12-amino-acid peptide found by an AI prohormone-cleavage screen at Stanford that cuts food intake by up to half in rodents and pigs through hypothalamic POMC neurons, apparently without the nausea that limits GLP-1 drugs.
Also known as BRINP2-related peptide, BRP, Stanford appetite peptide
Animal data only — Rodent or other animal studies. Dose translation to humans is genuinely uncertain.
One high-profile 2025 Nature paper plus follow-up work in mice and minipigs. Katrin Svensson has co-founded Merrifield Therapeutics to take it forward, but as of mid-2026 there is no registered human trial, no IND announcement and no human PK. Every claim about how it will feel in a person is extrapolation.
How it works
BRP is cleaved from the BRINP2 prohormone and was identified by a machine-learning model trained to predict which uncharacterised prohormones yield bioactive fragments. In mice and minipigs it acutely reduces food intake by up to 50% and produces fat-selective weight loss with preserved lean mass. It drives c-Fos expression in arcuate POMC neurons and its effect survives in GLP-1-receptor knockout animals, which is the core evidence that it works through a distinct circuit. Its receptor has not been definitively identified as of mid-2026, which is the single biggest open question about the molecule. Because it does not engage the area postrema the way GLP-1 agonists do, the working hypothesis is that it will avoid the nausea and vomiting that cap incretin dosing — but that is a hypothesis, not a finding, until humans are dosed.
Targets: Hypothalamic POMC neurons, Unidentified BRP receptor, Arcuate nucleus melanocortin circuit
Dosing
| Protocol | Dose | Frequency | Route |
|---|---|---|---|
| Preclinical rodent protocol (not a human protocol)Dosed before the dark-cycle feeding window in rodents. | — | twice daily in published animal work | subcutaneous |
- · Published work uses milligram-per-kilogram intraperitoneal or subcutaneous dosing in mice. There is no validated human-equivalent dose, no human PK, and no safety data. Any vendor selling a 'BRP dosing protocol' is inventing it.
Cycling
No human cycling framework exists. Animal studies ran 14 days continuously.
Pharmacology
- Half-life
- Short in rodents — the anorectic effect is largely gone within hours of a single injection, which is why preclinical work uses twice-daily dosing. No human pharmacokinetic data exist.
- Onset
- Food intake drops within the first hour of injection in rodents; body-composition changes accrue over roughly 14 days of twice-daily dosing.
- Routes
- subcutaneous
- Molecule
- Endogenous prohormone-derived 12-amino-acid peptide
- Sequence length
- 12 amino acids
Handling
- Diluent
- Bacteriostatic water
- Lyophilised
- Freezer at -20 C for anything beyond a few weeks.
- Reconstituted
- Refrigerated; small unmodified peptides of this size degrade quickly in solution.
- Light sensitive
- Yes — keep it out of the light
Mixing
Research-grade material appears as lyophilised powder in small quantities. Purity and even sequence identity of grey-market 'BRP' are unverified — this is a peptide most vendors could not correctly synthesise if they tried.
Side effects
- commonUnknown human safety profile— Nothing here has been characterised in people. The absence of reported side effects is the absence of data, not evidence of safety.
- commonAppetite suppression severe enough to cause under-eating— Observed in animals at effective doses; a 50% reduction in intake is not a small effect.
Do not use if
- Any human use — this compound has never completed a human safety study and no investigational new drug application had been filed as of mid-2026.
- History of an eating disorder — a peptide that halves food intake through an uncharacterised receptor is a bad match here.
Combining it
- cautionsemaglutide — Mechanistically additive on paper since BRP works outside the GLP-1 receptor, but stacking two uncharacterised appetite suppressors is how people end up hospitalised for dehydration.
What to monitor
- · Not applicable outside a formal trial. If someone uses it anyway, weight, food intake and hydration are the only meaningful trackable variables.
Legal status
Not approved anywhere. Not a dietary supplement. Sold, where it appears at all, as an unregulated research chemical.
References
- Coassolo et al. 2025, Nature — machine-learning identification of BRP and its anorectic effects in mice and minipigs (preclinical)
Mechanism in depth
Identified by computational screening of prohormone sequences for previously unannotated cleavage products, and reported in 2025 to reduce food intake in animal models through a pathway distinct from GLP-1 receptor signalling. The interest is specifically that appetite suppression appeared without the gastrointestinal aversion that limits incretin dosing.
What usually goes wrong
This is a recent preclinical finding being discussed as though it were a product. Animal appetite results have failed to translate to humans many times in this exact field, and the absence of nausea in a mouse is not evidence of tolerability in a person. Anything sold under this name today has no human data behind it whatsoever.
Receptor targets
- Reported to act independently of GLP-1R; receptor characterisation is incomplete — Not established
Reduced food intake in animal models
Genuinely uncertain
- Findings are preclinical and recent; no human trial has been reported.
- The receptor and mechanism are not fully characterised.
- Whether the reported absence of aversive effects survives translation to humans is entirely untested.