Fig. S1. Hydroxychavicol (HCH)-induced reactive oxygen species (ROS) originates from mitochondria.

Fig. S2. Pretreatment with diethyldithiocarbamate (DETC) (50 mM) enhances the accumulation of superoxide but lowers the level of H2O2 while pretreatment with aminotriazole (ATZ) (2.0 mM) enhances the accumulation of H2O2 after treatment of K562 cells with HCH (5.0 mg/mL).

Fig. S3. Hydroxychavicol (HCH) does not interact with N-acetylcysteine (NAC).

Fig. S4. Hydroxychavicol (HCH) treatment does not deplete intracellular glutathione.

Fig. S5. Contribution of JNK in hydroxychavicol (HCH)-induced nitric oxide (NO) production and apoptosis in K562 cells.

Fig. S6. Relative body weight profile of SCID mice bearing SCID mice bearing Ba/F3Bcr-Abl P210wild type or Ba/F3 T3151 Bcr-Abl P210T315I xenografts after oral administration of vehicle control or ICB3E twice daily for 10 days.

Data S1. xxx.

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