An arylsulphonamide that targets cell wall biosynthesis in Mycobacterium tuberculosis

We investigated the mechanism of action of an arylsulphonamide against Mycobacterium tuberculosis. We confirmed activity and selectivity against extracellular and intracellular bacilli. Bacterial cytological profiling suggested that mechanism of action was disruption of cell wall synthesis. The compound induced expression from the IniB promoter and boosted ATP production but did not induce reactive oxygen species. MmpL3 mutation led to low-level resistance. These data suggest the molecule targets cell wall biosynthesis with MmpL3 the probable target.