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Glucomannan is a promising isoniazid's enhancer that inducing macrophage phagocytosis.
J Adv Pharm Technol Res
July 2024
Department of Internal Medicine, Faculty of Medicine, Widya Mandala Surabaya Catholic University, Surabaya, Indonesia.
Isoniazid (INH) is a frontline antituberculosis agent effective against (Mtb), but the increasing challenge of avoiding multidrug-resistant tuberculosis, including INH resistance, necessitates innovative approaches. This study focused on enhancing macrophage phagocytosis to overcome INH resistance. Glucomannan, an immunomodulatory polysaccharide, emerged as a potential macrophage activator.
View Article and Find Full Text PDFGenetic mechanisms of co-emergence of INH-resistant strains during the standard course of antituberculosis therapy.
Microbiol Spectr
April 2024
Department of Health Technology and Informatics, The Hong Kong Polytechnic University, Kowloon, Hong Kong SAR, China.
The incidence of isoniazid (INH) resistant is increasing globally. This study aimed to identify the molecular mechanisms behind the development of INH resistance in strains collected from the same patients during the standard course of treatment. Three strains were collected from a patient before and during antituberculosis (anti-TB) therapy.
View Article and Find Full Text PDFCharacterization of a catalase-peroxidase variant (L333V-KatG) identified in an INH-resistant clinical isolate.
Biochem Biophys Rep
March 2024
Departamento de Ingeniería Celular y Biocatálisis, Instituto de Biotecnología, UNAM, Avenida Universidad 2001, Colonia Chamilpa, 62210, Cuernavaca, México.
catalase-peroxidase (-KatG) is a bifunctional heme-dependent enzyme that has been shown to activate isoniazid (INH), the widely used antibiotic against tuberculosis (TB). The L333V-KatG variant has been associated with INH resistance in clinical isolates from Mexico. To understand better the mechanisms of INH activation, its catalytic properties (catalase, peroxidase, and IN-NAD formation) and crystal structure were compared with those of the wild-type enzyme (WT-KatG).
View Article and Find Full Text PDFExploring natural products library to identify potential inhibitors targeting isoniazid-resistant tuberculosis.
J Biomol Struct Dyn
February 2025
Department of Biotechnology, Faculty of Biomedical Sciences & Technology, Sri Ramachandra Institute of Higher Education and Research (DU), Chennai, India.
(MTB) causing tuberculosis (TB) infection is a leading source of illness and death in developing nations, and the emergence of drug-resistant TB remains a significant global threat and a challenge in treating the disease. Mutations in the and genes are connected to the principal molecular mechanism of isoniazid (INH) resistance, and continuous treatment of INH for more than a decade led to the evolution of INH resistant-TB (inhR-TB). Structure-based drug discovery approaches on traditional natural compounds are the contemporary source to identify significant lead molecules.
View Article and Find Full Text PDFIdentification of potential inhibitors of InhA: a pharmacoinformatics approach.
J Biomol Struct Dyn
September 2024
Medicinal Chemistry Division, University College of Pharmaceutical Sciences, Kakatiya University, Warangal, Telangana, India.
The emergence of superbugs of multi-drug resistant (MDR/RR) and extensively drug-resistant (XDR) () strains at a faster rate is posing a serious threat to Tuberculosis (TB) control worldwide. enoyl-acyl carrier protein reductase (InhA) is a well-established target of the front-line anti-TB prodrug Isoniazid (INH), which requires activation by Catalase-peroxidase enzyme (KatG) in order to inhibit InhA enzyme, that is crucial for the biosynthesis of the mycobacterial cell wall. Currently, due to widespread resistance to this drug, it is necessary to identify new clinical candidates that directly inhibit InhA enzyme and do not require activation by KatG, thereby circumventing most of the resistance mechanisms.
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