Voglibose (Glustat), an N-substituted derivative of valiolamine, exhibits excellent inhibitory activity against α-glucosidases and action against hyperglycemia and various disorders caused by hyperglycemia.

Voglibose can inhibit the intestinal α-glucosidases, which are responsible for the digestion of disaccharides such as maltose and sucrose, including maltase and sucrase. The Ki values of Voglibose for sucrase and maltase are about 106and 105 times smaller than the Km values for sucrose and maltose. [1]

Voglibose (0.2 mg/kg) completely inhibits the insulin response to sucrose in rats. Voglibose (0.2 mg/kg) reduces the carbohydrate-induced increase in blood glucose in rats. Voglibose (0.2 mg/kg) reduces the carbohydrate-induced increase in blood glucose without causing sustained hypoglycemia in both normal and neonatal streptozotocin-induced diabetic rats. [2] Voglibose (0.001%) treatment increases GLP-1 secretion (Voglibose alone, 1.6-fold; Alogliptin plus Voglibose, 1.5-fold), while it decreases plasma glucose-dependent insulinotropic polypeptide (GIP) (Voglibose alone, 30%; Alogliptin plus voglibose, 29%) in prediabetic db/db mice after 3 weeks. Voglibose (0.001%) treatment decreases plasma DPP-4 activity by 15% in prediabetic db/db mice. Voglibose (0.001%) treatment increases plasma insulin by 1.8-fold and decreases plasma glucagon by 8% in prediabetic db/db mice. [3] Voglibose (0.001% and 0.005%) stimulates GLP-1 secretion in ob/ob mice, as evidenced by the 1.3- to 1.5-fold increase in plasma active plus inactive amidated GLP-1 levels. Voglibose (0.001% and 0.005%) decreases plasma DPP-4 activity unexpectedly by 40% to 51% in ob/ob mice, resulting from reduced plasma DPP-4 concentrations. Voglibose (0.001% and 0.005%) increases GLP-1 content by 1.5- to 1.6-fold and 1.4- to 1.6-fold in the lower intestine and colon, respectively, in ob/ob mice. [4]