{"title":"雷帕霉素衍生物作为雷帕霉素和GLS1双重抑制剂的首个哺乳动物靶点的设计、合成和生物学评价","authors":"Liushun Wu, Mengting Lyu, Dong-Quan Gu, Yin Li, Ying Li, Hongsu Zhao, Tongsheng Wang, Feng-Qing Xu, Deling Wu, Wuxi Zhou","doi":"10.1021/acs.jmedchem.5c01841","DOIUrl":null,"url":null,"abstract":"The mammalian target of rapamycin (mTOR) and glutaminase 1 (GLS1) are key enzymes regulating metabolic reprogramming in breast cancer. The first generation of mTOR and GLS1 dual inhibitors was designed and synthesized on the basis of anticancer synergism. Compound <b>9d</b> showed selective and potent antiproliferative activity against all breast cancer cell lines and displayed potent inhibitory activity against both mTOR (mTORC1 and mTORC2) and GLS1. Mechanism studies revealed that <b>9d</b> effectively modulated the level of biomarkers and metabolites associated with mTOR and GLS1 inhibition and triggered sustained and massive reactive oxygen species generation, leading to cell death by autophagy, apoptosis, and ferroptosis. Moreover, <b>9d</b> inhibited the metastasis, invasion, and angiogenesis of breast cancer cells. In vivo experiments demonstrated that <b>9d</b> significantly inhibited tumor growth and metastasis, without observable toxicity. These findings proved mTOR/GLS1 dual inhibitors’ great therapeutic potential for breast cancer.","PeriodicalId":46,"journal":{"name":"Journal of Medicinal Chemistry","volume":"11 1","pages":""},"PeriodicalIF":6.8000,"publicationDate":"2025-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Design, Synthesis, and Biological Evaluation of Rapamycin Derivatives as the First Mammalian Target of Rapamycin and GLS1 Dual Inhibitors\",\"authors\":\"Liushun Wu, Mengting Lyu, Dong-Quan Gu, Yin Li, Ying Li, Hongsu Zhao, Tongsheng Wang, Feng-Qing Xu, Deling Wu, Wuxi Zhou\",\"doi\":\"10.1021/acs.jmedchem.5c01841\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"The mammalian target of rapamycin (mTOR) and glutaminase 1 (GLS1) are key enzymes regulating metabolic reprogramming in breast cancer. The first generation of mTOR and GLS1 dual inhibitors was designed and synthesized on the basis of anticancer synergism. Compound <b>9d</b> showed selective and potent antiproliferative activity against all breast cancer cell lines and displayed potent inhibitory activity against both mTOR (mTORC1 and mTORC2) and GLS1. Mechanism studies revealed that <b>9d</b> effectively modulated the level of biomarkers and metabolites associated with mTOR and GLS1 inhibition and triggered sustained and massive reactive oxygen species generation, leading to cell death by autophagy, apoptosis, and ferroptosis. Moreover, <b>9d</b> inhibited the metastasis, invasion, and angiogenesis of breast cancer cells. In vivo experiments demonstrated that <b>9d</b> significantly inhibited tumor growth and metastasis, without observable toxicity. These findings proved mTOR/GLS1 dual inhibitors’ great therapeutic potential for breast cancer.\",\"PeriodicalId\":46,\"journal\":{\"name\":\"Journal of Medicinal Chemistry\",\"volume\":\"11 1\",\"pages\":\"\"},\"PeriodicalIF\":6.8000,\"publicationDate\":\"2025-10-17\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Medicinal Chemistry\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1021/acs.jmedchem.5c01841\",\"RegionNum\":1,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"CHEMISTRY, MEDICINAL\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Medicinal Chemistry","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1021/acs.jmedchem.5c01841","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"CHEMISTRY, MEDICINAL","Score":null,"Total":0}
Design, Synthesis, and Biological Evaluation of Rapamycin Derivatives as the First Mammalian Target of Rapamycin and GLS1 Dual Inhibitors
The mammalian target of rapamycin (mTOR) and glutaminase 1 (GLS1) are key enzymes regulating metabolic reprogramming in breast cancer. The first generation of mTOR and GLS1 dual inhibitors was designed and synthesized on the basis of anticancer synergism. Compound 9d showed selective and potent antiproliferative activity against all breast cancer cell lines and displayed potent inhibitory activity against both mTOR (mTORC1 and mTORC2) and GLS1. Mechanism studies revealed that 9d effectively modulated the level of biomarkers and metabolites associated with mTOR and GLS1 inhibition and triggered sustained and massive reactive oxygen species generation, leading to cell death by autophagy, apoptosis, and ferroptosis. Moreover, 9d inhibited the metastasis, invasion, and angiogenesis of breast cancer cells. In vivo experiments demonstrated that 9d significantly inhibited tumor growth and metastasis, without observable toxicity. These findings proved mTOR/GLS1 dual inhibitors’ great therapeutic potential for breast cancer.
期刊介绍:
The Journal of Medicinal Chemistry is a prestigious biweekly peer-reviewed publication that focuses on the multifaceted field of medicinal chemistry. Since its inception in 1959 as the Journal of Medicinal and Pharmaceutical Chemistry, it has evolved to become a cornerstone in the dissemination of research findings related to the design, synthesis, and development of therapeutic agents.
The Journal of Medicinal Chemistry is recognized for its significant impact in the scientific community, as evidenced by its 2022 impact factor of 7.3. This metric reflects the journal's influence and the importance of its content in shaping the future of drug discovery and development. The journal serves as a vital resource for chemists, pharmacologists, and other researchers interested in the molecular mechanisms of drug action and the optimization of therapeutic compounds.