BRP is a 12-peptide derived from BRINP2 that can cross the blood-brain barrier. BRP induces the central activation of FOS in neuronal cells via the cAMP-PKA-CREB signaling pathway. BRP exerts anorectic and anti-obesity effects without triggering nausea or aversive responses. The action of BRP is independent of the leptin, GLP-1 receptor and melanocortin 4 receptor pathways. BRP is applicable to obesity-related research [1].
In Vivo, BRP (0.5-20 mg/kg; i.p., i.n., i.c.v.; single dose) dose-dependently inhibits food intake in lean male and female C57BL/6J mice when administered via intraperitoneal, intranasal or intracerebroventricular routes[1]. BRP (5 mg/kg; i.p.; daily; 14 days) reverses obesity and improves glucose homeostasis in diet-induced obese male C57BL/6J mice by reducing food intake and fat mass[1]. BRP (2 mg/kg; i.m.; single dose) suppresses feeding behavior in male Yucatan miniature pigs without inducing anxiety-like behavior[1].
In Vitro, BRP (50-100 μg/mL; 0-24 h) induces potent, sustained, and non-desensitizing Fos expression in NS-1 rat neuronal cells, with EC50 values of 33.7 μM at 24 h and 37 μM at 1 h[1]. BRP (50-100 μg/ml; 0-24 h) induces potent, sustained and non-desensitizing Fos expression in mouse Neuro2a neuronal cells, with EC50 values of 33 μM at 24 h and 27 μM at 1 h, and activates the CREB and ERK1/2 signaling pathways[1]. BRP (100 μg/mL; 0-40 min) increases intracellular cAMP levels in Neuro2a mouse neuronal cells[1]. BRP (100 μg/mL; 15 min) induces phosphorylation of CREB at Ser133, phosphorylation of ERK1/2, and phosphorylation of PKA substrates in Neuro2a neuronal cells[1].
References:
[1]. Coassolo L, et al. Prohormone cleavage prediction uncovers a non-incretin anti-obesity peptide. Nature. 2025;641(8061):192-201.
In Vivo, BRP (0.5-20 mg/kg; i.p., i.n., i.c.v.; single dose) dose-dependently inhibits food intake in lean male and female C57BL/6J mice when administered via intraperitoneal, intranasal or intracerebroventricular routes[1]. BRP (5 mg/kg; i.p.; daily; 14 days) reverses obesity and improves glucose homeostasis in diet-induced obese male C57BL/6J mice by reducing food intake and fat mass[1]. BRP (2 mg/kg; i.m.; single dose) suppresses feeding behavior in male Yucatan miniature pigs without inducing anxiety-like behavior[1].
In Vitro, BRP (50-100 μg/mL; 0-24 h) induces potent, sustained, and non-desensitizing Fos expression in NS-1 rat neuronal cells, with EC50 values of 33.7 μM at 24 h and 37 μM at 1 h[1]. BRP (50-100 μg/ml; 0-24 h) induces potent, sustained and non-desensitizing Fos expression in mouse Neuro2a neuronal cells, with EC50 values of 33 μM at 24 h and 27 μM at 1 h, and activates the CREB and ERK1/2 signaling pathways[1]. BRP (100 μg/mL; 0-40 min) increases intracellular cAMP levels in Neuro2a mouse neuronal cells[1]. BRP (100 μg/mL; 15 min) induces phosphorylation of CREB at Ser133, phosphorylation of ERK1/2, and phosphorylation of PKA substrates in Neuro2a neuronal cells[1].
References:
[1]. Coassolo L, et al. Prohormone cleavage prediction uncovers a non-incretin anti-obesity peptide. Nature. 2025;641(8061):192-201.