Hyperglycemia is a defining characteristic of type 2 diabetes mellitus and is a 
major risk factor associated with the development of many microvascular 
complications. There are numerous therapies currently available to treat 
hyperglycemia, but glycemic control rates remain poor. One potential reason is 
the decline in ß-cell function over time, which decreases the effectiveness of 
therapies that rely on insulin action. The kidney occupies a central position in 
the control of glucose homeostasis by its role in gluconeogenesis and by 
regulating glucose excretion. Under normal conditions, glucose filtered by the 
kidney is virtually totally reabsorbed in the proximal tubule by the 
sodium-glucose co-transporter 2 (SGLT2). Inhibition of SGLT2 is an attractive, 
insulin-independent target for increasing glucose excretion in the setting of 
hyperglycemia. A number of SGLT2 inhibitors have been synthesized, and results 
from preclinical studies have shown that they increase glucose excretion and 
normalize plasma glucose in diabetic models. Initial clinical data are promising 
and suggest that SGLT2 inhibitors may be a new therapeutic option for treating 
type 2 diabetes mellitus.