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Fig 1.

Initial pharmacophore/Bayesian model-derived hits: A) chemical structures, in vitro antitubercular activity, and B) best fit to menadione pharmacophore of BAS04912643, C) best fit to menadione pharmacophore of B. BAS00623753 (grey).

D. best fit to indole-3-acetamide pharmacophore of BAS7571651, E best fit to lipoamide shape of BAS7571651. The pharmacophores consist of hydrogen bond acceptors (green) hydrogen bond donors (purple) and hydrophobic features (blue). The van der Waals surface was used to limit the number of compounds retrieved when screening the vendor library.

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Fig 1 Expand

Fig 2.

Synthetic routes to the A) arylamide and B) quinoxaline di-N-oxide families.

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Fig 2 Expand

Table 1.

Mtb growth inhibitory activities of BAS 00623753 and a small set of analogs.

Molecule structures are in S1 Data.

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Table 1 Expand

Table 2.

Structures and activities of the quinoxaline di-N-oxide family (nd = not determined).

Molecule structures are in S1 Data.

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Table 2 Expand

Fig 3.

Structures of quinoxaline di-N-oxides with the most promising antitubercular activities and selectivities.

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Fig 3 Expand

Table 3.

Physiochemical and ADME data.

For microsomal stability, verapamil was used as a high-metabolism control (0.24% remaining with NADPH) and warfarin was a low-metabolism control (85% remaining with NADPH). The kinetic solubility limit was the highest concentration with no detectable precipitate. For Caco-2 cell permeability, compounds at a concentration of 10 μM were incubated for 2 h. Papp = apparent permeability coefficient. All compounds showed poor recovery due to either low solubility or non-specific binding. Ranitidine, warfarin and talindol were used as low permeability, high permeability and P-gp efflux, controls respectively.

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Table 3 Expand

Table 4.

Activity of SRI50 against wild type and clinical MDR-TB strains.

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Table 4 Expand

Fig 4.

Mtb transcriptional response to SRI54 as compared to other small molecule antituberculars and environmental stresses.

100 SRI54 most induced and repressed genes (top-bottom) are clustered with responses to other treatments (left-right). The top dendrogram indicates relatedness of the Mtb perturbations based on gene clusters. Red indicates increase, blue indicates decrease and white no change in expression versus DMSO treatment. Amp, ampicillin; EMB, ethambutol; TLM, thiolactomycin; INH, isoniazid; ETH, ethionamide; 5-Cl-PZA, 5-chloropyrazinamide, CPZ, chlorpromazine; CCCP, carbonyl cyanide 3-chlorophenylhydrazone; GSNO, S-nitrosoglutathione; DNP, 2,4-dinitrophenol.

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Fig 4 Expand