Nintedanib exerts anti-pulmonary fibrosis activity via inhibiting TANK-binding kinase 1 (TBK1) phosphorylation.

Since triple angiokinase inhibitor could not fully explain the anti-pulmonary fibrosis activity of nintedanib (NDNB), the chemoproteomic strategy was performed to identify TANK-binding kinase 1 (TBK1) as the key target of NDNB in human pulmonary fibroblasts (HPFs). Functionally, NDNB exerts anti-fibrosis activity through impairing the p-TBK1-mediated Yes-associated protein (YAP)/transcriptional cofactor with PDZ-binding motif (TAZ) nuclear translocation.