<unk>  selectively binds to sulfonylurea receptors (SUR-1) on the surface of the pancreatic beta-cells. It was shown to provide cardiovascular protection as it does not bind to sulfonylurea receptors (SUR-2A) in the heart. This binding effectively closes these K+ ion channels. This decreases the efflux of potassium from the cell which leads to the depolarization of the cell. This causes voltage dependent Ca2+ ion channels to open increasing the Ca2+ influx. The calcium can then bind to and activate calmodulin which in turn leads to exocytosis of insulin vesicles leading to insulin release. The mouse model of MODY diabetes suggested that the reduced<unk>  clearance stands behind their therapeutic success in human MODY patients, but Urbanova et al. found that human MODY patients respond differently and that there was no consistent decrease in<unk>  clearance in randomly selected HNF1A-MODY and HNF4A-MODY patients. Its classification has been ambiguous, as literature uses it as both a first-generation and second-generation sulfonylurea.
Gliclazide
Glibenclamide
Linaclotide
Liranaftate
Lobeglitazone
Miglitol
Linagliptin
Saxagliptin