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) inhibits DMXAA-induced nuclear translocation of RelB in BMDCs[1].SN52 does not change the activation of canonical NF-κB signaling. The nuclear translocation of RelB is increased in DCs isolated from irradiated tumors, and SN52 abolishes this activation in activated DC cells[1].SN52 (40 μg/mL; 30 mins before co-cultured with irradiated or non-irradiated MC38 cells) inhibits the non-canonical NF-κB and increases?Ifn-b?expression in BMDCs stimulated with irradiated tumor cells[1].

SN52 (intrathecal injection; 40 μg/ml; day-1, day 1 and day 3 of 20Gy radiation of radiation) combines with IR enhances anti-tumor immune functions of both DCs and CD8 + T cells and subsequently reduced tumor burden more effectively compared with IR alone[1]. Animal Model: Tumor mice model[1]Dosage: 40 μg Administration: Intrathecal injection; 40 μg; day-1, day 1 and day 3 of 20Gy radiation of radiation Result: Reduced tumor burden than IR group alone.

Induced non-canonical NF-κB inhibition and potentiates the anti-tumor effect of IR.