Fig. 3
Secondary ALK or ROS1 mutations conferring drug resistance are responsive to APG-2449 in vivo. Antitumor activity of APG-2449 against acquired, drug-resistant mutations was evaluated in subcutaneous xenograft models derived from Ba/F3 cells carrying EML4-ALKL1196M mutation (A; treated for 2 weeks, n = 6 per treatment group), Ba/F3 cells carrying EML4-ALKG1202R mutation (B; treated for 2 weeks, n = 5 per treatment group), Ba/F3 cells carrying CD74-ROS1L2026M mutation (C; treated for 3 weeks while 2 groups were terminated earlier as indicated, n = 4 or 5 per treatment group), NSCLC PDX LD1–0006-390,637 harboring ALKL1196M_G1202R double mutations (D; treated for 3 weeks, n = 5 per treatment group), or NSCLC PDX LU-01-0582R with acquired resistance to crizotinib (E; treated for 4 weeks, n = 3 or 4 per treatment group)