Increasing evidence suggests that abnormalities in mitochondria are involved not only in aging, age-related neurodegenerative diseases, cancer, diabetes, and several other mitochondrial diseases, but also in the development of asthma. Therefore, pharma-cological approaches to studying mitochondrial regulation have been focused either clinically or experimentally. However, the precise connection between mitochondrial abnormalities and asthma is not well understood. NecroX-5, a novel compound is one of the derivatives of NecroX series compounds, which shows the mitochondrial ROS scavenging activity. In this study, we aimed to define the effects of Necrox-5 on airway inflammation and hyperresponsiveness in a murine model of bronchial asthma. The mice sensitized with OVA and LPS and then challenged with OVA (OVALPS-OVA mice) showed the typical features of neutrophilic asthma; increased airway inflammatory cells, the pathologic changes, the increased levels of Th2 cyto-kines and IL-17 in lungs of OVALPS-OVA mice, increased intracellular ROS generation, and increased bronchial hyperresponsiveness. Interestingly, we found that in OVALPS-OVA mice, Necrox-5, a novel mitochondrial targeting agent significantly reduced the increases in inflammatory cytokines, IL-17 levels, airway inflammation, and bronchial hyperresponsiveness. These findings indicate that mitochondrial dysfunction including oxidative damage may be implicated in the pathogenesis of bronchial asthma and provide the therapeutic potential of mitochondrial targeting agents for bronchial asthma.