BRP (BRINP2-related peptide)

BRP was identified by a machine-learning pipeline called Peptide Predictor that screened roughly 2,600 candidate human peptide fragments for signatures of secreted bioactive peptides. It acts on pro-opiomelanocortin neurons in the hypothalamus, activating an intracellular cAMP-PKA-CREB-FOS cascade and suppressing food intake. Critically, its transcriptional and behavioural signature differs from semaglutide's: in mice it did not produce the conditioned taste aversion, gastric slowing or reduced movement that GLP-1 agonists cause, and its effects persisted in GLP-1-receptor-knockout animals. Its own receptor has not been definitively identified, which is the biggest open question about the molecule. A single injection before feeding cut food intake by up to 50% within an hour in lean mice and minipigs.

Targets: Hypothalamic POMC neurons, Receptor not yet identified

• · All published dosing is weight-scaled rodent and minipig dosing. There is no human dose, no human pharmacokinetic data and no basis on which to convert the animal doses - anyone quoting a human protocol for BRP is making it up.

Work out your exact syringe units →

• commonInjection-site irritation— Expected for any subcutaneous peptide; not specifically characterised for BRP.
• rareUnknown in humans— No human has been dosed in a registered trial. Absence of reported side effects reflects absence of data, not safety.

• Everyone, at present - there is no human safety data of any kind.
• Pregnancy.
• The receptor it acts through has not been identified, so off-target effects cannot even be predicted.

• synergysemaglutide — Mechanistically independent of GLP-1 in animal work, so additive effects are plausible in theory. There is no data on the combination in any species.

• · Nothing established. This is a preclinical molecule.

Not approved and not in human trials; sold speculatively as a research chemical with no way to verify what is in the vial.

• Coassolo et al. 2025, BRINP2-related peptide suppresses food intake, Nature (preclinical)

BRP is genuinely novel and genuinely unproven, and both halves of that sentence matter. The discovery method is the interesting part: a machine-learning model was trained to predict which prohormone cleavage products are likely to be bioactive, applied across the human proteome, and BRP - a 12-residue fragment of BRINP2 - came out as a hit. It was then shown to reduce food intake in mice and minipigs. The mechanism is what makes it worth watching: BRP appears to act on hypothalamic POMC neurons through a receptor that is not GLP1R, and mice lacking GLP-1 receptors still respond to it, so it is not a covert incretin. The reported effect profile is also different in kind - reduced food intake without the gastric-emptying delay and without the nausea signature that defines the incretin and amylin classes. If that separation of appetite suppression from emesis holds in humans, it would be a bigger deal than any incremental weight-loss percentage in this document. The problem is that it is a single high-profile Nature paper from one group at Stanford, with mouse and minipig data, and no registered or reported human trial as of mid-2026. The history of obesity pharmacology is a long list of compounds that reduced food intake in rodents and did nothing useful in people - leptin being the most instructive example, since it was also a Nature-level discovery that transformed the field's understanding and then failed as a drug in common obesity. Anyone buying BRP from a research vendor is buying a 12-residue peptide with no human data, no established receptor, no dosing information, and no way to confirm identity.

The two failure modes are epistemic and practical. Epistemically: 'works in mice' is where a very long list of failed obesity drugs also started, and the nausea-free profile that makes BRP exciting is exactly the kind of finding that has historically not survived translation. Practically: a 12-residue peptide sold speculatively by research chemical vendors, for a target that was published eighteen months ago, has no quality standard, no reference material and no way for a buyer to confirm that the vial contains what the label says. Given that the sequence is published and short peptides are cheap to synthesise, it is equally plausible that a vial contains the right peptide and that it contains nothing.

• An unidentified receptor on hypothalamic POMC neurons — Not characterised

  Reduced food intake in mice and minipigs, apparently without gastric-emptying delay and without nausea behaviour. The receptor has not been identified, which is a substantial gap - it means there is no way to predict off-target effects or species differences.

• GLP-1 receptor — Not a target

  Explicitly ruled out in the source paper - GLP-1 receptor knockout mice still respond to BRP, which is the evidence that this is a genuinely distinct mechanism rather than a rediscovery.

Food intake fell within an hour of a single injection in animal studies, with the effect lasting a matter of hours. There is no human timeline because there is no human data.

There is nothing to say here that would be honest. No human dosing exists, no receptor is identified, and no interaction data of any kind is available. Combining an uncharacterised peptide with an approved drug means you cannot attribute anything that happens to either one.

Against every approved compound here: there is no comparison to make, because there is no human efficacy data. What makes BRP worth tracking rather than dismissing is the mechanism - if a non-incretin pathway can suppress appetite without engaging the emetic circuitry, that is a qualitatively different drug class rather than a better version of the existing one. The correct posture is to follow the phase 1 data when it appears, and not to be the phase 1 data.

$50–$200/month. Speculative research chemical pricing. Market observation, not verified pricing, and price here carries no information about identity or purity.

• ?No human data of any kind exists - no trial has been registered or reported as of mid-2026.
• ?The receptor BRP acts through has not been identified.
• ?The 12-residue sequence is published in the source paper but was not extracted and verified in this session.
• ?No pharmacokinetic parameters exist for any species in a form that was verified here.
• ?The nausea-free profile is inferred from animal behaviour and may not translate.
• ?Cost figures are market observations, not verified pricing.

• Prohormone cleavage prediction uncovers a non-incretin anti-obesity peptide Coassolo L et al., Nature, 2025 · PMID 40044869

  The entire evidence base for BRP. One paper, mouse and minipig data, no human trial.