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Development of novel small molecules for the treatment of ALS.
Bioorganic & Medicinal Chemistry Letters ( IF 2.5 ) Pub Date : 2020-01-07 , DOI: 10.1016/j.bmcl.2020.126950 Bini Mathew 1 , Pedro Ruiz 1 , Vibha Pathak 1 , Mark J Suto 1
Bioorganic & Medicinal Chemistry Letters ( IF 2.5 ) Pub Date : 2020-01-07 , DOI: 10.1016/j.bmcl.2020.126950 Bini Mathew 1 , Pedro Ruiz 1 , Vibha Pathak 1 , Mark J Suto 1
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Amyotrophic lateral sclerosis (ALS) is a rare and progressive neurodegenerative disease with unknown etiology. It is caused by the degeneration of motor neurons responsible for controlling voluntary muscles. It has been reported that mutations in the superoxide dismutase (SOD) 1 gene can lead to ALS. SOD1 abnormalities have been identified in both familial, as well as sporadic ALS cases. SOD2 is a highly inducible SOD that works in conjunction with SOD1. SOD2 can be induced through activation of NF-κBs. We previously reported that the novel small molecule, SRI-22818, increases NF-κB expression and activation and SOD2 levels in vitro and has activity in vivo in the SOD1-G93A reference model of ALS. We report herein the synthesis and biological evaluation of SRI-22818 analogs.
中文翻译：
开发用于治疗ALS的新型小分子。
肌萎缩性侧索硬化症（ALS）是一种病因不明的罕见的进行性神经退行性疾病。它是由负责控制随意肌肉的运动神经元变性引起的。据报道，超氧化物歧化酶（SOD）1基因的突变可导致ALS。在家族性和散发性ALS病例中均已发现SOD1异常。SOD2是高度诱导型SOD，可与SOD1协同工作。SOD2可以通过激活NF-κB来诱导。我们先前曾报道，新型小分子SRI-22818在体外可增加NF-κB的表达和激活以及SOD2的水平，并且在ALS的SOD1-G93A参考模型中具有体内活性。我们在此报告SRI-22818类似物的合成和生物学评估。
更新日期：2020-01-07
中文翻译：
开发用于治疗ALS的新型小分子。
肌萎缩性侧索硬化症（ALS）是一种病因不明的罕见的进行性神经退行性疾病。它是由负责控制随意肌肉的运动神经元变性引起的。据报道，超氧化物歧化酶（SOD）1基因的突变可导致ALS。在家族性和散发性ALS病例中均已发现SOD1异常。SOD2是高度诱导型SOD，可与SOD1协同工作。SOD2可以通过激活NF-κB来诱导。我们先前曾报道，新型小分子SRI-22818在体外可增加NF-κB的表达和激活以及SOD2的水平，并且在ALS的SOD1-G93A参考模型中具有体内活性。我们在此报告SRI-22818类似物的合成和生物学评估。
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