Biological evaluation of benzothiazole ethyl urea inhibitors of bacterial type II topoisomerases

Antimicrob Agents Chemother. 2013 Dec;57(12):5977-86. doi: 10.1128/AAC.00719-13. Epub 2013 Sep 16.

Abstract

The type II topoisomerases DNA gyrase (GyrA/GyrB) and topoisomerase IV (ParC/ParE) are well-validated targets for antibacterial drug discovery. Because of their structural and functional homology, these enzymes are amenable to dual targeting by a single ligand. In this study, two novel benzothiazole ethyl urea-based small molecules, designated compound A and compound B, were evaluated for their biochemical, antibacterial, and pharmacokinetic properties. The two compounds inhibited the ATPase activity of GyrB and ParE with 50% inhibitory concentrations of <0.1 μg/ml. Prevention of DNA supercoiling by DNA gyrase was also observed. Both compounds potently inhibited the growth of a range of bacterial organisms, including staphylococci, streptococci, enterococci, Clostridium difficile, and selected Gram-negative respiratory pathogens. MIC90s against clinical isolates ranged from 0.015 μg/ml for Streptococcus pneumoniae to 0.25 μg/ml for Staphylococcus aureus. No cross-resistance with common drug resistance phenotypes was observed. In addition, no synergistic or antagonistic interactions between compound A or compound B and other antibiotics, including the topoisomerase inhibitors novobiocin and levofloxacin, were detected in checkerboard experiments. The frequencies of spontaneous resistance for S. aureus were <2.3 × 10(-10) with compound A and <5.8 × 10(-11) with compound B at concentrations equivalent to 8× the MICs. These values indicate a multitargeting mechanism of action. The pharmacokinetic properties of both compounds were profiled in rats. Following intravenous administration, compound B showed approximately 3-fold improvement over compound A in terms of both clearance and the area under the concentration-time curve. The measured oral bioavailability of compound B was 47.7%.

MeSH terms

  • Adenosine Triphosphatases / antagonists & inhibitors
  • Adenosine Triphosphatases / genetics
  • Adenosine Triphosphatases / metabolism
  • Animals
  • Anti-Bacterial Agents / chemistry
  • Anti-Bacterial Agents / pharmacokinetics
  • Anti-Bacterial Agents / pharmacology*
  • Bacterial Proteins / antagonists & inhibitors*
  • Bacterial Proteins / genetics
  • Bacterial Proteins / metabolism
  • Benzothiazoles / chemistry
  • Benzothiazoles / pharmacokinetics
  • Benzothiazoles / pharmacology*
  • Cell Survival / drug effects
  • DNA Topoisomerase IV / antagonists & inhibitors*
  • DNA Topoisomerase IV / genetics
  • DNA Topoisomerase IV / metabolism
  • DNA Topoisomerases, Type II / genetics
  • DNA Topoisomerases, Type II / metabolism*
  • Escherichia coli / genetics
  • Escherichia coli / metabolism
  • Gene Expression
  • Gram-Negative Bacteria / drug effects*
  • Gram-Negative Bacteria / enzymology
  • Gram-Negative Bacteria / growth & development
  • Gram-Positive Bacteria / drug effects*
  • Gram-Positive Bacteria / enzymology
  • Gram-Positive Bacteria / growth & development
  • Hep G2 Cells
  • Humans
  • Interleukin-33
  • Interleukins
  • Levofloxacin / pharmacology
  • Male
  • Microbial Sensitivity Tests
  • Novobiocin / pharmacology
  • Rats
  • Rats, Sprague-Dawley
  • Recombinant Proteins / genetics
  • Recombinant Proteins / metabolism
  • Topoisomerase Inhibitors / chemistry
  • Topoisomerase Inhibitors / pharmacokinetics
  • Topoisomerase Inhibitors / pharmacology*
  • Urea / analogs & derivatives*
  • Urea / chemistry
  • Urea / pharmacokinetics
  • Urea / pharmacology

Substances

  • Anti-Bacterial Agents
  • Bacterial Proteins
  • Benzothiazoles
  • Il33 protein, mouse
  • Interleukin-33
  • Interleukins
  • Recombinant Proteins
  • Topoisomerase Inhibitors
  • Novobiocin
  • Levofloxacin
  • Urea
  • Adenosine Triphosphatases
  • DNA Topoisomerase IV
  • DNA Topoisomerases, Type II