“…In M. tuberculosis, DNA gyrase is the sole target, since it lacks the topoisomerase (Nagaraja et al, 2017;Aubry, 2004) Fluoroquinolones are attractive since they have activity against replicating, non-replicating and intracellular M. tuberculosis. Resistance to fluoroquinolones in M. tuberculosis is due to mutations in DNA gyrase (Avalos et al, 2015); high level resistance is generally conferred by mutation in the GyrA subunit in the quinolone resistance determining region covering codons 74-113 (Soudani et al, 2010;Singh et al, 2015;Singh et al, 2021;Chaoui et al, 2018). A single mutation can lead to resistance to the entire class of fluoroquinolones, therefore novel agents with different binding modes would be useful.…”