We therefore investigated whether (1) NPB112 binds and functionally antagonizes hGCGR in vitro and invivo; (2) chronic treatment with NPB112 effectively lowers invivo blood glucose level in diabetic animal models; (3) NPB112 effectively reduces the hepatic glucose output in those animals; and (4) prolonged treatment with NPB112 leads to elevation in glucagon or any unexpected adverse reactions including hypoglycemia or other laboratory abnormalities in hGCGR mice. This evidence concerns the gene GCG and Hypoglycemia.