For research use only. Not for therapeutic Use.
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[1].
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].
| Catalog Number | I044203 |
| CAS Number | 1071173-56-2 |
| Molecular Formula | C128H230N38O28 |
| Purity | ≥95% |
| Reference | [1]. Yong Xu, et al. SN52, a novel nuclear factor-kappaB inhibitor, blocks nuclear import of RelB:p52 dimer and sensitizes prostate cancer cells to ionizing radiation. Mol Cancer Ther [2]. Yuzhu Hou, et al. Non-canonical NF-κB Antagonizes STING Sensor-Mediated DNA Sensing in Radiotherapy. Immunity. 2018 Sep 18;49(3):490-503.e4 |
