Glucocorticosteroids are principal drugs for the treatment of bronchial asthma. However, around 10 % of asthmatic patients do not respond adequately to the steroid therapy. The intractable asthma is considered to associate with dysregulated Th17 cells and resulting neutrophil invasion. In this presentation, we show that the inhibition of LAT1, a transporter of large neutral amino acids, provides a possible option to improve steroid-resistant asthma. We investigated the effect of JPH203, a LAT1 specific inhibitor, on allergic airway inflammation developed in BALB/c mice transferred with in vitro-differentiated ovalbumin-specific Th17 cells. JPH203 administration suppressed the allergen-induced bronchial hyperresponsiveness and neutrophil accumulation in the lungs, whereas no significant effects were observed by dexamethasone treatment. JPH203 inhibited cytokine production of Th17 cells along with reducing mTOR activity, in contrast to the less effect of dexamethasone, suggesting the possible mechanisms underlying the suppression of Th17-dependent and steroid-resistant airway inflammation by LAT1 inhibition. Our results propose LAT1 as a novel target for the treatment of steroid-resistant asthma.