目前，多种抗有丝分裂抑制剂应用于肿瘤治疗。然而，这些抑制剂在一定程度上表现出靶向毒性。作为一种运动蛋白，驱动蛋白家族成员 18A (KIF18A) 对于纺锤体的形成至关重要，并且与表现出染色体非整倍性、全基因组加倍和染色体不稳定等特征的肿瘤相关。与传统的抗有丝分裂靶标不同，KIF18A 表现出肿瘤特异性选择性。 KIF18A 的功能丧失或减弱会导致具有倍性特异性特征的肿瘤细胞的脆弱性，对二倍体细胞的影响较小。针对具有倍性特异性致死性的 KIF18A 抑制剂的研究具有重要意义。本综述简要概述了倍性特异性致死靶点KIF18A的调控机制及其抑制剂的研究进展，旨在促进KIF18A抑制剂的开发。版权所有©2024 Elsevier Ltd.保留所有权利。

Currently, various antimitotic inhibitors applied in tumor therapy. However, these inhibitors exhibit targeted toxicity to some extent. As a motor protein, kinesin family member 18A (KIF18A) is crucial to spindle formation and is associated with tumors exhibiting characteristics such as chromosomal aneuploidy, whole-genome doubling, and chromosomal instability. Differing from traditional antimitotic targets, KIF18A exhibits tumor-specific selectivity. The functional loss or attenuation of KIF18A results in vulnerability of tumor cells with ploidy-specific characteristics, with lesser effects on diploid cells. Research on inhibitors targeting KIF18A with ploidy-specific lethality holds significant importance. This review provides a brief overview of the regulatory mechanisms of the ploidy-specific lethality target KIF18A and the research advancements in its inhibitors, aiming to facilitate the development of KIF18A inhibitors.Copyright © 2024 Elsevier Ltd. All rights reserved.