Recent crystallographic studies have shown that BMS-202, a small molecule compound with a methoxy-1-pyridine chemical structure, interacts well with PD-L1 dimerization. However, its roles and mechanisms of BMS-202 in glioma have not yet been reported. The aims of this work were to study BMS-202 antitumor activity and its underlying mechanisms in glioma. In the study, the multi-omics and bioinformatics tools, a series of experiments, including CCK-8, flow cytometry, co-immunoprecipitation, siRNA transfection, PCR, western blot, and cell migration and invasion, were performed to investigate the underlying mechanisms of BMS-202 in glioma. BMS-202 was shown to inhibit glioma cell proliferation and invasion. Mechanistically, BMS-202 downregulated PD-L1 expression on the GBM cell surface and regulated PD-L1/AKT/BCAT1 signaling pathways in an mTOR-independent manner. BMS-202 is expected to delay metabolism and extend life span. Thus, our data identify that BMS-202 potentially acts as an effective candidate for patients diagnosed with GBM.