Key findings showed that CDN’s core IPF-related target (e.g., IGF1) was identified; molecular docking and dynamics confirmed stable CDN-IGF1 binding; and in vitro experiments verified CDN alleviated BLM-induced A549 cell fibrosis and EMT by inhibiting the IGF1/PI3K/AKT axis. This evidence concerns the gene NT5C and idiopathic pulmonary fibrosis.