Hardes Kornelia, Becker Gero L, Lu Yinghui, Dahms Sven O, Köhler Susanne, Beyer Wolfgang, Sandvig Kirsten, Yamamoto Hiroyuki, Lindberg Iris, Walz Lisa, von Messling Veronika, Than Manuel E, Garten Wolfgang, Steinmetzer Torsten
Institute of Pharmaceutical Chemistry, Philipps University, Marbacher Weg 6, 35032 Marburg (Germany).
Institute of Virology, Philipps University, Hans-Meerwein-Strasse 2, Marburg (Germany).
ChemMedChem. 2015 Jul;10(7):1218-31. doi: 10.1002/cmdc.201500103. Epub 2015 May 14.
New peptidomimetic furin inhibitors with unnatural amino acid residues in the P3 position were synthesized. The most potent compound 4-guanidinomethyl-phenylacteyl-Arg-Tle-Arg-4-amidinobenzylamide (MI-1148) inhibits furin with a Ki value of 5.5 pM. The derivatives also strongly inhibit PC1/3, whereas PC2 is less affected. Selected inhibitors were tested in cell culture for antibacterial and antiviral activity against infectious agents known to be dependent on furin activity. A significant protective effect against anthrax and diphtheria toxin was observed in the presence of the furin inhibitors. Furthermore, the spread of the highly pathogenic H5N1 and H7N1 avian influenza viruses and propagation of canine distemper virus was strongly inhibited. Inhibitor MI-1148 was crystallized in complex with human furin. Its N-terminal guanidinomethyl group in the para position of the P5 phenyl ring occupies the same position as that found previously for a structurally related inhibitor containing this substitution in the meta position, thereby maintaining all of the important P5 interactions. Our results confirm that the inhibition of furin is a promising strategy for a short-term treatment of acute infectious diseases.
合成了在P3位置带有非天然氨基酸残基的新型拟肽类弗林蛋白酶抑制剂。最有效的化合物4-胍基甲基-苯乙酰基-精氨酸-叔亮氨酸-精氨酸-4-脒基苄酰胺(MI-1148)抑制弗林蛋白酶的Ki值为5.5 pM。这些衍生物也强烈抑制PC1/3,而对PC2的影响较小。在细胞培养中测试了选定的抑制剂对已知依赖弗林蛋白酶活性的感染因子的抗菌和抗病毒活性。在存在弗林蛋白酶抑制剂的情况下,观察到对炭疽毒素和白喉毒素有显著的保护作用。此外,高致病性H5N1和H7N1禽流感病毒的传播以及犬瘟热病毒的增殖受到强烈抑制。抑制剂MI-1148与人弗林蛋白酶形成复合物结晶。其P5苯环对位的N端胍基甲基占据了先前在间位含有该取代基的结构相关抑制剂所发现的相同位置,从而维持了所有重要的P5相互作用。我们的结果证实,抑制弗林蛋白酶是急性传染病短期治疗的一种有前景的策略。