Idiopathic pulmonary fibrosis (IPF) is a fatal lung disease of unknown etiology. Under pathological conditions in lungs with IPF, myofibroblasts (MyoF) play a crucial role in fibrogenesis through the accumulation of an excessive amount of extracellular matrix. To develop effective therapeutic interventions against IPF, dedifferentiation of MyoF has recently attracted considerable attention from the point of view of tissue regeneration. Here, we screened various small-molecule inhibitors using dedifferentiation assay of human lung MyoF and chose several different types of inhibitors. In addition, differentially expressed genes (DEGs) in MyoF treated with the dedifferentiating agent were comprehensively investigated by an RNA-seq/transcriptome analysis. Then, we focused on the downregulated DEGs as key candidate genes to maintain the characteristics of MyoF. To specify the therapeutic target of IPF, furthermore, the drug-target molecules as well as the downregulated DEGs were subjected to a pathway analysis. We will discuss new candidate molecules having therapeutic potential against IPF.