计算生物学
分子动力学
同源建模
对接(动物)
化学
药代动力学
结合亲和力
药品
血浆蛋白结合
同源(生物学)
药理学
亲缘关系
生物信息学
小分子
药物发现
分子模型
生物
仿形(计算机编程)
靶蛋白
鉴定(生物学)
生物物理学
蛋白质结构
蛋白质-蛋白质相互作用
结合位点
分子
作者
Felix Oluwasegun Ishabiyi,Haruna Isiyaku Umar,Tanmoy Duttaa,Okoyenta Celestina Onyinye,Olusola Daniel Damola,Leyla Budagova,Denekew Temesgen,Mohammed Bourhia,Ridwan Opeyemi Bello,Esmael M. Alyami,Mona Alsolami,Omar A. Almohammed
标识
DOI:10.1038/s41598-025-31607-9
摘要
The GPR176 protein is a cell membrane protein implicated in human diseases, especially cancers. Numerous studies have highlighted its overexpression, which is considered a major driver of tumorigenesis. Reducing its overexpression has been shown by many studies to be a viable pharmacological strategy for cancer therapy, prompting this study to search for drug molecules from existing FDA-approved drugs. We performed homology modeling of the GPR176 protein to obtain its 3D structure, conducted docking simulations of FDA-approved drugs retrieved from ReDO_DB to identify compounds with strong binding affinities, and carried out density functional theory quantum calculations and molecular dynamic simulations to assess stability and compactness. Additionally, pharmacokinetic profiling and drug-likeness analyses were performed to identify molecules capable of inhibiting and potentially deorphanizing GPR176. We identified Fostamatinib and Ticagrelor as both compounds exhibited binding affinities of -11.503 kcal/mol and − 11.882 kcal/mol, which indicates that both compounds effectively interact with the protein; they both had minimal deviations from their natural states as the RMSD values of 0.35 and 0.45 characterize their stability profile; energy gap of -0.1327 eV and − 0.1371 eV, which illuminates their reactivity to the protein and favorable pharmacokinetic profiles compared to the control, Vismodegib. This leads to the identification of Fostamatinib and Ticagrelor as potential inhibitors of the protein, and thus, we recommend further experimental studies to validate these findings.
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