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. 2021 Feb 2;11(2):88. doi: 10.3390/metabo11020088

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© 2021 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Mechanisms of action of various antituberculosis (anti-TB) drugs and compounds targeting the metabolism of Mycobacterium tuberculosis (Mtb). Many anti-TB drugs and compounds target different aspects of metabolism, and consequently lead to bacteriostasis or bactericidal effects. Some anti-TB drugs and compounds may share the same cellular targets. Others may act on different targets, which can affect common metabolic pathway(s). Drugs approved for treatment are colored in orange. Compounds undergoing clinical trials are colored in yellow. Compounds still in vitro developmental phase are colored in red. Text colored in grey are the proposed mechanisms. Abbreviations: INH = isoniazid; ETH = ethionamide; ISO = isoxyl; TAC = thioacetazone; BDQ = bedaquiline; FadDs = fatty acid adenylating enzymes; ICL = isocitrate lyase; EMB = ethambutol; ATP = adenosine triphosphate; NAD = nicotinamide adenine dinucleotide; LprG = Lipoarabinomannan carrier protein LprG; EthA = flavin adenine dinucleotide (FAD)-containing monooxygenase; HadAB = β-hydroxyacyl-ACP dehydratase HadAB complex; KatG = catalase-peroxidase; FAS II = type II fatty acid synthase; InhA = enoyl-ACP reductase; RNS = reactive nitrogen species; AG = arabinogalactan; TG = triacylglycerol; LAM = lipoarabinomannan; FAAL = fatty acyl AMP ligase; PDIM = phthiocerol dimycocerosates; SL-1 = sulfolipid-1; MA = mycolic acid.