Mito-DHH chloride

Mito-DHH (0.25-2.8 μM; 48 h) potently and selectively kills A549, HepG2, A375, and SW620 cancer cells over normal L02 cells, with the highest potency against A549 cells (IC₅₀ = 0.25 μM) and a selectivity index of 11.2^[1].
Mito-DHH (0.25-0.5 μM; 10 days) impairs long-term clonogenic survival of A549 cells at concentrations of 0.25 μM and 0.5 μM^[1].
Mito-DHH (1 μM; 0.5-3 h) rapidly and selectively accumulates in the mitochondria of A549 cells within 0.5 h, with minimal enrichment in L02 cell mitochondria^[1].
Mito-DHH (50 μM; 2 h) under alkaline conditions (pH 8 and 10) promotes auto-oxidation to generate reactive oxygen species, with more robust ROS production at higher pH^[1].
Mito-DHH (1 μM; 2 h) preferentially induces mitochondrial superoxide anion generation in A549 cells over L02 cells after 2 h of treatment^[1].
Mito-DHH (1 μM; 3 h) preferentially induces intracellular hydroxyl radical generation in A549 cells over L02 cells after 3 h of treatment^[1].
Mito-DHH (1-2 μM; 6-12 h) induces a ROS-dependent reduction in ATP production in A549 cells after 6 and 12 h, with no effect on ATP levels in L02 cells at 10 μM^[1].
Mito-DHH (2 μM; 5 h) inhibits both mitochondrial oxidative phosphorylation and cytoplasmic glycolysis in A549 cells after 5 h of treatment, inducing a dual-effect energy crisis^[1].
Mito-DHH (1-2 μM; 18-24 h) preferentially disrupts mitochondrial membrane potential in A549 cells after 18 and 24 h of treatment, with no effect on L02 cells^[1].
Mito-DHH (10 μM; 1-12 h) induces late-stage apoptosis in A549 cells, with detectable PI nuclear localization starting at 6 h and progressing over time^[1].
Mito-DHH (1-2 μM; 48 h) preferentially induces apoptosis in A549 cells over L02 cells after 48 h of treatment^[1].
Mito-DHH (1-2 μM; 24 h) preferentially induces G0/G1 cell cycle arrest in A549 cells over L02 cells after 24 h of treatment^[1].

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