Firestine Steven M, Paritala Hanumantharao, McDonnell Jane E, Thoden James B, Holden Hazel M
Department of Pharmaceutical Sciences, Eugene Applebaum College of Pharmacy and Health Sciences, Wayne State University, Detroit, MI 48201, United States.
Bioorg Med Chem. 2009 May 1;17(9):3317-23. doi: 10.1016/j.bmc.2009.03.043. Epub 2009 Mar 26.
The increasing risk of drug-resistant bacterial infections indicates that there is a growing need for new and effective antimicrobial agents. One promising, but unexplored area in antimicrobial drug design is de novo purine biosynthesis. Recent research has shown that de novo purine biosynthesis in microbes is different from that in humans. The differences in the pathways are centered around the synthesis of 4-carboxyaminoimidazole ribonucleotide (CAIR) which requires the enzyme N(5)-carboxyaminoimidazole ribonucleotide (N(5)-CAIR) synthetase. Humans do not require and have no homologs of this enzyme. Unfortunately, no studies aimed at identifying small-molecule inhibitors of N(5)-CAIR synthetase have been published. To remedy this problem, we have conducted high-throughput screening (HTS) against Escherichia coliN(5)-CAIR synthetase using a highly reproducible phosphate assay. HTS of 48,000 compounds identified 14 compounds that inhibited the enzyme. The hits identified could be classified into three classes based on chemical structure. Class I contains compounds with an indenedione core. Class II contains an indolinedione group, and Class III contains compounds that are structurally unrelated to other inhibitors in the group. We determined the Michaelis-Menten kinetics for five compounds representing each of the classes. Examination of compounds belonging to Class I indicates that these compounds do not follow normal Michaelis-Menten kinetics. Instead, these compounds inhibit N(5)-CAIR synthetase by reacting with the substrate AIR. Kinetic analysis indicates that the Class II family of compounds are non-competitive with both AIR and ATP. One compound in Class III is competitive with AIR but uncompetitive with ATP, whereas the other is non-competitive with both substrates. Finally, these compounds display no inhibition of human AIR carboxylase:SAICAR synthetase indicating that these agents are selective inhibitors of N(5)-CAIR synthetase.
耐药细菌感染风险的不断增加表明,对新型有效抗菌药物的需求日益增长。抗菌药物设计中一个有前景但尚未探索的领域是从头嘌呤生物合成。最近的研究表明,微生物中的从头嘌呤生物合成与人类不同。这些途径的差异集中在4-羧基氨基咪唑核糖核苷酸(CAIR)的合成上,这需要N(5)-羧基氨基咪唑核糖核苷酸(N(5)-CAIR)合成酶。人类不需要这种酶,也没有其同源物。不幸的是,尚未发表旨在鉴定N(5)-CAIR合成酶小分子抑制剂的研究。为了解决这个问题,我们使用高度可重复的磷酸盐测定法对大肠杆菌N(5)-CAIR合成酶进行了高通量筛选(HTS)。对48,000种化合物的高通量筛选鉴定出14种抑制该酶的化合物。根据化学结构,所鉴定的命中化合物可分为三类。第一类包含具有茚二酮核心的化合物。第二类包含吲哚二酮基团,第三类包含与该组中其他抑制剂结构无关的化合物。我们确定了代表每一类的五种化合物的米氏动力学。对属于第一类的化合物的研究表明,这些化合物不遵循正常的米氏动力学。相反,这些化合物通过与底物AIR反应来抑制N(5)-CAIR合成酶。动力学分析表明,第二类化合物家族对AIR和ATP均无竞争性。第三类中的一种化合物与AIR竞争但与ATP非竞争性,而另一种与两种底物均无竞争性。最后,这些化合物对人AIR羧化酶:SAICAR合成酶没有抑制作用,表明这些药物是N(5)-CAIR合成酶的选择性抑制剂。