Jia Xiuzhi, Han Qinglian, Ma Xiaoqun, Sun Zhongwen
Department of Immunology and Pathogen Biology, College of Medicine, Lishui University, Lishui, 323000, Zhejiang, China.
Center of Disease Immunity and Intervention, College of Medicine, Lishui University, Lishui, 323000, Zhejiang, China.
J Comput Aided Mol Des. 2025 Aug 19;39(1):69. doi: 10.1007/s10822-025-00650-z.
The highly aggressive primary brain tumor, glioma, presents significant therapeutic challenges, particularly in its diffuse form, which remains resistant to curative treatment even after surgical intervention. Conventional approaches such as surgery, radiotherapy, and chemotherapy often fail to achieve satisfactory outcomes, underscoring the urgent need for more effective targeted therapies. In this study, we have developed novel AKT inhibitors-compounds 3260-0411, V012-5231, and V016-4965. These compounds demonstrate a substantial reduction in both AKT protein and mRNA levels in U251 and T98G glioma cells. Furthermore, our in vitro experiments reveal that these inhibitors effectively suppress AKT1 enzyme activity and induce apoptosis in glioma cells. Molecular dynamics simulations indicate that all three compounds exhibit excellent dynamic stability when bound to AKT; notably V016-4965 demonstrates the highest binding stability among them. Collectively, our findings suggest that compounds 3260-0411, V012-5231, and V016-4965 hold great promise as targeted therapies against AKT for treating glioma-a challenging malignancy with limited management options.
高度侵袭性的原发性脑肿瘤——胶质瘤,带来了重大的治疗挑战,尤其是其弥漫性形式,即使在手术干预后仍对根治性治疗具有抗性。手术、放疗和化疗等传统方法往往无法取得令人满意的效果,这凸显了对更有效靶向治疗的迫切需求。在本研究中,我们开发了新型AKT抑制剂——化合物3260 - 0411、V012 - 5231和V016 - 4965。这些化合物在U251和T98G胶质瘤细胞中使AKT蛋白和mRNA水平大幅降低。此外,我们的体外实验表明,这些抑制剂能有效抑制AKT1酶活性并诱导胶质瘤细胞凋亡。分子动力学模拟表明,这三种化合物与AKT结合时均表现出优异的动态稳定性;值得注意的是,V016 - 4965在它们之中具有最高的结合稳定性。总体而言,我们的研究结果表明,化合物3260 - 0411、V012 - 5231和V016 - 4965作为针对AKT的靶向治疗药物,有望用于治疗胶质瘤——一种治疗选择有限的具有挑战性的恶性肿瘤。