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靶向血管内皮生长因子受体2(VEGFR2)和黏着斑激酶(FAK)的双激酶抑制剂的发现:基于结构的药效团建模、虚拟筛选及分子对接研究

Discovery of dual kinase inhibitors targeting VEGFR2 and FAK: structure-based pharmacophore modeling, virtual screening, and molecular docking studies.

作者信息

Fouad Marwa A, Osman Alaa A, Abdelhamid Noha M, Rashad Mai W, Nabawy Ashrakat Y, El Kerdawy Ahmed M

机构信息

Pharmaceutical Chemistry Department, Faculty of Pharmacy, Cairo University, Kasr El-Aini St., Cairo, 11562, Egypt.

Pharmaceutical Chemistry Department, School of Pharmacy, Newgiza University (NGU), Newgiza, Km 22 Cairo-Alexandria Desert Road, Cairo, Egypt.

出版信息

BMC Chem. 2024 Feb 12;18(1):29. doi: 10.1186/s13065-024-01130-5.

Abstract

VEGFR2 and FAK signaling pathways are interconnected and have synergistic effects on tumor angiogenesis, growth, and metastasis. Thus, instead of the conventional targeting of each of these proteins individually with a specific inhibitor, the present work aimed to discover novel dual inhibitors targeting both VEGFR2 and FAK exploiting their association. To this end, receptor-based pharmacophore modeling technique was opted to generate 3D pharmacophore models for VEGFR2 and FAK type II kinase inhibitors. The generated pharmacophore models were validated by assessing their ability to discriminate between active and decoy compounds in a pre-compiled test set of VEGFR2 and FAK active compounds and decoys. ZINCPharmer web tool was then used to screen the ZINC database purchasable subset using the validated pharmacophore models retrieving 42,616 hits for VEGFR2 and 28,475 hits for FAK. Subsequently, they were filtered using various filters leaving 13,023 and 6,832 survived compounds for VEGFR2 and FAK, respectively, with 124 common compounds. Based on molecular docking simulations, thirteen compounds were found to satisfy all necessary interactions with VEGFR2 and FAK kinase domains. Thus, they are predicted to have a possible dual VEGFR2/FAK inhibitory activity. Finally, SwissADME web tool showed that compound ZINC09875266 is not only promising in terms of binding pattern to our target kinases, but also in terms of pharmacokinetic properties.

摘要

血管内皮生长因子受体2(VEGFR2)和黏着斑激酶(FAK)信号通路相互关联,对肿瘤血管生成、生长和转移具有协同作用。因此,本研究并非采用传统方法分别用特定抑制剂单独靶向这些蛋白,而是旨在利用VEGFR2和FAK之间的关联发现新型双靶点抑制剂。为此,选择基于受体的药效团建模技术来生成VEGFR2和FAK II型激酶抑制剂的三维药效团模型。通过评估所生成的药效团模型在VEGFR2和FAK活性化合物及诱饵的预编译测试集中区分活性化合物和诱饵化合物的能力,对其进行验证。然后使用ZINCPharmer网络工具,利用经过验证的药效团模型筛选可购买的ZINC数据库子集,VEGFR2检索到42,616个命中结果,FAK检索到28,475个命中结果。随后,使用各种过滤器对它们进行筛选,分别留下13,023个和6,832个VEGFR2和FAK的存活化合物,其中有124个共同化合物。基于分子对接模拟,发现有13种化合物与VEGFR2和FAK激酶结构域满足所有必要的相互作用。因此,预计它们具有可能的双靶点VEGFR2/FAK抑制活性。最后,SwissADME网络工具显示,化合物ZINC09875266不仅在与我们的目标激酶的结合模式方面有前景,而且在药代动力学性质方面也有前景。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c34/10863211/1311c76996da/13065_2024_1130_Fig1_HTML.jpg

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