Stanford Medicine researchers have identified a naturally occurring 12-amino-acid peptide called BRP that suppressed appetite and drove fat loss in animals, with a mechanism that looks narrower than the one behind semaglutide.
The work was done in laboratory neurons, lean mice, obese mice and minipigs. No human testing has begun, and senior author Katrin Svensson, an assistant professor of pathology, says the team is eager to learn whether BRP is safe and effective in people. The study was published in Nature.
Why the brain target matters
Semaglutide (sold as Ozempic and Wegovy) mimics the hormone GLP-1, whose receptors sit in the brain but also the gut, pancreas and other tissues. That spread, Svensson said, is why the drug slows the movement of food through the digestive tract and lowers blood sugar alongside its effect on appetite.
BRP appears to act specifically in the hypothalamus, the region that governs hunger and energy use. The researchers report it activates different populations of brain cells rather than copying GLP-1 signaling.
How an algorithm found it
The team built a program called Peptide Predictor and ran it across the roughly 20,000 genes encoding human proteins, looking for sequences an obesity-linked enzyme was likely to cut. Filtering for secreted proteins with at least four cut sites narrowed the field to 373 prohormones and an estimated 2,683 possible peptides.
From there, 100 peptides were tested on cultured nerve cells. GLP-1 tripled neuronal activity against untreated controls; BRP increased it tenfold, which is what pulled it out of the pile.
Key results
In the hour after a muscle injection, treated animals ate up to 50% less food than expected. Over 14 days of daily injections, obese mice lost an average of 3 grams while controls gained about 3 grams, and nearly all of the loss came from fat rather than muscle.
The treated animals also showed improved glucose and insulin tolerance. Researchers monitoring movement, water intake, anxiety-related behavior and fecal output found no significant differences from controls, which is notable given that constipation is a known side effect of GLP-1 drugs.
Limitations
These are animal experiments, and the source is explicit that animal work cannot establish whether BRP would prevent nausea in people. The receptors BRP binds have not been identified, and peptides break down quickly, so durability is unresolved. Svensson and Coassolo are named inventors on BRP patents, and Svensson cofounded a company to develop it.
Bottom line
A tenfold neuronal response and a clean behavioral panel in two species is a genuinely interesting start, and the algorithm-first discovery route may matter more long term than this one molecule. Everything that counts, safety, dosing and whether any of it holds in humans, is still ahead.
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