Lupala Cecylia S, Gomez-Gutierrez Patricia, Perez Juan J
Department of Chemical Engineering, Universitat Politecnica de Catalunya, ETSEIB. Av. Diagonal, 647, 08028, Barcelona, Spain.
J Comput Aided Mol Des. 2016 Jan;30(1):85-101. doi: 10.1007/s10822-015-9890-z. Epub 2015 Dec 24.
Bradykinin (BK) is a member of the kinin family, released in response to inflammation, trauma, burns, shock, allergy and some cardiovascular diseases, provoking vasodilatation and increased vascular permeability among other effects. Their actions are mediated through at least two G-protein coupled receptors, B1 a receptor up-regulated during inflammation episodes or tissue trauma and B2 that is constitutively expressed in a variety of cell types. The goal of the present work is to carry out a structure-activity study of BK B2 antagonism, taking into account the stereochemical features of diverse non-peptide antagonists and the way these features translate into ligand anchoring points to complementary regions of the receptor, through the analysis of the respective ligand-receptor complex. For this purpose an atomistic model of the BK B2 receptor was built by homology modeling and subsequently refined embedded in a lipid bilayer by means of a 600 ns molecular dynamics trajectory. The average structure from the last hundred nanoseconds of the molecular dynamics trajectory was energy minimized and used as model of the receptor for docking studies. For this purpose, a set of compounds with antagonistic profile, covering maximal diversity were selected from the literature. Specifically, the set of compounds include Fasitibant, FR173657, Anatibant, WIN64338, Bradyzide, CHEMBL442294, and JSM10292. Molecules were docked into the BK B2 receptor model and the corresponding complexes analyzed to understand ligand-receptor interactions. The outcome of this study is summarized in a 3D pharmacophore that explains the observed structure-activity results and provides insight into the design of novel molecules with antagonistic profile. To prove the validity of the pharmacophore hypothesized a virtual screening process was also carried out. The pharmacophore was used as query to identify new hits using diverse databases of molecules. The results of this study revealed a set of new hits with structures not connected to the molecules used for pharmacophore development. A few of these structures were purchased and tested. The results of the binding studies show about a 33% success rate with a correlation between the number of pharmacophore points fulfilled and their antagonistic potency. Some of these structures are disclosed in the present work.
缓激肽(BK)是激肽家族的一员,在炎症、创伤、烧伤、休克、过敏和一些心血管疾病发生时释放,可引起血管舒张和血管通透性增加等效应。其作用至少通过两种G蛋白偶联受体介导,即炎症发作或组织创伤时上调的B1受体和在多种细胞类型中组成性表达的B2受体。本研究的目的是进行BK B2拮抗剂的构效关系研究,通过分析相应的配体-受体复合物,考虑多种非肽拮抗剂的立体化学特征以及这些特征如何转化为受体互补区域的配体锚定点。为此,通过同源建模构建了BK B2受体的原子模型,随后通过600纳秒的分子动力学轨迹在脂质双层中进行优化。分子动力学轨迹最后一百纳秒的平均结构进行了能量最小化,并用作对接研究的受体模型。为此,从文献中选择了一组具有拮抗特性、涵盖最大多样性的化合物。具体而言,该组化合物包括法西替班、FR173657、阿那替班、WIN64338、缓激肽抑制剂、CHEMBL442294和JSM10292。将分子对接至BK B2受体模型并分析相应的复合物,以了解配体-受体相互作用。本研究的结果总结在一个三维药效团中,该药效团解释了观察到的构效关系结果,并为设计具有拮抗特性的新型分子提供了见解。为了证明所假设药效团的有效性,还进行了虚拟筛选过程。该药效团用作查询,使用不同的分子数据库识别新的命中物。本研究的结果揭示了一组新的命中物,其结构与用于药效团开发的分子无关。购买并测试了其中一些结构。结合研究的结果显示成功率约为33%,满足的药效团点数与其拮抗效力之间存在相关性。本研究中披露了其中一些结构。