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Isoniazid (H) • It is a prodrug activated by catalase-peroxidase (coded by KatG). Active metabolite inhibits the enzyme ketoenoylreductase (coded by inh A), required for mycolic acid synthesis, an essential component of mycobacterial cell wall. It acts by O2 dependent pathway such as catalase peroxidase reaction. • It is bacteriostatic against resting and bactericidal against rapidly multiplying organisms. • It is effective against intra- as well as extra-cellular mycobacteria. • Action is most marked against rapidly multiplying bacilli (less effective against slow multipliers). • It is widely distributed in the body and has maximum CSF penetration. • It is effective orally and metabolized by ACETYLATION which is genetically controlled. Fast acetylators require high dose and slow acetylators are predisposed to toxicity (particularly peripheral neuritis). • It is an essential component of multi-drug therapy of tuberculosis and is drug of choice (used solely) for prophylaxis of tuberculosis and for treatment of latent tuberculosis infection. • Resistance occurs due to mutation in Kat G (gene for catalse-peroxidase) or inhA. Mutation in kat G is responsible for high level resistance whereas mutation in inhA confers cross resistance to ethionamide. • It causes peripheral neuritis that can be prevented and treated by pyridoxine. • It is also hepatotoxic and can cause hemolysis in G-6 PD deficient patients. Incidence of hepatotoxicity increases with age, daily alcohol consumption and in post partum (3 months) period. • Isoniazid also inhibits MAO-A; thus can result in cheese reaction. • Rash, fever, anemia, optic neuritis, seizures, lupus like syndrome, transient memory loss, psychosis and gynaecomastia has also been reported with this drug.