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American Society for Microbiology, Antimicrobial Agents and Chemotherapy, 2(62), 2018

DOI: 10.1128/aac.02222-17

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Revisiting Activation of and Mechanism of Resistance to Compound IQG-607 in Mycobacterium tuberculosis

Journal article published in 2017 by Bruno L. Abbadi ORCID, Anne D. Villela, Valnês S. Rodrigues-Junior, Fernanda T. Subtil, Pedro F. Dalberto, Ana P. S. Pinheiro, Diógenes S. Santos, Pablo Machado, Luiz A. Basso, Cristiano V. Bizarro ORCID
This paper was not found in any repository, but could be made available legally by the author.
This paper was not found in any repository, but could be made available legally by the author.

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Abstract

ABSTRACT IQG-607 is a metal complex previously reported as a promising anti-tuberculosis (TB) drug against isoniazid (INH)-resistant strains of Mycobacterium tuberculosis . Unexpectedly, we found that INH-resistant clinical isolates were resistant to IQG-607. Spontaneous mutants resistant to IQG-607 were subjected to whole-genome sequencing, and all sequenced colonies carried alterations in the katG gene. The katG (S315T) mutation was sufficient to confer resistance to IQG-607 in both MIC assays and inside macrophages. Moreover, overexpression of the InhA(S94A) protein caused IQG-607's resistance.