In diabetic rats induced by a high-fat diet and streptozotocin, saxagliptin treatment at 1 mg/kg for 12 weeks leads to significant improvements in pancreatic insulin secretion capacity and an increased β-cell to α-cell areas ratio^[1].

Saxagliptin also demonstrates dose-dependent inhibition of plasma DPP-4 activity in Han-Wistar rats, achieving about 70% inhibition with 1 mg/kg and approximately 90% with 10 mg/kg at 7 hours post-dose. At 24 hours post-dose, approximately 20% and 70% inhibition levels are observed, respectively^[2].

Saxagliptin hydrochloride has the potential for type 2 diabetes mellitus research. In vitro, treatment with Saxagliptin 100 nM for 48 hours, Saxagliptin significantly induces β-cell proliferation. This proliferation is accompanied by increases in phosphorylated AKT and active β-catenin protein levels, along with elevated expression of c-myc and cyclin D1 proteins^[1].

Saxagliptin's mechanism involves the inhibition of DPP-4 activity, which prevents the degradation of glucagon-like peptide-1, thus promoting insulin secretion while decreasing glucagon secretion^[3].