Tuberculosis, a disease caused by Mycobacterium tuberculosis, constitutes a substantial health concern that affects 10.3 million of the global population. Throughout the latent phase of infection, Mycobacterium tuberculosis bacilli can endure within granulomas for extended durations as they are exhibiting low metabolic activity and are therefore slow or non-replicating. Isoniazid (INH), a hydrazide which acts as a tight-binding inhibitor of enoyl reductase (InhA), is the main component of current TB drugs. INH is activated by the KatG catalase-peroxidase to inhibit bacterial cell wall synthesis. Another hydrazine compound used against TB, thiacetazone (TAC), undergoes activation through the action of mono-oxygenase EthA and hydroxymycolate synthase (MmaA4). This activation process alters the structure of hydroxyl-acyl-dehydratases (HadAB, HadBC), prominent enzymes which catalyze Mtb's mycolic acid biosynthesis and elongation pathway. However, external host-induced factors, notably low oxygen levels, altered pH conditions and exposure to reactive nitrogen species (RNS) and reactive oxygen species (ROS) may result in enhanced antibiotic resistance to INH and TAC.