NIH Chemical Genomics Center, National Human Genome Research Institute, National Institutes of Health, Rockville, Maryland 20850, USA.
J Med Chem. 2011 Sep 22;54(18):6215-33. doi: 10.1021/jm200497t. Epub 2011 Aug 19.
Spinal muscular atrophy (SMA) is an autosomal recessive disorder affecting the expression or function of survival motor neuron protein (SMN) due to the homozygous deletion or rare point mutations in the survival motor neuron gene 1 (SMN1). The human genome includes a second nearly identical gene called SMN2 that is retained in SMA. SMN2 transcripts undergo alternative splicing with reduced levels of SMN. Up-regulation of SMN2 expression, modification of its splicing, or inhibition of proteolysis of the truncated protein derived from SMN2 have been discussed as potential therapeutic strategies for SMA. In this manuscript, we detail the discovery of a series of arylpiperidines as novel modulators of SMN protein. Systematic hit-to-lead efforts significantly improved potency and efficacy of the series in the primary and orthogonal assays. Structure-property relationships including microsomal stability, cell permeability, and in vivo pharmacokinetics (PK) studies were also investigated. We anticipate that a lead candidate chosen from this series may serve as a useful probe for exploring the therapeutic benefits of SMN protein up-regulation in SMA animal models and a starting point for clinical development.
脊髓性肌萎缩症(SMA)是一种常染色体隐性疾病,由于生存运动神经元基因 1(SMN1)的纯合缺失或罕见点突变,影响生存运动神经元蛋白(SMN)的表达或功能。人类基因组包括第二个几乎相同的基因,称为 SMN2,它在 SMA 中保留。SMN2 转录本通过选择性剪接,SMN 的水平降低。上调 SMN2 表达、修饰其剪接或抑制源自 SMN2 的截短蛋白的蛋白水解已被讨论为 SMA 的潜在治疗策略。在本文中,我们详细描述了一系列芳基哌啶作为新型 SMN 蛋白调节剂的发现。系统的从头开始努力显著提高了该系列在主要和正交测定中的效力和功效。还研究了结构-性质关系,包括微粒体稳定性、细胞通透性和体内药代动力学(PK)研究。我们预计,从该系列中选择的一个先导候选药物可能成为探索 SMA 动物模型中 SMN 蛋白上调治疗益处的有用探针,也是临床开发的起点。