HCV-NS3 inhibitors: determination of their kinetic parameters and mechanism

Biochim Biophys Acta. 2009 Oct;1794(10):1441-8. doi: 10.1016/j.bbapap.2009.06.004. Epub 2009 Jun 6.

Abstract

Existing HCV protease inhibitors fall into two categories: reversible and non-covalent, such as BILN-2061, and covalent and reversible, exemplified by SCH-503034 and VX-950. In this work, the characterization of the kinetics of these three inhibitors is presented. SCH-503034 and VX-950 initially bind to the genotype 1b HCV NS3/4A protease to form a low affinity complex, with K(i) values of 5 and 5.8 microM respectively. The ability of those two compounds to form a second covalent complex (EI) results in a potency increase, with overall K(i) values of 20 and 45 nM, respectively. The increase in potency can be explained by their slow dissociation rate, forming complexes with half-lives of 2 h (VX-950) and 5 h (SCH-503034). Although BILN-2061 has been described as a fast reversible, non-covalent inhibitor, our results show a slow binding two-step mechanism. Contrary to SCH-503034 and VX-950, BILN-2061 can form a high affinity first complex with a K(i) value of 3.9 nM, and an overall K(i) of 0.14 nM. The half-life of the BILN-2061 EI complex is shorter (t(1/2) approximately 0.7 h) than that of the other two compounds. The potency of these compounds is genotype dependent, and a kinetic analysis using NS3/4A from genotype 3a indicates that the loss of potency of SCH-503034 and VX-950 relative to genotype 1 is mainly due to the slow on-rate and faster off-rate for the formation of the EI complex. In the case of BILN-2061, a better fit is obtained using a one-step model, indicating that the loss of potency is due to an increase in the off-rate of the EI complex.

MeSH terms

  • Amino Acid Substitution
  • Antiviral Agents / pharmacokinetics
  • Antiviral Agents / pharmacology*
  • Carbamates / pharmacokinetics
  • Carbamates / pharmacology
  • Drug Resistance, Viral / genetics
  • Genotype
  • Half-Life
  • Hepacivirus / drug effects*
  • Hepacivirus / enzymology*
  • Hepacivirus / genetics
  • Humans
  • Kinetics
  • Macrocyclic Compounds / pharmacokinetics
  • Macrocyclic Compounds / pharmacology
  • Models, Biological
  • Mutation
  • Oligopeptides / pharmacokinetics
  • Oligopeptides / pharmacology
  • Proline / analogs & derivatives
  • Proline / pharmacokinetics
  • Proline / pharmacology
  • Quinolines / pharmacokinetics
  • Quinolines / pharmacology
  • Recombinant Proteins / antagonists & inhibitors
  • Recombinant Proteins / genetics
  • Serine Endopeptidases / genetics
  • Serine Proteinase Inhibitors / pharmacokinetics
  • Serine Proteinase Inhibitors / pharmacology*
  • Thiazoles / pharmacokinetics
  • Thiazoles / pharmacology
  • Viral Nonstructural Proteins / antagonists & inhibitors*
  • Viral Nonstructural Proteins / genetics

Substances

  • Antiviral Agents
  • BILN 2061
  • Carbamates
  • Macrocyclic Compounds
  • NS3 protein, hepatitis C virus
  • Oligopeptides
  • Quinolines
  • Recombinant Proteins
  • Serine Proteinase Inhibitors
  • Thiazoles
  • Viral Nonstructural Proteins
  • telaprevir
  • N-(3-amino-1-(cyclobutylmethyl)-2,3-dioxopropyl)-3-(2-((((1,1-dimethylethyl)amino)carbonyl)amino)-3,3-dimethyl-1-oxobutyl)-6,6-dimethyl-3-azabicyclo(3.1.0)hexan-2-carboxamide
  • Proline
  • Serine Endopeptidases