Ipragliflozin exhibits antihyperglycemic effects, with dose-dependent inhibition of increases in blood glucose levels. In both STZ-induced type 1 diabetic rats and KK-Ay type 2 diabetic mice, this effect is significant at various tested doses^[1].

In streptozotocin-induced type 1 diabetic rats, repeated administration of Ipragliflozin (0.3 and 1 mg/kg) demonstrates antidiabetic effects^[1].

In Streptozotocin (STZ; 50 mg/kg)-induced type 1 diabetic rats and KK-Ay type 2 diabetic mice, doses ranging from 0.1 to 1 mg/kg were orally administered once in the fed state. Blood glucose levels were then monitored for 8 hours under fasting conditions. The results indicated a dose-dependent reduction in blood glucose levels, which was statistically significant at all tested doses. This experiment utilized a repeated administration animal model^[1].

In Streptozotocin (STZ; 50 mg/kg)-induced type 1 diabetic rats, doses of 0.3 and 1 mg/kg were orally administered once daily at night for 4 weeks. The outcome revealed significant reductions in both HbA1c and blood glucose levels. Furthermore, pancreatic insulin content significantly increased at a dose of 1 mg/kg. Urinary glucose excretion exhibited a dose-dependent increase, reaching significance at the 1 mg/kg dose^[1].

In MCF-7 human breast cancer cell lines, Ipragliflozin (1-50 μM) significantly and dose-dependently suppresses growth. Knocking down SGLT2 expression using siRNA abolishes the attenuation of cell proliferation induced by Ipragliflozin, indicating its action through SGLT2 inhibition. Additionally, Ipragliflozin at high doses (50 and 100 μM) significantly inhibits DNA synthesis of MCF-7 cells, as revealed by BrdU assay^[2].