Pfizer Neuroscience Princeton, NJ 08852, USA.
J Med Chem. 2011 Nov 10;54(21):7621-38. doi: 10.1021/jm2009138. Epub 2011 Oct 11.
The identification of highly potent and orally active phenylpyrazines for the inhibition of PDE10A is reported. The new analogues exhibit subnanomolar potency for PDE10A, demonstrate high selectivity against all other members of the PDE family, and show desired druglike properties. Employing structure-based drug design approaches, we methodically explored two key regions of the binding pocket of the PDE10A enzyme to alter the planarity of the parent compound 1 and optimize its affinity for PDE10A. Bulky substituents at the C9 position led to elimination of the mutagenicity of 1, while a crucial hydrogen bond interaction with Glu716 markedly enhanced its potency and selectivity. A systematic assessment of the ADME and PK properties of the new analogues led to druglike development candidates. One of the more potent compounds, 96, displayed an IC(50) for PDE10A of 0.7 nM and was active in predictive antipsychotic animal models.
报道了用于抑制 PDE10A 的高活性和口服活性的苯基吡嗪的鉴定。新类似物对 PDE10A 具有亚纳摩尔效力,对 PDE 家族的所有其他成员表现出高度选择性,并表现出所需的类药性。通过基于结构的药物设计方法,我们系统地探索了 PDE10A 酶结合口袋的两个关键区域,以改变母体化合物 1 的平面性并优化其对 PDE10A 的亲和力。C9 位置的大取代基导致 1 的致突变性消除,而与 Glu716 的关键氢键相互作用则显著增强了其效力和选择性。对新类似物的 ADME 和 PK 性质进行了系统评估,得到了具有类药性的开发候选物。其中一种更有效的化合物 96 对 PDE10A 的 IC50为 0.7 nM,并在预测性抗精神病动物模型中具有活性。