Эмпаглифлозин

Empagliflozin, a sodium-glucose co-transporter 2 (SGLT2) inhibitor, was originally discovered by Boehringer Ingelheim and codeveloped and co-marketed through research collaboration with Eli Lilly and Co. It was first approved by European Medicine Agency (EMA) in May 2014, followed by the approval of the US FDA in August 2014. SGLT2 inhibitors are anewclass of glucose-lowering agents developed for the treatment of type 2 diabetes mellitus, which have a mechanism of action that is independent of pancreatic b-cell function or the degree of insulin resistance. Consequently, SGLT2 inhibitors have the potential to be of use not only as standalone therapy but also in combination with any of the existing classes of glucose-lowering agents, including insulin. Empagliflozin selectively inhibits SGLT2, which in turn prevents glucose reabsorption by excreting excess glucose in the urine.

Empagliflozin is a novel, potent and selective SGLT-2 inhibitor, improves glycaemic control and features of metabolic syndrome in diabetic rats.

ChEBI: Empagliflozin is a C-glycosyl compound consisting of a beta-glucosyl residue having a (4-chloro-3-{4-[(3S)-tetrahydrofuran-3-yloxy]benzyl}phenyl group at the anomeric centre. A sodium-glucose co-transporter 2 inhibitor used as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus. It has a role as a sodium-glucose transport protein subtype 2 inhibitor and a hypoglycemic agent. It is a C-glycosyl compound, an aromatic ether, a tetrahydrofuryl ether and a member of monochlorobenzenes.

Empagliflozin is an orally available competitive inhibitor of sodium-glucose co-transporter 2 (SGLT2; SLC5A2) with antihyperglycemic activity. Upon oral administration, empagliflozin selectively and potently inhibits SGLT2 in the kidneys, thereby suppressing the reabsorption of glucose in the proximal tubule. Inhibition of SGLT2 increases urinary glucose excretion by the kidneys, resulting in a reduction of plasma glucose levels in an insulin-independent manner. Inhibition of SGLT2 in the kidneys also suppresses the renal reabsorption of 1,5-anhydroglucitol (1,5AG). This lowers serum 1,5AG and neutrophil 1,5-anhydroglucitol-6-phosphate (1,5AG6P) levels, which may improve neutropenia and neutrophil dysfunction in patients with glycogen storage disease type Ib (GSD Ib). SGLT2, a transport protein exclusively expressed in the proximal renal tubules, mediates approximately 90% of renal glucose reabsorption from tubular fluid.
pubchem.ncbi.nlm.nih.gov/compound/Empagliflozin