Malleability of the SARS-CoV-2 3CL Mpro Active-Site Cavity Facilitates Binding of Clinical Antivirals

Structure. 2020 Dec 1;28(12):1313-1320.e3. doi: 10.1016/j.str.2020.10.007. Epub 2020 Oct 23.

Abstract

The COVID-19 pandemic caused by SARS-CoV-2 requires rapid development of specific therapeutics and vaccines. The main protease of SARS-CoV-2, 3CL Mpro, is an established drug target for the design of inhibitors to stop the virus replication. Repurposing existing clinical drugs can offer a faster route to treatments. Here, we report on the binding mode and inhibition properties of several inhibitors using room temperature X-ray crystallography and in vitro enzyme kinetics. The enzyme active-site cavity reveals a high degree of malleability, allowing aldehyde leupeptin and hepatitis C clinical protease inhibitors (telaprevir, narlaprevir, and boceprevir) to bind and inhibit SARS-CoV-2 3CL Mpro. Narlaprevir, boceprevir, and telaprevir are low-micromolar inhibitors, whereas the binding affinity of leupeptin is substantially weaker. Repurposing hepatitis C clinical drugs as COVID-19 treatments may be a useful option to pursue. The observed malleability of the enzyme active-site cavity should be considered for the successful design of specific protease inhibitors.

Keywords: 3CL M(pro); 3CL main protease; SARS-CoV-2; drug design; enzyme kinetics; hepatitis C clinical drugs; protease inhibitor; repurposing clinical drugs; room temperature X-ray crystallography.

Publication types

  • Research Support, U.S. Gov't, Non-P.H.S.
  • Comment

MeSH terms

  • Antiviral Agents* / pharmacology
  • Betacoronavirus* / metabolism
  • COVID-19*
  • Catalytic Domain
  • Coronavirus Infections* / drug therapy
  • Crystallography, X-Ray
  • Cysteine Endopeptidases / metabolism
  • Humans
  • Pandemics
  • Protease Inhibitors / pharmacology
  • SARS-CoV-2
  • Temperature
  • Viral Nonstructural Proteins

Substances

  • Antiviral Agents
  • Protease Inhibitors
  • Viral Nonstructural Proteins
  • Cysteine Endopeptidases