BRS3

BRS3, or bombesin receptor subtype-3, is a G protein-coupled receptor in the bombesin receptor family. It is encoded by the BRS3 gene in humans and is generally treated as an orphan receptor because a definitive endogenous ligand has not been identified in humans. In non-human species and in experimental systems, bombesin-related peptides such as gastrin-releasing peptide and neuromedin B can activate BRS3, but ligand specificity and physiological relevance can vary.

Expression studies show that BRS3 is enriched in the central nervous system, particularly in the hypothalamus, with additional expression in peripheral tissues. Its physiological roles are linked to energy balance and feeding regulation, and it may influence autonomic functions, thermogenesis, and glucose homeostasis. Genetic deletion or disruption of BRS3 in mice leads to obesity and altered feeding patterns, while pharmacological activation in rodent models can reduce food intake and promote energy expenditure, indicating a role in appetite control and metabolism.

Pharmacologically, researchers have identified several small molecules that act as BRS3 agonists or antagonists in vitro. However, no BRS3-targeted therapies have been approved for clinical use, and translational research remains ongoing. The receptor is of interest as a potential target for obesity and metabolic disorder interventions, but its exact endogenous signaling mechanisms and therapeutic potential in humans require further clarification.

See also: Bombesin receptor family, GRPR, NMBR.