EM-1 could induce K562 cells apoptosis time-dependently and dose-dependently. The mechanism of action could be related to bcl-2/bax access activated.

• EM1能诱导K562细胞凋亡,抑制肿瘤细胞增殖呈一定的浓度和时间依赖关系,其作用机制可能与bcl2/bax通路激活有关。