Glibenclamide

Glibenclamide (Glyburide) is an orally active ATP-sensitive K⁺ channel (K_ATP) inhibitor and can be used for the research of diabetes and obesity^[1]. Glibenclamide inhibits P-glycoprotein. Glibenclamide directly binds and blocks the SUR1 subunits of K_ATP and inhibits the cystic fibrosis transmembrane conductance regulator protein (CFTR)^[3]. Glibenclamide interferes with mitochondrial bioenergetics by inducing changes on membrane ion permeability^[4]. Glibenclamide can induce autophagy^[5]. IC50 & Target: K_ATP^[1] In Vitro: Glibenclamide (Brown adipocytes; 10 μΜ; 1 day) has no effect on adipocyte differentiation. Glibenclamide (Ucp1-2A-GFP brown adipocyte) significantly increases UCP1 expression. Glibenclamide directly binds and blocks the SUR1 subunits of ATP-dependent potassium channels (K_ATP) and consequently increases insulin secretion from the pancreatic β cells^[2]. Glibenclamide interferes with mitochondrial bioenergy by permeating mitochondrial intima with Cl^- and promoting mitochondrial net Cl^-/K⁺ cotransport^[4]. Glibenclamide induced autophagy inhibits its insulin secretion-improving function in β cells^[5]. In Vivo: Glibenclamide (2 mg/kg; p.o.) increases of insulin release and rapid drop of blood glucose level^[2].
Glibenclamide (50 μg/kg; p.o.) does not cause significant change, such as body weight or body composition^[2].