Rationale: Ca²⁺ signaling controls the production of Th2 cytokines known to be deleterious in asthma. Recently, we showed that Ca²⁺ signaling was dihydropyridine (DHP)-sensitive in Th2 lymphocytes and that the DHP derivate nicardipine, used in the treatment of cardiovascular pathologies prevent Th2-dependent B cell polyclonal activation. Objective : Herein, we tested the effect of nicardipine in experimental allergic asthma. Methodology : BALB/c mice immunized with OVA in alum, and challenged with intranasal OVA were treated with nicardipine once the Th2 response or even airway inflammation was induced. We also tested the effect of nicardipine in asthma induced by transferring OVA-specific Th2 cells in BALB/c mice, exposed to intranasal OVA. We checked the impact of nicardipine on T-cell responses and airway inflammation. Measurements and main results: Nicardipine inhibited in vitro Ca²⁺ response in Th2 cells. In vivo, it impeded the development of Th2 mediated airway inflammation and reduced the capacity of lung draining lymphocytes to secrete Th2 but not Th1 cytokines. Nicardipine did not affect antigen presentation to CD⁴⁺ T lymphocytes, nor the initial localization of Th2 cells into the lungs of mice exposed to intranasal OVA. However, it reduced the production of type-2 cytokines and the amplification of the Th2 response in asthmatic mice. Conversely, nicardipine had no effect on Th1-mediated airway inflammation. Conclusion : Nicardipine improves experimental asthma by impairing Th2-dependent inflammation. This study could be a rationale for developing drugs selectively targeting DHP receptors of Th2 lymphocytes, potentially beneficial in the treatment of asthma.