Monoamine oxidases (MAOs) have become a potential target for the treatment and slow down of several neurodegenerative diseases. These are flavoenzymes that are present in the exterior of the mitochondrial membrane (Patil et al., 2013). Members of the monoamine oxidase family of flavoproteins catalyze the breakdown of primary, secondary amines, polyamines, and amino acids, including lysine demethylation in proteins (Gaweska & Fitzpatrick, 2011). MAOs are also found in almost any brain area as well as most of the peripheral organs. MAO exists in two isoforms: MAO-A and MAO-B (Saura et al., 1996). The oxidative deamination of neurochemicals such as dopamine (DA), serotonin, phenylethylamine, adrenaline, and noradrenaline is catalyzed by these enzymes. MAO-A shows an affinity toward substrates serotonin (5-HT), norepinephrine (NE), and dopamine (DA), while MAO-B has it toward phenylethylamine (PEA) and benzylamine . The degradation of serotonin, norepinephrine, and tyramine by MAO-A is therefore
Background: Tuberculosis is one of the oldest known infectious diseases to mankind, caused by Mycobacterium tuberculosis. Although current treatment using first-line anti-tubercular drugs is proven to be effective, an infection caused by resistant strains as in multidrug-resistant and extensive drug- resistant tuberculosis is still an impending challenge to treat. Objective: Our objective is to focus on reporting benzimidazole derivatives that are targeting mycobacterial membrane biosynthesis, particularly the mycobacterial mycolyl-arabinogalactan-peptidoglycan complexes. From the literature survey, it has been noted that targeting Mycobacterium tuberculosis cell membrane biosynthesis is an effective approach to fight against drug resistance in tuberculosis. Methods: Articles on benzimidazole derivatives as inhibitors of proteins responsible for the biosynthesis of the mycobacterial mycolyl-arabinogalactan-peptidoglycan complex have been selected. Results: By reviewing the anti-tubercular activity of the reported benzimidazole derivatives, we have concluded that there exists a correlation between benzimidazole derivatives and their biological activity. It has been noted that benzimidazole derivative with substitution at N1, C2, C5, and C6 positions have shown greater affinity towards target proteins. Conclusion: Even though scientific advancement towards the prevention of tuberculosis has been quite significant in the past few decades, still infection caused by resistant strains is a major concern. We have collected data on benzimidazole derivatives that inhibit the biosynthesis of mycolic acid, arabinogalactan and, peptidoglycan and from our observations, we conclude that majority of the molecules have given anti-tubercular activity in nanomolar range but there are few mycobacterial membrane biosynthesis proteins where benzimidazole as an inhibitor has yet to be explored.
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