Bompiani Kristin M, Caglič Dejan, Krutein Michelle C, Benoni Galit, Hrones Morgan, Lairson Luke L, Bian Haiyan, Smith Garry R, Dickerson Tobin J
Department of Chemistry, The Scripps Research Institute , 10550 North Torrey Pines Road, La Jolla, California 92037, United States.
Fox Chase Chemical Diversity Center , 3805 Old Easton Road, Doylestown, Pennsylvania 18902, United States.
ACS Comb Sci. 2016 Aug 8;18(8):461-74. doi: 10.1021/acscombsci.6b00033. Epub 2016 Jul 20.
Botulism is caused by potent and specific bacterial neurotoxins that infect host neurons and block neurotransmitter release. Treatment for botulism is limited to administration of an antitoxin within a short time window, before the toxin enters neurons. Alternatively, current botulism drug development targets the toxin light chain, which is a zinc-dependent metalloprotease that is delivered into neurons and mediates long-term pathology. Several groups have identified inhibitory small molecules, peptides, or aptamers, although no molecule has advanced to the clinic due to a lack of efficacy in advanced models. Here we used a homogeneous high-throughput enzyme assay to screen three libraries of drug-like small molecules for new chemotypes that modulate recombinant botulinum neurotoxin light chain activity. High-throughput screening of 97088 compounds identified numerous small molecules that activate or inhibit metalloprotease activity. We describe four major classes of inhibitory compounds identified, detail their structure-activity relationships, and assess their relative inhibitory potency. A previously unreported chemotype in any context of enzyme inhibition is described with potent submicromolar inhibition (Ki = 200-300 nM). Additional detailed kinetic analyses and cellular cytotoxicity assays indicate the best compound from this series is a competitive inhibitor with cytotoxicity values around 4-5 μM. Given the potency and drug-like character of these lead compounds, further studies, including cellular activity assays and DMPK analysis, are justified.
肉毒中毒由强效且特异性的细菌神经毒素引起,这些毒素感染宿主神经元并阻断神经递质释放。肉毒中毒的治疗仅限于在毒素进入神经元之前的短时间窗内给予抗毒素。另外,目前肉毒中毒药物研发的靶点是毒素轻链,它是一种锌依赖性金属蛋白酶,可进入神经元并介导长期病理过程。尽管由于在先进模型中缺乏疗效,尚无分子进入临床,但已有多个研究小组鉴定出了抑制性小分子、肽或适配体。在此,我们使用一种均相高通量酶分析法,从三个类药物小分子文库中筛选可调节重组肉毒杆菌神经毒素轻链活性的新化学类型。对97088种化合物进行高通量筛选,鉴定出了许多激活或抑制金属蛋白酶活性的小分子。我们描述了鉴定出的四类主要抑制性化合物,详细阐述了它们的构效关系,并评估了它们的相对抑制效力。描述了一种在酶抑制的任何背景下均未报道过的化学类型,其具有强效的亚微摩尔抑制作用(Ki = 200 - 300 nM)。进一步详细的动力学分析和细胞毒性试验表明,该系列中最佳的化合物是一种竞争性抑制剂,细胞毒性值约为4 - 5 μM。鉴于这些先导化合物的效力和类药物特性,包括细胞活性测定和药物代谢动力学分析在内的进一步研究是合理的。