CRM1 degrader 1

CRM1 degrader 1 (compound 1l) inhibits the proliferation of MGC803 gastric cancer cells with an IC₅₀ value of 2.314 μM^[1].
CRM1 degrader 1 (1.25-10 μM; 24 h) reduces the viability of MGC803 and HGC27 gastric cancer cells in a dose-dependent manner; at 10 μM, the viability of the two gastric cancer cell lines decreases by approximately 40-60%, while almost no toxicity is observed in GES1 normal gastric epithelial cells^[1].
CRM1 degrader 1 (1.25-10 μM) reduces the mitochondrial membrane potential (MMP, ΔΨ) of MGC803 and HGC27 cells in a dose-dependent manner^[1].
CRM1 degrader 1 dose-dependently reduces CRM1 protein levels and increases p53 protein levels in MGC803 and HGC27 cells^[1].
CRM1 degrader 1 (10 μM; 6 h) reduces the co-immunoprecipitation signal of CRM1-p53 in MGC803 cells, promotes the nuclear accumulation of p53 and Ranbp1, and simultaneously decreases the cytoplasmic levels of Ranbp1 and CRM1^[1].
The reduction of CRM1 protein in MGC803 and HGC27 cells induced by CRM1 degrader 1 (5 μM; 24 h) is almost completely blocked by MG132 (0.05 μM), supporting that CRM1 degradation depends on the ubiquitin-proteasome pathway^[1].
The inhibitory effect of CRM1 degrader 1 on the viability of MGC803 cells is significantly attenuated after p53 siRNA knockdown, which supports the involvement of p53 in the cellular actions of CRM1 degrader 1^[1].
CRM1 degrader 1 (1.25-10 μM; 24 h) dose-dependently increases the proportion of Annexin V-positive cells in MGC803 and HGC27 cells, and induces cell apoptosis^[1].
CRM1 degrader 1 (1.25-10 μM; 24 h) reduces CRM1 protein levels and increases the levels of p53, cleaved PARP and cleaved caspase-3; it also increases Bax and cleaved caspase-9, and decreases Bcl-2 and Bcl-xL^[1].
CRM1 degrader 1 (10 μM; 24 h) acts synergistically with the proteasome inhibitor MG132 (HY-13259) to enhance apoptosis in MGC803 and HGC27 gastric cancer cells; the expression of pro-apoptotic proteins is still upregulated even though the degradation of CRM1 is blocked^[1].
Combination treatment with CRM1 degrader 1 (10 μM; 24 h) and MG132 (0.05 μM; 1 h pre-incubation) further enhances apoptosis in MGC803 and HGC27 cells, and increases the levels of p53, cleaved PARP, cleaved caspase-3 and Bax, compared with exposure to either agent alone^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.