BRP (BRINP2-Related Peptide)

Published in Nature (March 2026) by Coassolo et al., BRP emerged from a model trained to predict which fragments of inactive prohormones are proteolytically cleaved into bioactive peptides. In mice and minipigs, a single injection before feeding reduced food intake by up to 50% within an hour; 14 daily injections in obese mice produced roughly 4 g of fat-predominant weight loss (versus 3 g gained by controls), with improved glucose and insulin tolerance and no measurable loss of lean mass.

Unlike GLP-1 agonists, treated animals showed no signs of nausea, delayed gastric emptying, or reduced activity/anxiety-like behavior in testing. A company co-founded by senior author Katrin Svensson has indicated plans to begin human trials, but none had started as of this writing.

// POMC NEURON ACTIVATION

BRP activates pro-opiomelanocortin (POMC) neurons in the hypothalamus, triggering an intracellular cAMP-PKA-CREB-FOS signalling cascade — a direct-neuronal mechanism rather than the peripheral incretin-receptor route GLP-1 drugs use.

// UNIDENTIFIED RECEPTOR

The specific cell-surface receptor BRP binds has not yet been identified; the research team describes this as an open question under active investigation.

// MINIMAL PHARMACOPHORE

Structure-activity work found that both the leucine at position 8 and C-terminal amidation are required for activity — removing either eliminates the appetite-suppressing effect.

Preclinical only. No human dosing, safety data, or purity standards exist. No CAS number has been assigned. Any product marketed as "BRP" today is unregulated research material at best, sourced well ahead of any human trial data.