Saravanan Venkatesan, Palani Sathiya Priya, Chagaleti Bharath Kumar, Gao Quan-Ze, Valsaladevi Anjana Gopi, Kumaradoss Kathiravan Muthu
Department of Pharmaceutical Chemistry, SRM College of Pharmacy, SRM Institute of Science and Technology, Kattankulathur, Chengalpattu, 603203, India.
National Applied Research Laboratories, National Centre for High-Performance Computing, Hsinchu City, 30076, Taiwan.
Biochem Biophys Res Commun. 2025 Mar 19;753:151471. doi: 10.1016/j.bbrc.2025.151471. Epub 2025 Feb 11.
Human carbonic anhydrase (CA) isoenzymes IX and XII are overexpressed in cancer cells, contributing to tumor microenvironment acidification and representing important targets for cancer therapy. In this study, we identified compound V35 (ZINC09419065) as a selective inhibitor of CA IX and CA XII with enhanced binding stability and selectivity compared to standard inhibitors. We analyzed conserved regions in CA I, CA II, CA IX, and CA XII to investigate their isozyme selectivity, revealing critical selectivity determinants at positions 95, 141, and 203. Molecular docking results indicated that V35 interacts robustly with CA XII, forming a metal ion coordination complex with Zn via HIS94, HIS96, HIS119, and THR199, similar to the interaction pattern of standard inhibitor SLC-0111. Molecular dynamics (MD) simulations conducted over 500 ns under hypoxic conditions showed that V35 has high binding stability, with root mean square deviation (RMSD) and fluctuation (RMSF) values comparable to SLC-0111, demonstrating its conformational stability in CA XII. Binding free energy calculations using the MMGBSA method showed that V35 achieves binding free energy of -44.17 kcal/mol with CA XII, closely matching SLC-0111 (-49.41 kcal/mol). Density functional theory (DFT) calculations further highlighted V35's electrostatic potential distribution, supporting its isozyme selectivity. Post-dynamics analysis indicated that the ester functional groups and the inward movement of HIS64 stabilize V35's interactions in CA XII, a feature absent in CA I.
人类碳酸酐酶(CA)同工酶IX和XII在癌细胞中过表达,导致肿瘤微环境酸化,是癌症治疗的重要靶点。在本研究中,我们鉴定出化合物V35(ZINC09419065)是CA IX和CA XII的选择性抑制剂,与标准抑制剂相比,其结合稳定性和选择性增强。我们分析了CA I、CA II、CA IX和CA XII中的保守区域,以研究它们的同工酶选择性,揭示了95、141和203位的关键选择性决定因素。分子对接结果表明,V35与CA XII强烈相互作用,通过HIS94、HIS96、HIS119和THR199与Zn形成金属离子配位络合物,类似于标准抑制剂SLC-0111的相互作用模式。在缺氧条件下进行的500 ns以上的分子动力学(MD)模拟表明,V35具有高结合稳定性,其均方根偏差(RMSD)和波动(RMSF)值与SLC-0111相当,证明了其在CA XII中的构象稳定性。使用MMGBSA方法进行的结合自由能计算表明,V35与CA XII的结合自由能为-44.17 kcal/mol,与SLC-0111(-49.41 kcal/mol)非常匹配。密度泛函理论(DFT)计算进一步突出了V35的静电势分布,支持其同工酶选择性。动力学后分析表明,酯官能团和HIS64的向内移动稳定了V35在CA XII中的相互作用,这是CA I中不存在的特征。