SN52 is a powerful, competitive, and cell-permeable inhibitor of NF-κB2. It is a variant of the SN50 peptide. SN52 effectively prevents the nuclear translocation of p52-RelB heterodimers, exhibiting a robust radiosensitization effect on prostate cancer cells. This compound holds significant potential for cancer research purposes.

SN52 (40 μg/ml; 30 mins before DMXAA) effectively prevents DMXAA-induced nuclear migration of RelB in BMDCs[1]. It does not affect the canonical NF-κB signaling pathway. Moreover, while the nuclear relocation of RelB intensifies in DCs from irradiated tumors, SN52 negates this effect in activated DC cells[1]. Additionally, when pre-treated (40 μg/mL; 30 mins prior) and co-cultured with both irradiated and non-irradiated MC38 cells, SN52 not only impedes the non-canonical NF-κB pathway but also elevates Ifn-b expression in BMDCs influenced by irradiated tumor cells[1].

SN52, administered via intrathecal injection at a dosage of 40 μg/ml on days -1, 1, and 3 during a 20Gy radiation course, synergistically enhances the antitumor immune responses of dendritic cells (DCs) and CD8+ T cells when combined with ionizing radiation (IR), leading to a more effective reduction in tumor burden in a tumor mouse model compared to IR treatment alone. This combination also induces non-canonical NF-κB inhibition, further potentiating IR's antitumor efficacy.