Liu Xinyu, Zhang Yiwen, Duan Huaichuan, Luo Qing, Liu Wei, Liang Li, Wan Hua, Chang Shan, Hu Jianping, Shi Hubing
Laboratory of Tumor Targeted and Immune Therapy, Clinical Research Center for Breast, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University and Collaborative Innovation Center for Biotherapy, Chengdu, China.
Key Laboratory of Medicinal and Edible Plants Resources Development of Sichuan Education Department, College of Pharmacy and Biological Engineering, Sichuan Industrial Institute of Antibiotics, Chengdu University, Chengdu, China.
Front Mol Biosci. 2020 Jan 28;6:164. doi: 10.3389/fmolb.2019.00164. eCollection 2019.
For cancer treatment, in addition to the three standard therapies of surgery, chemotherapy, and radiotherapy, immunotherapy has become the fourth internationally-recognized alternative treatment. Indoleamine 2, 3-dioxygenase 1 (IDO1) catalyzes the conversion of tryptophan to kynurenine causing lysine depletion, which is an important target in the research and development of anticancer drugs. Epacadostat (INCB024360) is currently one of the most potent IDO1 inhibitors, nevertheless its inhibition mechanism still remains elusive. In this work, comparative molecular dynamics simulations were performed to reveal that the high inhibitory activity of INCB024360 mainly comes from two aspects: disturbing the ligand delivery tunnel and then preventing small molecules such as oxygen and water molecules from accessing the active site, as well as hindering the shuttle of substrate tryptophan with product kynurenine through the heme binding pocket. The scanning of key residues showed that L234 and R231 residues both were crucial to the catalytic activity of IDO1. With the association with INCB024360, L234 forms a stable hydrogen bond with G262, which significantly affects the spatial position of G262-A264 loop and then greatly disturbs the orderliness of ligand delivery tunnel. In addition, the cleavage of hydrogen bond between G380 and R231 increases the mobility of the GTGG conserved region, leading to the closure of the substrate tryptophan channel. This work provides new ideas for understanding action mechanism of amidoxime derivatives, improving its inhibitor activity and developing novel inhibitors of IDO1.
对于癌症治疗,除了手术、化疗和放疗这三种标准疗法外,免疫疗法已成为国际公认的第四种替代治疗方法。吲哚胺2,3-双加氧酶1(IDO1)催化色氨酸转化为犬尿氨酸,导致色氨酸耗竭,这是抗癌药物研发中的一个重要靶点。依帕卡托(INCB024360)是目前最有效的IDO1抑制剂之一,但其抑制机制仍不清楚。在这项工作中,进行了比较分子动力学模拟,以揭示INCB024360的高抑制活性主要来自两个方面:扰乱配体输送通道,从而阻止氧气和水分子等小分子进入活性位点,以及阻碍底物色氨酸与产物犬尿氨酸通过血红素结合口袋穿梭。关键残基扫描表明,Lys234和Arg231残基对IDO1的催化活性都至关重要。与INCB024360结合后,Lys234与Gly262形成稳定的氢键,这显著影响了Gly262-Ala264环的空间位置,进而极大地扰乱了配体输送通道的有序性。此外Gly380与Arg231之间氢键的断裂增加了GTGG保守区域的流动性,导致底物色氨酸通道关闭。这项工作为理解偕胺肟衍生物的作用机制、提高其抑制活性以及开发新型IDO1抑制剂提供了新的思路。