Ramos-Molina Bruno, Lick Adam N, Blanco Elias H, Posada-Salgado J Alejandro, Martinez-Mayorga Karina, Johnson Alan T, Jiao Guan-Sheng, Lindberg Iris
Department of Anatomy and Neurobiology, School of Medicine, University of Maryland-Baltimore, MD, USA.
Instituto de Química, Universidad Nacional Autónoma de México, Mexico City, Mexico.
Biochem Pharmacol. 2015 Jul 15;96(2):107-18. doi: 10.1016/j.bcp.2015.05.008. Epub 2015 May 21.
The proprotein convertase furin is implicated in a variety of pathogenic processes such as bacterial toxin activation, viral propagation, and cancer. Several groups have identified non-peptide compounds with high inhibitory potency against furin in vitro, although their efficacy in various cell-based assays is largely unknown. In this study we show that certain guanidinylated 2,5-dideoxystreptamine derivatives exhibit interesting ex vivo properties. Compound 1b (1,1'-(4-((2,4-diguanidino-5-(4-guanidinophenoxy)cyclohexyl)oxy)-1,3-phenylene)diguanidine) is a potent and cell-permeable inhibitor of cellular furin, since it was able to retard tumor cell migration, block release of a Golgi reporter, and protect cells against Bacillus anthracis (anthrax) and Pseudomonas aeruginosa intoxication, with no evident cell toxicity. Other compounds based on the 2,5-dideoxystreptamine scaffold, such as compound 1g (1,1'-(4,6-bis(4-guanidinophenoxy)cyclohexane-1,3-diyl)diguanidine) also efficiently protected cells against anthrax, but displayed only moderate protection against Pseudomonas exotoxin A and did not inhibit cell migration, suggesting poor cell permeability. Certain bis-guanidinophenyl ether derivatives such as 2f (1,3-bis(2,4-diguanidinophenoxy) benzene) exhibited micromolar potency against furin in vitro, low cell toxicity, and highly efficient protection against anthrax toxin; this compound only slightly inhibited intracellular furin. Thus, compounds 1g and 2f both represent potent furin inhibitors at the cell surface with low intracellular inhibitory action, and these particular compounds might therefore be of preferred therapeutic interest in the treatment of certain bacterial and viral infections.
前体蛋白转化酶弗林蛋白酶与多种致病过程有关,如细菌毒素激活、病毒传播和癌症。几个研究小组已经鉴定出在体外对弗林蛋白酶具有高抑制效力的非肽化合物,尽管它们在各种基于细胞的检测中的功效在很大程度上尚不清楚。在本研究中,我们表明某些胍基化的2,5-二脱氧链霉胺衍生物具有有趣的体外特性。化合物1b(1,1'-(4-((2,4-二胍基-5-(4-胍基苯氧基)环己基)氧基)-1,3-亚苯基)二胍)是一种有效的细胞可渗透的细胞内弗林蛋白酶抑制剂,因为它能够延缓肿瘤细胞迁移、阻断高尔基体报告分子的释放,并保护细胞免受炭疽芽孢杆菌(炭疽)和铜绿假单胞菌中毒,且没有明显的细胞毒性。其他基于2,5-二脱氧链霉胺支架的化合物,如化合物1g(1,1'-(4,6-双(4-胍基苯氧基)环己烷-1,3-二基)二胍)也能有效地保护细胞免受炭疽感染,但对铜绿假单胞菌外毒素A的保护作用仅为中等,并且不抑制细胞迁移,表明细胞通透性较差。某些双胍基苯醚衍生物,如2f(1,3-双(2,4-二胍基苯氧基)苯)在体外对弗林蛋白酶具有微摩尔效力、低细胞毒性,并对炭疽毒素具有高效保护作用;该化合物仅轻微抑制细胞内弗林蛋白酶。因此,化合物1g和2f都是细胞表面有效的弗林蛋白酶抑制剂,细胞内抑制作用较低,因此这些特定化合物可能在治疗某些细菌和病毒感染方面具有优先的治疗意义。