Because the epidermal growth factor receptor (EGFR) inhibitor icotinib has a structural feature of a terminal alkyne, it reacted with 3-chlorophenyl azide to produce compound 5, which showed excellent inhibitory effects on mutant lung cancer cells (PC-9) and wild-type lung cancer cells (A549), and had a stronger effect than icotinib. The gene discussed is EGFR; the disease is lung cancer.