Fig 1.
Structures of the compounds used in the study.
Table 1.
Activity of compounds against Staphylococcal planktonic cells (including clinical isolates).
Fig 2.
Propensity to induce resistance development in Gram-positive bacteria.
Fold of increase in MICs of Norfloxacin and NCK-10 against S. aureus.
Fig 3.
Antibacterial activity of NCK-10 at different physiological conditions.
Fig 4.
Kinetics of killing of S. aureus persister cells by NCK-10 at 5 × MIC.
(*) indicate that no colony was observed.
Fig 5.
Mechanism of action against persister cells.
(A) Depolarization of the membranes of S. aureus persister cells. (B) Permeabilization of S. aureus persister cells. The concentration of NCK-10 used is 5 × MIC.
Fig 6.
Ability of NCK-10 to disrupt methicillin resistant S. aureus biofilms.
(A) Reduction in viable bacterial count with respect to control at different concentrations of NCK-10. (B) Reduction in biofilm mass by crystal violet staining (Concentration of NCK-10 was 10×MIC). (C) Confocal of image of untreated biofilm and after treatment with NCK-10 (Concentration of NCK-10 was 10×MIC).
Fig 7.
(A) Bacterial titer in MRSA skin infection model (with planktonic cells). (B) Scanning electron micrographs of the wound tissue surface 24 h post inoculation. (C) Bacterial titer in MRSA skin infection model (Biofilm).
Fig 8.
(A) Untreated (B) Treated with Fusidic acid and (C) Treated with NCK-10.