慢性粒细胞白血病(CML)为一种起源于骨髓内异常多能干细胞的骨髓增殖性疾病,以持续表达 bcr-abl 融合基因为特征,这段融合基因的翻译产物 bcr-abl 蛋白具有较高的蛋白酪氨酸激酶活性,可激活一系列下游信号传导通路而导致 CML 的发生,因而成为 CML 治疗的明确靶向。伊马替尼(IM)可竞争性结合 abl 酪氨酸激酶催化部位的 ATP 结合位点,使该激酶不能与 ATP 结合,从而失去催化活性。应用 TM治疗的几乎所有 CML 急变期患者和近15%～20%的 CML Chronic myeloid leukemia (CML), a myeloproliferative disorder that originates from abnormal marrow cells, is characterized by the persistent expression of the bcr-abl fusion gene. The bcr-abl protein, the translation product of this fusion gene, Protein tyrosine kinase activity, which activates a series of downstream signaling pathways leading to the development of CML, has become a clear target for CML therapy. Imatinib (IM) competitively binds to the ATP binding site of the catalytic site of abl tyrosine kinase, rendering the kinase unable to bind to ATP, losing its catalytic activity. Almost all CML patients treated with TM and nearly 15% to 20% of CML