NF-κB-IN-22

NF-κB-IN-22 (complex 11) (72 h) potently inhibits the proliferation of NCI-H460, HepG-2, HCT-116, and MGC-803 cancer cells, with IC₅₀ values ranging from 0.38 to 0.91 μM after 72 h of incubation^[1].
NF-κB-IN-22 (72 h) effectively inhibits the proliferation of cisplatin-sensitive A549 and Cisplatin-resistant A549/CDDP lung cancer cells, with IC₅₀ values of 0.31 μM and 0.57 μM, respectively; it exhibits low toxicity toward normal HL-7702 and BEAS-2B cells^[1].
NF-κB-IN-22 (1 mM) remains stable in PBS at pH 7.4 and 5.5, undergoes partial degradation in cell culture medium containing 10% FBS, and can undergo reductive activation in the presence of ascorbic acid to release ligand 6 and Oxaliplatin^[1].
NF-κB-IN-22 (10 μM; 12 h) induces significantly higher intracellular platinum accumulation in A549 and A549/CDDP cells than Oxaliplatin (HY-17371) or the Oxaliplatin/1a combination^[1].
NF-κB-IN-22 (5 μM; 24 h with TNF-α stimulation) effectively inhibits TNF-α-induced activation of the NF-κB pathway in A549 cells by reducing the phosphorylation levels of p65, IKKβ and IκBα^[1].
NF-κB-IN-22 (5 μM; 24 h with TNF-α stimulation) effectively blocks TNF-α-induced nuclear translocation of phosphorylated NF-κB/p65 in A549 cells^[1].
NF-κB-IN-22 (5 μM; 24 h) effectively induces apoptosis in A549 cells, arrests the cells at the G2/M phase, and significantly inhibits their migration and invasion abilities^[1].
NF-κB-IN-22 (5 μM; 24 h) induces significant DNA damage and DNA double-strand breaks in A549 cells^[1].
NF-κB-IN-22 (5 μM; 24 h) significantly upregulates the expression of γ-H2AX protein in A549 cells^[1].
NF-κB-IN-22 (5 μM; 24 h) induces significant mitochondrial dysfunction in A549 cells, characterized by a 41.72% decrease in mitochondrial membrane potential^[1].

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