[Introduction or background] Recent studies suggest that the cellular senescence of epithelial cell is related to the pathogenesis of lung fibrosis. ARV825, a recently developed BRD4 degrader, has been reported as a novel senolytic drug. On the other hand, BRD4 also regulates the pro-fibrotic gene expression of fibroblasts. Therefore, in this study, we evaluated both senolytic effect and anti-fibrotic effect of ARV825 on lung fibrosis.  [Methods] The murine and human lung fibroblasts were used in the present study. Murine lung fibroblasts were rendered senescent by serial passage. The expression of senescent markers and profibrotic markers were determined by quantitative PCR or immunoblot analysis. For in vivo experiments, lung fibrosis was induced in mice by intratracheal administration of bleomycin. The histology of lung fibrosis was analyzed by Ashcroft score. Total lung collagen was determined by hydroxyproline assay. The respiratory mechanics analysis was performed using a flexiVent system.  [Results] For senescent cells, ARV825 induced the expression of an apoptosis marker together with the reduction of the expression of BRD4 and senescence markers. On the other hand, for early passage pre-senescent lung fibroblasts, ARV825 reduced the expression of collagen type 1 and ?-smooth muscle actin in a dose-dependent manner. In an experimental lung fibrosis mouse model, ARV825 attenuated lung fibrosis and ameliorated the lung function. Immunohistochemical staining revealed that the number of senescent alveolar type 2 cells in lung tissue was significantly decreased by ARV825. [Conclusions] These results suggest that ARV825 may impact the progressive and irreversible course of fibrotic lung diseases.