Diabetes mellitus is a complex metabolic disorder characterized by impaired glucose homeostasis and chronic inflammation. In recent years, the role of various molecular targets in the pathogenesis of diabetes has gained significant attention. This study aimed to explore the potential therapeutic effects of Vildagliptin, a dipeptidyl peptidase-4 (DPP-4) inhibitor, against key diabetic targets including interleukin-1 β (IL-1 β), phosphoinositide 3-kinase (PI3K), and Akt substrate of 160 kDa (AS160). IL-1 β is a pro-inflammatory cytokine known to contribute to the development of insulin resistance and pancreatic β-cell dysfunction. Experimental evidence suggests that Vildagliptin may exert an inhibitory effect on IL-1β production and signaling, thereby attenuating inflammation in diabetes. The PI3K/Akt pathway plays a crucial role in glucose metabolism and insulin signaling. Impaired PI3K signaling has been implicated in insulin resistance, a hallmark of type 2 diabetes. Studies have demonstrated that Vildagliptin treatment can enhance PI3K activity, leading to improved insulin sensitivity and glucose uptake in peripheral tissues. AS160, an Akt substrate, regulates glucose transport by modulating the translocation of glucose transporter 4 (GLUT4) to the plasma membrane. Reduced AS160 phosphorylation has been observed in insulin-resistant states. Vildagliptin has been reported to enhance AS160 phosphorylation, promoting GLUT4 translocation and enhancing glucose uptake in skeletal muscle and adipose tissue. This study comprehensively examines the effects of Vildagliptin on IL-1β, PI3K, and AS160 in the context of diabetes using molecular docking