Infliximab is a monoclonal antibody, a human-mouse chimeric monoclonal antibody that inhibits TNF-α and prevents TNF-α from interacting with TNFR1 and TNFR2. Infliximab can be used to treat Crohn's disease and rheumatoid arthritis.

METHODS: Human lung cancer cells A549 were pretreated with ML162 (0.1-15 µM) for 4-24 h. TXNRD1 activity was measured with the RX1 activity probe.
RESULTS: RX1 signaling was significantly dose-dependently inhibited at ML162 concentrations of 0.5 µM or higher. there was also a fairly rapid onset of concentration-dependent inhibition of cellular TXNRD1 activity by ML162, and a 4 h incubation with 1 µM or higher ML162 treatment was sufficient to inhibit RX1 signaling. ML162 effectively inhibited cellular TXNRD1 activity.[1]
METHODS: Melanoma cells A2058 and A375 were pretreated with ferrostatin (10 µM), Z-VAD-FMK (10 µM), or necrosulfonamide (0.5 µM) for 24 h, and cell viability was measured after ML162 (1-16 µM) treatment.
RESULTS: ML162 caused cell death in a dose-dependent manner in the A2058 and A375 melanoma cell lines, which could be reversed by ferrostatin-1, a ferritin-specific inhibitor, but not by Z-VAD-FMK, an inhibitor of apoptosis, or necrosulfonamide, an inhibitor of necroptosis. [2]

METHODS: To detect anti-tumor activity in vivo, ML162 (40 mg/kg once daily) and anti-PD-1 antibody (200 µg every three days) were intraperitoneally injected into BALB/c mice bearing TS/A tumors once daily for two weeks.
RESULTS: The combination of GPX4 inhibitor and anti-PD-1 antibody significantly inhibited tumor growth compared to monotherapy. The combination therapy did not result in additional immune cell infiltration compared to monotherapy, but the combination therapy induced a significant immune response with an increased proportion of PRF1+CD8+ T cells and GZMB+CD8+ T cells. [3]