Lysophosphatidic acid (LPA) mediated signaling is relevant to fibrosis and the proliferation of pulmonary cells, such as the promotion of fibroblast accumulation and stimulation of the TGF-β signal. One of the essential mechanisms to reduce lysophosphatidic acid production is inhibiting autotaxin activity, which can block the hydrolysis of a lysophosphatidylcholine (LPC) into LPA, leading to the alleviation of the development of pulmonary fibrosis. Recently, 3,4-difluorobenzyl(1-ethyl-5-(4-((4-hydroxypiperidin-1-yl)-methyl)-thiazol-2-yl)-1H-indol-3-yl)carbamate (NAI59), a novel autotaxin inhibitor, showed outstanding anti-pulmonary fibrosis therapeutic effectiveness; however, the metabolic information of NAI59 has not been comprehensively expounded yet. Therefore, in this study, we aim to identify the metabolites of NAI59 in rats using ultra-high-performance liquid chromatography-high-resolution tandem mass spectrometry, and we analyze the potential anti-fibrosis of metabolites in plasma using molecular docking with the crystal structure autotaxin. As a result, a total of 24 metabolites, namely, 15 phase I metabolites and 9 phase II metabolites, were identified, all of which are the novel discovered metabolites. The metabolic pathways of NAI59 were primarily hydroxylation, oxidation, hydrogenation, glucuronic acid conjugation, sulfate conjugation, acetylation, and glucosylation. The molecular docking result showed that the identified metabolites in plasma had great affinities upon docking into the active site of autotaxin, indicating they may have potential anti-pulmonary fibrosis activity. The interaction plots revealed the importance of fluorophenyl and the hydroxyl groups on piperidine that contribute toward the formation of hydrogen bonds with autotaxin. Additionally, we found that the metabolite possessed a better docking result when the structure contained a glucuronic acid group. To the best of our knowledge, this study is the first research into the metabolic fate of NAI59 in rats, and we analyze the potential anti-fibrosis aspects of metabolites using molecular docking. This study provides a metabolic rationale for further preclinical research and imparts new insights for developing improved ATX inhibitors.