When cultured without serum for 72 h, Drp1 association with the Fis1 and not the other adaptors (Mff, Mid49, and Mid51) increased significantly, which was reduced by P110 treatment (Fig EV2C). Association of Drp1 with mitochondria was 2.6‐fold higher in NSC‐34 cells expressing SOD1 G93A mutant relative to control cells (P = 0.0008; Figs 2B and EV2D), indicating Drp1 hyperactivation, which was significantly reduced by P110 treatment (P = 0.0008). P110 treatment also significantly blocked the subsequent release of cytochrome c from the mitochondria (P = 0.0397; Fig EV3A), reduced the accumulation of active Bax on the mitochondria (P = 0.0065), and improved decreased Bcl‐2 levels on the mitochondria in NSC‐34 cells expressing SOD1 G93A mutant vs. control cells (P = 0.0002). Thus, P110 treatment significantly inhibited the initiation of apoptosis in these mutant cells.