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发现基于吡啶的衍生物作为治疗急性髓性白血病的FLT3抑制剂。

Discovery of pyridine-based derivatives as FLT3 inhibitors for the treatment of acute myeloid leukemia.

作者信息

Chen Beijing, Wang Zhongyuan, Chen Qi, Zhang Ying, Wu Shengfei, Zhang Yu, Li Aihong, Ouyang Weiwei, Sima Lijie, Li Xiaoxu, Zhao Dongsheng, Luo Bilan, Wang Jianta, Tang Lei, Su Xiaoming, Liao Weike

机构信息

Guizhou Provincial Engineering Technology Research Center for Chemical Drug R&D, Guizhou Medical University, Guiyang, 550004, China.

Department of Pharmacy, Guizhou Provincial People's Hospital, Guiyang, 550002, China.

出版信息

Eur J Med Chem. 2025 Feb 5;283:117173. doi: 10.1016/j.ejmech.2024.117173. Epub 2024 Dec 16.

Abstract

FMS-like tyrosine receptor kinase 3 (FLT3) mutations, the most common genetic alterations found in acute myeloid leukemia (AML) patients, have been pursued as an ideal drug discovery target for the AML therapy. Taking compound 2 as lead, a series of pyridine derivatives bearing 1,2,3-triazole moiety were rationally designed and synthesized. The bioassays confirmed that these derivatives exerted potent antileukemia effects, and compound 12y was found to be the most potent one. 12y displayed double-digital nanomolar inhibitory activities against FLT3-ITD and FLT3-ITD driven human AML MOLM-13 cells as well as high selectivity over FLT3-ITD non-addicted cell lines. In addition, kinase profiling versus over 51 kinases demonstrated that 12y was potent against FLT3-ITD and VEGFR2. Moreover, treatment of MOLM-13 cells with 12y resulted in downregulated phosphorylation levels of FLT3 and STAT5, as well as cell cycle arrest and apoptosis. With the acceptable oral bioavailability of 19.2 % in SD rats, 12y prolonged the survival rate of NSG mice dose-dependently in MOLM-13 inoculated xenograft model without obvious toxicity. Overall, this study might provide a new insight for the development of novel FLT3 inhibitors.

摘要

FMS样酪氨酸受体激酶3(FLT3)突变是急性髓系白血病(AML)患者中最常见的基因改变,一直被视为AML治疗的理想药物研发靶点。以化合物2为先导,合理设计并合成了一系列带有1,2,3-三唑部分的吡啶衍生物。生物活性测定证实这些衍生物具有强大的抗白血病作用,发现化合物12y是其中活性最强的。12y对FLT3-ITD以及FLT3-ITD驱动的人AML MOLM-13细胞表现出双位数纳摩尔抑制活性,并且对非FLT3-ITD依赖的细胞系具有高选择性。此外,针对51种以上激酶的激酶谱分析表明,12y对FLT3-ITD和血管内皮生长因子受体2(VEGFR2)具有活性。而且,用12y处理MOLM-13细胞导致FLT3和信号转导子和转录激活子5(STAT5)的磷酸化水平下调,以及细胞周期停滞和凋亡。在SD大鼠中12y具有19.2%的可接受口服生物利用度,在接种MOLM-13的异种移植模型中,12y剂量依赖性地延长了NSG小鼠的存活率,且无明显毒性。总体而言,本研究可能为新型FLT3抑制剂的开发提供新的见解。

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