SN52 is a potent, competitive, and cell-permeable inhibitor of NF-κB2 . SN52 is a variant of the SN50 peptide and inhibits the nuclear translocation of p52-RelB heterodimers. SN52 has a strong radiosensitization effect on prostate cancer cells. SN52 can be used for cancer research In Vitro SN52 (40 μg/ml; 30 mins before DMXAA) inhibits DMXAA-induced nuclear translocation of RelB in BMDCs. 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. 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. MCE has not independently confirmed the accuracy of these methods. They are for reference only. In Vivo 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 . MCE has not independently confirmed the accuracy of these methods. They are for reference only. Animal Model: Tumor mice model 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. Form:Solid IC50& Target:IC50: NF-κB2