Poulsen Anders, Bjørnholm Berith, Gundertofte Klaus, Pogozheva Irina D, Liljefors Tommy
Department of Medicinal Chemistry, The Danish University of Pharmaceutical Sciences, 2 Universitetsparken, DK-2100 Copenhagen, Denmark.
J Comput Aided Mol Des. 2003 Nov;17(11):765-83. doi: 10.1023/b:jcam.0000017497.58165.d8.
Three neurokinin (NK) antagonist pharmacophore models (Models 1-3) accounting for hydrogen bonding groups in the 'head' and 'tail' of NK receptor ligands have been developed by use of a new procedure for treatment of hydrogen bonds during superimposition. Instead of modelling the hydrogen bond acceptor vector in the strict direction of the lone pair, an angle is allowed between the hydrogen bond acceptor direction and the ideal lone pair direction. This approach adds flexibility to hydrogen bond directions and produces more realistic RMS values. By using this approach, two novel pharmacophore models were derived (Models 2 and 3) and a hydrogen bond acceptor was added to a previously published NK2 pharmacophore model [Poulsen et al., J. Comput.-Aided Mol. Design, 16 (2002) 273] (Model 1). Model 2 as well as Model 3 are described by seven pharmacophore elements: three hydrophobic groups, three hydrogen bond acceptors and a hydrogen bond donor. Model 1 contains the same hydrophobic groups and hydrogen bond donor as Models 2 and 3, but only one hydrogen bond acceptor. The hydrogen bond acceptors and donor are represented as vectors. Two of the hydrophobic groups are always aromatic rings whereas the other hydrophobic group can be either aromatic or aliphatic. In Model 1 the antagonists bind in an extended conformation with two aromatic rings in a parallel displaced and tilted conformation. Model 2 has the same two aromatic rings in a parallel displaced conformation whereas Model 3 has the rings in an edge to face conformation. The pharmacophore models were evaluated using both a structure (NK receptor homology models) and a ligand based approach. By use of exhaustive conformational analysis (MMFFs force field and the GB/SA hydration model) and least-squares molecular superimposition studies, 21 non-peptide antagonists from several structurally diverse classes were fitted to the pharmacophore models. More antagonists could be fitted to Model 2 with a low RMS and a low conformational energy penalty than to Models 1 and 3. Pharmacophore Model 2 was also able to explain the NK1, NK2 and NK3 subtype selectivity of the compounds fitted to the model. Three NK 7TM receptor models were constructed, one for each receptor subtype. The location of the antagonist binding site in the three NK receptor models is identical. Compounds fitted to pharmacophore Model 2 could be docked into the NK1, NK2 and NK3 receptor models after adjustment of the conformation of the flexible linker connecting the head and tail. Models I and 3 are not compatible with the receptor models.
通过使用一种在叠合过程中处理氢键的新方法,已开发出三种神经激肽(NK)拮抗剂药效团模型(模型1 - 3),该模型考虑了NK受体配体“头部”和“尾部”中的氢键基团。与在孤对严格方向上对氢键受体向量进行建模不同,允许氢键受体方向与理想孤对方向之间存在一个角度。这种方法增加了氢键方向的灵活性,并产生了更现实的均方根(RMS)值。通过使用这种方法,得出了两种新型药效团模型(模型2和3),并在先前发表的NK2药效团模型[Poulsen等人,《计算机辅助分子设计杂志》,16(2002)273](模型1)中添加了一个氢键受体。模型2和模型3由七个药效团元素描述:三个疏水基团、三个氢键受体和一个氢键供体。模型1包含与模型2和3相同的疏水基团和氢键供体,但只有一个氢键受体。氢键受体和供体表示为向量。其中两个疏水基团始终是芳香环,而另一个疏水基团可以是芳香族或脂肪族的。在模型1中,拮抗剂以伸展构象结合,两个芳香环呈平行错位和倾斜构象。模型2具有相同的两个平行错位构象的芳香环,而模型3中的环呈面对面构象。使用结构(NK受体同源模型)和基于配体的方法对药效团模型进行了评估。通过使用详尽的构象分析(MMFFs力场和GB/SA水合模型)和最小二乘分子叠合研究,将来自几个结构不同类别的21种非肽拮抗剂拟合到药效团模型中。与模型1和3相比,更多的拮抗剂能够以低均方根和低构象能量罚分拟合到模型2中。药效团模型2还能够解释拟合到该模型的化合物的NK1、NK2和NK3亚型选择性。构建了三个NK 7TM受体模型,每个受体亚型一个。拮抗剂结合位点在三个NK受体模型中的位置是相同的。在调整连接头部和尾部的柔性接头的构象后,拟合到药效团模型2的化合物可以对接至NK1、NK2和NK3受体模型中。模型1和3与受体模型不兼容。