PbQ

PbQ (2.5-50 μM; 24 h) reduces the viability of human type II pulmonary epithelial (A549) cells in a dose-dependent manner, with an IC₅₀ of 5-10 μM^[1].
PbQ (5-10 μM; 24 h) disrupts cell cycle progression in human type II pulmonary epithelial (A549) cells, causing a dose-dependent accumulation of cells in the sub-G₀/G₁ phase, accompanied by decreased proportions of cell populations in the G₀/G₁ and G₂/M phases^[1].
PbQ (10 μM; 6-24 h) induces time-dependent apoptosis in human type II pulmonary epithelial (A549) cells and also triggers nuclear DNA fragmentation^[1].
PbQ (5-10 μM; 24 h) induces dose-dependent release of cytochrome c into the cytoplasm in human type II pulmonary epithelial (A549) cells^[1].
PbQ (10 μM; 24 h) induces specific degradation of α-tubulin (without affecting β-actin) in human type II pulmonary epithelial (A549) cells, and this effect occurs after 24 h of treatment with 10 μM PbQ^[1].
When co-incubated with Cu⁺ ions, PbQ (250 μM; 24 h) exhibits high biocompatibility with RAW 264.7 macrophages, maintaining approximately 80% cell viability after incubation at 250 μM for 24 h^[2].
PbQ (10 μM; 1 h) can penetrate the cell membrane of peripheral blood mononuclear cells (PBMCs), and after exposure to Cu ^(I) ions (10 μM CuCl; 30 min), it exhibits a unique, selective, and highly enhanced fluorescence response in PBMCs, enabling the visualization of labile intracellular Cu ^(I) ions^[2].

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