Metabolic reprogramming is a hallmark of cancer that promotes tumor progression and immune evasion. Pyruvate kinase M2(PKM2), a key glycolytic enzyme frequently expressed in tumor tissues, regulates glycolytic flux and cellular metabolism. Metabolic alterations in tumors, including extracellular acidification, may influence the expression of immune checkpoint molecules such as programmed death-ligand 1 (PD-L1). In this study, we investigated whether pharmacological activation of PKM2 using TEPP-46 alters tumor metabolism and PD-L1 expression in triple-negative breast cancer (TNBC) cells. Metabolic activity was evaluated by measuring extracellular acidification rate (ECAR), and PKM2 oligomerization status was analysed after TEPP-46 treatment. PD-L1 expression and JAK/STAT signalling were examined to explore mechanisms linking metabolic regulation and immune checkpoint expression. TEPP-46 treatment did not induce significant cytotoxicity in MDA-MB-231 cells but reduced glycolytic activity, indicated by decreased ECAR. PKM2 oligomerization analysis showed an increased tetrameric PKM2 fraction after TEPP-46 treatment. TEPP-46 also reduced PD-L1 expression and altered JAK/STAT3 signalling, including decreased levels of p-JAK1/2, HIF-1α, and p-STAT3. Long-term TEPP-46 treatment suppressed tumor spheroid growth in MDA-MB-231 cells. These findings suggest that PKM2-mediated metabolic reprogramming may regulate PD-L1 expression and contribute to tumor immune tolerance in TNBC cells.