Benzosceptrin C is a PD-L1 inhibitor that promotes the degradation of programmed cell death ligand (PD-L1) via a lysosomal pathway, enhances T-cell cytotoxicity, and demonstrates antitumor activity [1].

Benzosceptrin C (0-10 μM) inhibits PD-L1 expression in CRC cancer cells, thereby enhancing T cell cytotoxicity by disrupting the PD-L1 checkpoint, and impedes the proliferation of CRC cancer cells RKO and HCT116. It promotes lysosomal degradation of PD-L1 by blocking its palmitoylation through the inhibition of DHHC3 activity, which prevents the direct interaction between PD-L1 and PD-1, exerting an immune antitumor effect [1]. In a Cell Proliferation Assay with a concentration of 0-10 μM over 24 days, it demonstrated a dose-dependent inhibition of tumor cell proliferation. Western Blot Analysis showed reduced PD-L1 levels in RKO and HCT116 cells in a time- and dose-dependent manner after 24 hours [1].

Benzosceptrin C, administered at 5-50 mg/kg/day via intraperitoneal injection for 16 days, suppresses tumor growth in MC38 xenograft C57BL/6 mice by activating tumor-infiltrating T cells and inducing apoptosis. [1] Animal Model: MC38 xenograft C57BL/6 mice [1] Dosage: 5-50 mg/kg Administration: i.p., Once a day for 16 days Result: Tumor growth inhibition (TGI) of 30.4% and 43.1% was observed at doses of 25 and 50 mg/kg, respectively, with the presence of T cells.