Beta-3 adrenergic receptor (ADRB3)

The Beta-3 adrenergic receptor (ADRB3) is a member of the beta-adrenergic receptor family, which are G protein-coupled receptors primarily responsive to catecholamines such as epinephrine and norepinephrine[1][6][7]. It is most abundantly expressed in adipose tissue, where it promotes lipolysis and thermogenesis, and in the bladder, where it mediates relaxation of smooth muscle[1][2][6]. Activation of this receptor by selective agonists leads to increased intracellular cAMP, driving its biological activities. Clinically, beta-3 agonists such as mirabegron and vibegron have become established therapies for overactive bladder syndrome; ongoing research also explores roles for beta-3 adrenergic targeting in metabolic, cardiovascular, and potentially neurological disease and cancer[1][2][3][6]. The receptor is targeted by a range of experimental and approved therapeutics, and genetic variation in ADRB3 may influence metabolic function and drug responsiveness[2]. Its tissue expression profile, molecular signaling, and role in disease make it an important and validated therapeutic target.

Other names

Beta-3 adrenoceptorβ3-adrenergic receptorβ3-adrenoceptorADRB3Beta-3 AR

Agonists increase cAMP via Gs-protein–stimulated adenylyl cyclase activation, leading to smooth muscle relaxation (notably bladder), lipolysis, and thermogenesis[1][2][3]. Some agonists (e.g., mirabegron) cause bladder muscle relaxation by direct activation, used to treat overactive bladder[1][2][3]. Agonists and some beta-blockers (nebivolol) may induce vasodilation via nitric oxide pathways[2][3]. Antagonists inhibit cAMP production and block receptor-mediated physiological effects.