Peddibhotla Satyamaheshwar, Fontaine Pauline, Leung Chi K, Maloney Patrick, Hershberger Paul M, Wang Ying, Bousquet Michelle S, Luesch Hendrik, Mangravita-Novo Arianna, Pinkerton Anthony B, Smith Layton H, Malany Siobhan, Choe Keith
†Conrad Prebys Center for Chemical Genomics at Sanford-Burnham Medical Research Institute, Orlando, Florida 32827, United States.
⊥Department of Biology and Genetics Institute, University of Florida, Gainesville, Florida 32611, United States.
ACS Chem Biol. 2015 Aug 21;10(8):1871-9. doi: 10.1021/acschembio.5b00304. Epub 2015 May 22.
Nematodes parasitize ∼1/3 of humans worldwide, and effective treatment via administration of anthelmintics is threatened by growing resistance to current therapies. The nematode transcription factor SKN-1 is essential for development of embryos and upregulates the expression of genes that result in modification, conjugation, and export of xenobiotics, which can promote resistance. Distinct differences in regulation and DNA binding relative to mammalian Nrf2 make SKN-1 a promising and selective target for the development of anthelmintics with a novel mode of action that targets stress resistance and drug detoxification. We report 17 (ML358), a first in class small molecule inhibitor of the SKN-1 pathway. Compound 17 resulted from a vanillamine-derived hit identified by high throughput screening that was advanced through analog synthesis and structure-activity studies. Compound 17 is a potent (IC50 = 0.24 μM, Emax = 100%) and selective inhibitor of the SKN-1 pathway and sensitizes the model nematode C. elegans to oxidants and anthelmintics. Compound 17 is inactive against Nrf2, the homologous mammalian detoxification pathway, and is not toxic to C. elegans (LC50 > 64 μM) and Fa2N-4 immortalized human hepatocytes (LC50 > 5.0 μM). In addition, 17 exhibits good solubility, permeability, and chemical and metabolic stability in human and mouse liver microsomes. Therefore, 17 is a valuable probe to study regulation and function of SKN-1 in vivo. By selective targeting of the SKN-1 pathway, 17 could potentially lead to drug candidates that may be used as adjuvants to increase the efficacy and useful life of current anthelmintics.
线虫寄生在全球约三分之一的人类体内,而通过施用驱虫药进行有效治疗正受到对当前疗法不断增加的耐药性的威胁。线虫转录因子SKN-1对胚胎发育至关重要,并上调导致外源性物质修饰、结合和输出的基因的表达,这可能会促进耐药性。与哺乳动物Nrf2相比,SKN-1在调控和DNA结合方面存在明显差异,这使得SKN-1成为开发具有针对应激抗性和药物解毒新作用模式的驱虫药的有前景且具选择性的靶点。我们报道了化合物17(ML358),它是SKN-1通路的首个小分子抑制剂。化合物17源自高通量筛选鉴定出的一种香草胺衍生的活性化合物,通过类似物合成和构效关系研究得到优化。化合物17是SKN-1通路的强效(IC50 = 0.24 μM,Emax = 100%)且具选择性的抑制剂,可使模式线虫秀丽隐杆线虫对氧化剂和驱虫药敏感。化合物17对同源的哺乳动物解毒通路Nrf2无活性,对秀丽隐杆线虫(LC50 > 64 μM)和Fa2N-4永生化人肝细胞(LC50 > 5.0 μM)无毒。此外,化合物17在人和小鼠肝微粒体中表现出良好的溶解性、渗透性以及化学和代谢稳定性。因此,化合物17是研究体内SKN-1调控和功能的有价值的探针。通过选择性靶向SKN-1通路,化合物17可能会催生可作为佐剂使用的候选药物,以提高当前驱虫药的疗效和使用寿命。