背景:结核病是人类已知的最古老的传染病之一,由结核分枝杆菌引起。尽管目前使用一线抗结核药物的治疗被证明是有效的,由耐药菌株引起的感染,耐多药和广泛耐药的结核病仍然是一个迫在眉睫的挑战治疗。
目的:我们的目标是重点报告针对分枝杆菌膜生物合成的苯并咪唑衍生物,特别是分枝杆菌霉菌-阿拉伯半乳聚糖肽聚糖复合物。从文献调查来看,已经注意到,靶向结核分枝杆菌细胞膜生物合成是对抗结核病耐药性的有效方法。
方法:选择了关于苯并咪唑衍生物作为负责分枝杆菌霉菌-阿拉伯半乳聚糖-肽聚糖复合物生物合成的蛋白质抑制剂的文章。
结果:通过回顾已报道的苯并咪唑衍生物的抗结核活性,我们得出的结论是苯并咪唑衍生物与其生物活性之间存在相关性。已经注意到,在N1、C2、C5和C6位置具有取代的苯并咪唑衍生物对靶蛋白显示出更大的亲和力。
结论:尽管在过去的几十年中,预防结核病的科学进步相当显著,耐药菌株引起的感染是一个主要问题。我们收集了有关苯并咪唑衍生物的数据,这些衍生物抑制了霉菌酸的生物合成,阿拉伯半乳聚糖和,肽聚糖。根据我们的观察,我们得出的结论是,大多数分子在纳摩尔范围内具有抗结核活性。仍然很少有分枝杆菌膜生物合成蛋白,其中苯并咪唑作为抑制剂尚待探索。
Tuberculosis is one of the oldest known infectious diseases to mankind, caused by Mycobacterium tuberculosis. Although current treatment using first-line anti-tubercular drugs is proven to be effective, an infection caused by resistant strains, as in multidrug-resistant and extensive drug- resistant tuberculosis is still an impending challenge to treat.
Our objective is to focus on reporting benzimidazole derivatives that are targeting mycobacterial membrane biosynthesis, particularly the mycobacterial mycolyl-arabinogalactanpeptidoglycan complexes. From the literature survey, it has been noted that targeting Mycobacterium tuberculosis cell membrane biosynthesis is an effective approach to fight against drug resistance in tuberculosis.
Articles on benzimidazole derivatives as inhibitors of proteins responsible for the biosynthesis of the mycobacterial mycolyl-arabinogalactan-
peptidoglycan complex have been selected.
By reviewing the anti-tubercular activity of the reported benzimidazole derivatives, we have concluded that a correlation between benzimidazole derivatives and their biological activity is found. It has been noted that benzimidazole derivatives with substitution at N1, C2, C5, and C6 positions have shown a greater affinity towards target proteins.
Even though scientific advancement toward the prevention of tuberculosis has been quite significant in the past few decades, infection caused by resistant strains is a major concern. We have collected data on benzimidazole derivatives that inhibit the biosynthesis of mycolic acid, arabinogalactan and,
peptidoglycan. From our observations, we conclude that majority of the molecules have given anti-tubercular activity in nanomolar range. Still there are few mycobacterial membrane biosynthesis proteins where benzimidazole as an inhibitor has yet to be explored.