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用于设计和开发潜在变构AKT抑制剂的骨架跃迁方法

Scaffold Hopping Method for Design and Development of Potential Allosteric AKT Inhibitors.

作者信息

Poustforoosh Alireza

机构信息

Medicinal and Natural Products Chemistry Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.

出版信息

Mol Biotechnol. 2024 Oct 27. doi: 10.1007/s12033-024-01307-2.

Abstract

Targeting AKT is a practical strategy for cancer therapy in many cancer types. Targeted inhibitors of AKT are attractive solutions for inhibiting the interconnected signaling pathways, like PI3K/Akt/mTOR. Allosteric inhibitors are more desirable among different classes of AKT inhibitors as they could be more specific with fewer off-target proteins. In this study, a ligand/structure-based pipeline was developed to design new allosteric AKT inhibitors by employing the core hopping method. Triciribine, a traditional allosteric AKT inhibitor was used as the template, and the FDA-approved kinase inhibitors for cancer treatment were considered as the cores. The allosteric site in the crystal structure of AKT1 was used to screen the designed compounds. The results were further evaluated using molecular docking, ADME/T analysis, molecular dynamics (MD) simulation, and binding free energy calculations. The outcomes introduced 24 newly designed inhibitors, amongst which three compounds C6, C20, and C16 showed remarkable binding affinity to AKT1. While the docking scores for triciribine was around - 8.6 kcal/mol, the docking scores of these compounds were about - 11 to - 13 kcal/mol. The MD results indicated that designed compounds target the essential residues of the PH domain and kinase domain of AKT, such as Trp80, Thr211, Tyr272, Asp274, and Asp292. Scaffold hopping is a tremendous tool for designing novel anti-cancer agents by improving already known and potential drug compounds. The designed compounds are worth to be examined by experimental investigation in vitro and in vivo.

摘要

在许多癌症类型中,靶向AKT是一种切实可行的癌症治疗策略。AKT的靶向抑制剂是抑制相互关联的信号通路(如PI3K/Akt/mTOR)的有吸引力的解决方案。在不同类型的AKT抑制剂中,变构抑制剂更受青睐,因为它们可能更具特异性,脱靶蛋白更少。在本研究中,开发了一种基于配体/结构的流程,通过采用核心跳跃方法设计新的变构AKT抑制剂。将传统的变构AKT抑制剂曲西立滨用作模板,并将FDA批准的用于癌症治疗的激酶抑制剂视为核心。利用AKT1晶体结构中的变构位点筛选设计的化合物。使用分子对接、ADME/T分析、分子动力学(MD)模拟和结合自由能计算进一步评估结果。结果引入了24种新设计的抑制剂,其中化合物C6、C20和C16对AKT1表现出显著的结合亲和力。曲西立滨的对接分数约为-8.6 kcal/mol,而这些化合物的对接分数约为-11至-13 kcal/mol。MD结果表明,设计的化合物靶向AKT的PH结构域和激酶结构域的关键残基,如Trp80、Thr211、Tyr272、Asp274和Asp292。骨架跳跃是一种通过改进已知和潜在的药物化合物来设计新型抗癌药物的强大工具。设计的化合物值得通过体外和体内实验研究进行检验。

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