The more common of these occurrences is 'drug resistance among previously treated patients', in which inadequate treatment or lack of adherence by the patient results in the selection of naturally occurring resistant mutants .Less common is cross-resistance, in which resistance occurs between drugs that are chemically related and/or have a similar target within the mycobacterial cell (ie rifampin and other rifamycin derivatives, or isoniazid and ethionamide) [ is not always clear.Moreover, this moiety is crucial for the affinity of the arylamide–Inh A interactions with Tyr158 and NADH to form hydrogen bonds.
Rather, MDR develops by sequential acquisition of mutations at different loci, usually because of inappropriate patient treatment.
Recent research has probed the mechanism of action of isoniazid (INH), a key drug in the chemotherapy of tuberculosis and also the anti-mycobacterial potential of derivatives of isoniazid has been evaluated.
We have made an attempt to compile an account of various derivatives of isoniazid reported for their diverse biological activities like anti-mycobacterial, -bacterial, -fungal and -viral activities.
Arylamides show high potency in Inh A enzyme assay, but they fail in antimycobacterial assay.
To achieve the structural basis to improve antimycobacterial activity, the dynamic behavior of arylamide inhibitors and a substrate, -acetylcysteamine)-thioester, were carried out by molecular dynamics (MD) simulations.