酪氨酸激酶抑制剂（TKIs）在慢性髓细胞性白血病（CML）的治疗中产生了重大变革，并且改善了慢性期（CML-CP）和加速期（AP）CML患者的预后。现在，临床医生拥有了众多有效的治疗选择，必须考虑选择最合适的TKI时涉及的多种患者和疾病特定因素。虽然由于TKI的成功，大多数CML患者预计有接近正常的预期寿命，但重点已经扩展到了除响应和生存外的因素，如生活质量、耐受性和长期毒性管理。重要的是，一部分患者可以实现持久的深度分子应答，并达到无需治疗的缓解状态。尽管取得了这些成功，但与CML治疗相关的不满足需求仍然存在，包括治疗耐药和不耐受的持续挑战，为耐药突变或严重合并症患者拓宽治疗选择，以及关注特定人群，如儿童和年轻成人。特别地，此前对于携带T315I突变的CML-CP患者，唯一的可用治疗方法是泊那汀帕、奥汉布替尼（在此撰写时仅在中国获准使用）、雷沙替尼和造血干细胞移植。Asciminib已成为CML治疗领域的一种新选择，适用于已接受过≥2种TKIs或携带T315I突变的成年CML-CP患者。Asciminib独特的作用机制即针对ABL酰肌酸酯口袋，使其与传统的三磷酸腺苷竞争性TKIs区别开来。虽然asciminib可能满足CML-CP患者的不满需求，并继续在其他新领域进行研究，但需要有关如何在治疗算法中整合asciminib的指导。本综述关注临床数据以及asciminib如何满足当前的不满需求，并讨论如何个体化患者选择，并重点强调未来研究asciminib在早期治疗和儿童青少年中的方向。©2023 Hijiya和Mauro。

Tyrosine kinase inhibitors (TKIs) have significantly changed the treatment of chronic myeloid leukemia (CML) and improved outcomes for patients with CML in chronic phase (CML-CP) and accelerated phase (AP). Now armed with numerous effective therapeutic options, clinicians must consider various patient- and disease-specific factors when selecting the most appropriate TKI across lines of therapy. While most patients with CML expected to have a near-normal life expectancy due to the success of TKIs, emphasis has expanded beyond response and survival to include factors like quality of life, tolerability, and long-term toxicity management. Importantly, a subset of patients can achieve sustained deep molecular response and can attain treatment-free remission. Despite these successes, unmet needs remain related to CML treatment, including the persistent challenge of treatment resistance and intolerance, broadening treatment options for patients with resistance mutations or serious comorbidities, and focus on specific populations such as children and young adults. In particular, the only previously available treatments for patients with CML-CP with the T315I mutation were ponatinib, olverembatinib (exclusively approved for use in China at the time of this writing), omacetaxine, and hematopoietic stem cell transplantation. Asciminib has entered the CML treatment landscape as a new option for adult patients with CML-CP who have received ≥2 prior TKIs or those with the T315I mutation. Asciminib's unique mechanism of action, Specifically Targeting the ABL Myristoyl Pocket, sets it apart from traditional adenosine triphosphate-competitive TKIs. While asciminib may overcome unmet needs for patients with CML-CP and continues to be studied in other novel settings, guidance on how to integrate asciminib in treatment algorithms is needed. This review focuses on clinical data and how asciminib can overcome current unmet needs, discusses how to individualize patient selection, and highlights future directions to investigate asciminib in earlier lines of therapy and in children and adolescents.© 2023 Hijiya and Mauro.