AbstractBACKGROUNDMagnaporthe oryzae is the causal agent of rice blast disease. Pydiflumetofen, a novel succinate dehydrogenase inhibitor (SDHI), has promising potential for controlling rice blast owing to the antifungal activity of this fungicide.RESULTSThe median effective concentration (EC50) of 18 M. oryzae isolates obtained from the field to pydiflumetofen ranged from 0.3197 to 0.7381 μg mL−1. Further investigation revealed eight point‐mutation types in the MoSdhB/C/D genes, including MoSdhBR243H, MoSdhBH245Y/L/Q, MoSdhBI247T, MoSdhCS77N and MoSdhDD122N/E. These mutations were identified through pydiflumetofen adaptation and resulted in mutants with a resistance factor (RF) > 213. These mutations partially impacted the fitness of the fungus, yet, interestingly, had no effect on pathogenicity. Meanwhile, the expression of MoSdhs genes, and mitochondria fission, fusion and morphology related genes also were influenced. The point mutations exhibited reduced succinate dehydrogenase (SDH) activity. However, the mutations on MoSdhBR243H, MoSdhBH245Q, MoSdhBI247T, and MoSdhDD122N/E enhanced the adaptability of SDH to pydiflumetofen, except mutations on MoSdhBH245Y/L and MoSdhCS77N. Additionally, positive cross‐resistance existed between pydiflumetofen and carboxin.CONCLUSIONThe potential resistant risk of M. oryzae to pydiflumetofen could be high. Eight mutations in MoSdhB/C/D are responsible for conferring resistance to this fungicide. © 2025 Society of Chemical Industry.