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.
IC50 & Target
IC50: NF-κB2
(In Vitro)
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.
(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[1].
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.