A peptide that targets hunger centers
Stanford researchers flagged a brain/CSF peptide called BRINP2 that appears to act on the hypothalamus in ways similar to GLP‑1 drugs and could influence appetite and metabolism without the same muscle loss or GI side effects reported for some therapies. (x.com) The work is still at an early, mechanistic stage but points to alternative ways to modulate central appetite circuits. (x.com)
Appetite drugs work by dialing down the body’s “eat now” signals, and Stanford researchers say a 12-amino-acid peptide called BRP may do that by acting mainly in the brain’s hypothalamus. (med.stanford.edu) The peptide’s full name is BRINP2-related peptide, or BRP. In a Nature paper published March 5, 2025, Stanford’s Katrin Svensson and lead author Laetitia Coassolo reported that BRP reduced food intake and had anti-obesity effects in mice and pigs. (nature.com; pubmed.ncbi.nlm.nih.gov) The team found BRP by using a computational tool to scan more than 2,600 previously uncharacterized peptide fragments generated from human proteins by prohormone convertases, the enzymes that cut larger proteins into smaller signaling pieces. (pubmed.ncbi.nlm.nih.gov; nature.com) That matters because today’s best-known obesity drugs, including semaglutide-based medicines, mimic glucagon-like peptide-1, a gut hormone released after eating. Those drugs act in several organs, including the brain, gut and pancreas, and they are commonly associated with gastrointestinal side effects. (med.stanford.edu; med.stanford.edu) Stanford said BRP appears to take a narrower route. Svensson said semaglutide’s receptors are spread across multiple tissues, while BRP “appears to act specifically in the hypothalamus,” the brain region that helps regulate appetite and metabolism. (med.stanford.edu) In the animal work, the researchers reported that BRP suppressed appetite and reduced weight gain without causing nausea, constipation, food aversion or the significant lean-muscle loss seen with some current therapies. The paper also said the effect was independent of leptin, the glucagon-like peptide-1 receptor and melanocortin 4 receptor pathways. (med.stanford.edu; pubmed.ncbi.nlm.nih.gov; lifescience.net) The mechanistic work points to a specific brain circuit. A Journal of the Endocrine Society meeting abstract described BRP as circulating in human cerebrospinal fluid and said it activates a central cyclic AMP-protein kinase A-CREB-Fos signaling pathway in POMC-negative hypothalamic neurons. (academic.oup.com; pubmed.ncbi.nlm.nih.gov) The findings are still preclinical. The Stanford study was done in animals, not people, and the Stanford news release said Svensson has co-founded a company, Merrifield Therapeutics, to move toward human clinical trials. (med.stanford.edu; crossmark.crossref.org) Nature Reviews Endocrinology summarized the result in one line: a “novel anti-obesity peptide” that targets the hypothalamus. For now, that means a new lead in the search for weight-loss drugs that may change appetite by acting closer to the brain’s control center. (nature.com)
