Those taking Ozempic so far have to accept nausea, constipation, and muscle loss. Stanford researchers have now identified a naturally-occurring peptide called BRP that in animal models suppresses appetite just as strongly as semaglutide, without causing these side effects. They discovered it using an AI tool that scanned all 20,000 human protein-coding genes.
What is BRP and where does it come from?
BRP stands for BRINP2-related peptide. It is a naturally occurring molecule that the human body produces itself, consisting of just twelve amino acids. The parent molecule is the protein BRINP2, from which BRP is enzymatically released as a small fragment.
The research team led by Dr. Katrin Svensson, assistant professor of pathology at Stanford University, with lead author Dr. Laetitia Coassolo, found BRP not through classical laboratory search but via algorithm. Their AI tool called Peptide Predictor scanned all 20,000 human protein-coding genes, identified 373 candidate prohormones, and distilled 2,683 potential peptide fragments, of which 100 were selected for lab testing. BRP prevailed. The original work appeared in March 2025 in Nature (Vol. 641); a follow-up study using miniature pig data published by the team in July 2026 confirmed results on an animal model with metabolism more similar to humans.
Why Ozempic has so many side effects
Semaglutide, the active ingredient in Ozempic and Wegovy, acts as a GLP-1 agonist: it binds to receptors in the digestive tract, pancreas, and brain. This broad effect explains both efficacy and side effects. Nausea occurs in up to 44 percent of patients, constipation in around 24 percent. Add muscle loss: in the STEP1 study, 39 to 40 percent of total weight loss with semaglutide came from muscle mass, which long-term reduces body strength and fall stability.
BRP does not take this path. It specifically activates POMC neurons (proopiomelanocortin neurons) in the hypothalamus, the brain region regulating hunger and satiety. The signal cascade proceeds via molecules cAMP, PKA, CREB, and FOS, completely separate from the GLP-1 system. In cell experiments, BRP activated these neurons tenfold more strongly than untreated control cells, according to the study. Since the effect remains confined to the brain, gastrointestinal effects are eliminated.
What the animal data show
Obese mice receiving daily BRP injections reduced food intake by up to 50 percent within an hour of injection. Over 14 days, these animals lost an average of three grams of body fat; the control group gained three grams in the same period. Muscle mass remained preserved, nausea responses were not observed, glucose and insulin tolerance improved.
For the follow-up study, the team tested BRP on miniature pigs, whose metabolism is significantly more similar to humans than that of mice. There too, animals reduced food intake substantially after a single injection, without stress responses or digestive disturbances. Svensson explained that BRP appeared to work specifically in the hypothalamus, which controls appetite and metabolism.
In comparison: how long other obesity drugs took
Semaglutide was originally developed as a diabetes medication. It received FDA approval in 2017 as Ozempic, for obesity only in 2021 as Wegovy, roughly 25 years after initial GLP-1 laboratory work in the early 1990s. Tirzepatide (Zepbound) from Eli Lilly, a dual GLP-1/GIP agonist, received FDA approval for obesity in November 2023 and showed weight loss of up to 15.7 percent in the SURMOUNT-2 study in people with obesity and type 2 diabetes. Both drugs share known gastrointestinal side effects.
Demand for alternatives is real: roughly one-third of semaglutide patients discontinue therapy in the first year due to intolerance, as analysis of U.S. insurance data shows. Globally, over one billion adults are affected by obesity, according to the World Health Organization.
Three conditions for clinical breakthrough
Dr. Svensson has founded Merrifield Therapeutics, a spinoff, to advance BRP into clinical development. Human trials have not yet begun, no IND application (Investigational New Drug) with the FDA has been announced. In the best case, industry experts expect five to seven years until possible approval.
Three hurdles must be cleared. First, BRP must work in the human hypothalamus just as effectively as in mice and miniature pigs. That is not certain: many obesity candidates have convincingly passed animal trials and failed in phase II human studies. The FDA demands randomized controlled trials with hundreds of participants over months. Second, the supply problem must be solved. Peptides are broken down in the digestive tract, making a tablet difficult. Likely, like semaglutide, a weekly injection or depot patch would be needed. Third, all safety data so far come from experiments lasting at most 14 days. Long-term effects in humans are completely unknown.
What speaks to the seriousness of the approach is that the Stanford research group founded the commercial spinoff Merrifield Therapeutics only after animal data were replicated and published in Nature, not before. Whether BRP clears clinical hurdles will become clearer earliest in 2028 or 2029. What is now clear: AI-guided search for endogenous peptides opens a systematic research field for pharmacology that was barely tapped before.