TY - JOUR
T1 - USP2 inhibition prevents infection with ACE2-dependent coronaviruses in vitro and is protective against SARS-CoV-2 in mice
AU - Dang, Fabin
AU - Bai, Lei
AU - Dong, Jiazhen
AU - Hu, Xiaoping
AU - Wang, Jingchao
AU - Paulo, Joao A.
AU - Xiong, Yan
AU - Liang, Xiaowei
AU - Sun, Yishuang
AU - Chen, Yuncai
AU - Guo, Ming
AU - Wang, Xin
AU - Huang, Zhixiang
AU - Inuzuka, Hiroyuki
AU - Chen, Li
AU - Chu, Chen
AU - Liu, Jianping
AU - Zhang, Tao
AU - Rezaeian, Abdol Hossein
AU - Liu, Jing
AU - Kaniskan, Husnu Ümit
AU - Zhong, Bo
AU - Zhang, Jinfang
AU - Letko, Michael
AU - Jin, Jian
AU - Lan, Ke
AU - Wei, Wenyi
N1 - Publisher Copyright:
Copyright © 2023 The Authors, some rights reserved.
PY - 2023
Y1 - 2023
N2 - Targeting angiotensin-converting enzyme 2 (ACE2) represents a promising and effective approach to combat not only the COVID-19 pandemic but also potential future pandemics arising from coronaviruses that depend on ACE2 for infection. Here, we report ubiquitin specific peptidase 2 (USP2) as a host-directed antiviral target; we further describe the development of MS102, an orally available USP2 inhibitor with viable antiviral activity against ACE2-dependent coronaviruses. Mechanistically, USP2 serves as a physiological deubiquitinase of ACE2, and targeted inhibition with specific small-molecule inhibitor ML364 leads to a marked and reversible reduction in ACE2 protein abundance, thereby blocking various ACE2-dependent coronaviruses tested. Using human ACE2 transgenic mouse models, we further demonstrate that ML364 efficiently controls disease caused by infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), as evidenced by reduced viral loads and ameliorated lung inflammation. Furthermore, we improved the in vivo performance of ML364 in terms of both pharmacokinetics and antiviral activity. The resulting lead compound, MS102, holds promise as an oral therapeutic option for treating infections with coronaviruses that are reliant on ACE2.
AB - Targeting angiotensin-converting enzyme 2 (ACE2) represents a promising and effective approach to combat not only the COVID-19 pandemic but also potential future pandemics arising from coronaviruses that depend on ACE2 for infection. Here, we report ubiquitin specific peptidase 2 (USP2) as a host-directed antiviral target; we further describe the development of MS102, an orally available USP2 inhibitor with viable antiviral activity against ACE2-dependent coronaviruses. Mechanistically, USP2 serves as a physiological deubiquitinase of ACE2, and targeted inhibition with specific small-molecule inhibitor ML364 leads to a marked and reversible reduction in ACE2 protein abundance, thereby blocking various ACE2-dependent coronaviruses tested. Using human ACE2 transgenic mouse models, we further demonstrate that ML364 efficiently controls disease caused by infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), as evidenced by reduced viral loads and ameliorated lung inflammation. Furthermore, we improved the in vivo performance of ML364 in terms of both pharmacokinetics and antiviral activity. The resulting lead compound, MS102, holds promise as an oral therapeutic option for treating infections with coronaviruses that are reliant on ACE2.
UR - http://www.scopus.com/inward/record.url?scp=85179020470&partnerID=8YFLogxK
U2 - 10.1126/scitranslmed.adh7668
DO - 10.1126/scitranslmed.adh7668
M3 - Article
C2 - 38055802
AN - SCOPUS:85179020470
SN - 1946-6234
VL - 15
JO - Science Translational Medicine
JF - Science Translational Medicine
IS - 725
M1 - eadh7668
ER -