Purpose <p>Nasopharyngeal carcinoma (NPC) is the most common cancer in Southern China. In this study, we investigated the anti-NPC effect of delphinidin (DN) on MAPK/Akt/STAT-2, vis induces apoptotic signalling in human NPC cells -in vitro and in silico-based work.</p> Methods <p>Cell viability and apoptosis were confirmed by MTT assays and AO/EtBR, DAPI, and PI staining. RT‑qPCR used to analyze pro‑apoptotic genes (caspase‑3, caspase‑8, caspase‑9) and survival‑related genes in the PI3K/AKT/mTOR together with modulation of MAPK components (ERK1/2, p38, JNK). In silico molecular docking revealed that DN interacts with multiple proliferation‑ and apoptosis‑related proteins—such as MAPK, Akt, PI3K, mTOR, Jun, ERK1, PARP2, CDK, Cyclin‑B1, Cyclin‑D3, CDC2, CDC6, Bax, Bcl‑2, caspase‑3, caspase‑9, and STAT‑2—with low binding energy and high binding affinity.</p> Results <p>DN inhibited NPC cell viability and induced apoptosis; we used in-silico analysis. DN therapy causes a dose-dependent up-regulation of pro-apoptotic genes, particularly caspase-3, caspase-8, and caspase-9, according to RT-qPCR research. On the other hand, the substance successfully suppresses the expression of genes that promote survival in the PI3K/AKT/mTOR signalling axis and modifies elements of the MAPK pathway, such as ERK1/2, p38, and JNK. The docking analysis of DN with cell proliferation markers, Cell cycle regulation protein and apoptotic marker by in silico. Docking analysis was used in this study to predict the DN interaction with interacting amino acid residues in proteins that have a low binding energy and a greater binding affinity. These findings indicate that DN exerts a cytostatic effect through apoptosis by targeting the MAPK/Akt/STAT-2 pathway, supporting the study in human nasopharyngeal carcinoma cells.</p> Conclusions <p>Therefore, DN is a promising therapeutic agent for treating human nasopharyngeal cancer cells. DN as an adjunct or targeted intervention for the management of nasopharyngeal carcinoma (NPC).</p>