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1 sis to the second-line antituberculosis drug ethionamide.
2 amic studies are needed for pyrazinamide and ethionamide.
3 ere levofloxacin, amikacin, capreomycin, and ethionamide.
4 ikacin, 97.4% for capreomycin, and 88.9% for ethionamide.
5 eron encoding a monooxygenase that activates ethionamide.
6 s have the potential to activate the prodrug ethionamide.
7 racy (e.g., sensitivity: pyrazinamide + 25%; ethionamide + 10%).
8 pecificity was over 95% for all drugs except ethionamide (91.4%), moxifloxacin (91.6%) and ethambutol
9 erculosis (Mtb) that reduces the efficacy of ethionamide, a second-line antitubercular drug used to c
10 n mshA mutants was likely due to a defect in ethionamide activation.
11 ld allow a fourfold reduction in the dose of ethionamide administered while retaining the same effica
12 tients were included in the cohort receiving ethionamide and 4244 in the cohort receiving linezolid.
13 l of second-line drugs bioactivation such as ethionamide and has been shown to impair the sensitivity
14 ere resistant to the anti-tuberculosis drugs ethionamide and isoniazid were isolated and found to map
15 100 person-months with a fluoroquinolone and ethionamide, and 4.4 per 100 person-months with a fluoro
16 EthA, the bacterial monooxygenase activating ethionamide, and is thus largely responsible for the low
17                                Regimens with ethionamide are more likely to result in AEs.
18  observed with substitution of linezolid for ethionamide as a part of an all-oral 9-month regimen.
19 isk of AEs was higher in contacts prescribed ethionamide as compared to ethambutol adjusting for age,
20 r ethambutol, clofazimine, streptomycin, and ethionamide as regression graded considerably more resis
21 ed on a larger scale and confirmed as potent ethionamide boosters on M. tuberculosis -infected macrop
22 g design and in vitro/ex vivo evaluations of ethionamide boosters on the targeted protein EthR and on
23 nhibitors leading to the discovery of potent ethionamide boosters.
24 floxacin, moxifloxacin, amikacin, kanamycin, ethionamide, clofazimine, linezolid, delamanid, and beda
25 four antibiotics in clinical use: isoniazid, ethionamide, delamanid and pretomanid.
26 and high-dose L alone or in combination with ethionamide (Et), amikacin (A), and Z given for 2 or 7 m
27                                              Ethionamide (ETA) is an important component of second-li
28                                              Ethionamide (ETA), a prodrug that must undergo metabolic
29                             Thioamide drugs, ethionamide (ETH) and prothionamide (PTH), are clinicall
30 ds, were tested for their resistance to INH, ethionamide (ETH) or thiolactomycin (TLM).
31 t DA-CB has a general MoA related to that of ethionamide (ETH), a mycolic acid inhibitor that targets
32  to isoniazid (INH), fluoroquinolones (FLQ), ethionamide (ETH), and second-line injectable drugs (SLI
33 ity to detect resistance to isoniazid (INH), ethionamide (ETH), fluoroquinolones (FLQ), and second-li
34 rt treated with a 9-month regimen containing ethionamide for four months, was compared with a cohort
35 d putative resistance markers in katG, ethA (ethionamide), gyrA and gyrB (fluoroquinolones), and pncA
36                                              Ethionamide has been used for more than 30 years as a se
37  (i) coresistance to INH and a related drug, ethionamide; (ii) thermosensitive lethality; and (iii) a
38  to regimens including linezolid in 2019 and ethionamide in 2017.
39      SMARt751 also restored full efficacy of ethionamide in mice infected with M. tuberculosis strain
40    Linezolid is an acceptable alternative to ethionamide in this shorter regimen for treatment of mul
41             SMARt751 boosted the efficacy of ethionamide in vitro and in mouse models of acute and ch
42                   Activation of the pro-drug ethionamide is regulated by the Baeyer-Villiger monooxyg
43 twork analyses on cerulenin, chlorpromazine, ethionamide, ofloxacin, thiolactomycin and triclosan.
44 I 1.1-6.0]), ofloxacin (aOR: 2.5 [1.6-3.9]), ethionamide or prothionamide (aOR: 1.7 [1.3-2.3]), use o
45  [1.7-4.3]), ofloxacin (aOR: 2.3 [1.3-3.8]), ethionamide or prothionamide (aOR: 1.7 [1.4-2.1]), use o
46 namide, ethambutol, kanamycin, moxifloxacin, ethionamide, or clofazimine.
47 binations of moxifloxacin with pyrazinamide, ethionamide, or ethambutol were more active than pyrazin
48 ciated with use of certain fluoroquinolones, ethionamide, or prothionamide, and greater total number
49 mycin, capreomycin, ofloxacin, moxifloxacin, ethionamide, para-aminosalicylic acid, cycloserine, and
50 mycin, capreomycin, ofloxacin, moxifloxacin, ethionamide, para-aminosalicylic acid, linezolid, and cy
51 ifference was observed between linezolid and ethionamide regimens for treatment success (aRR = 0.96,
52 nd in vivo, and provide a novel mechanism of ethionamide resistance in M. tuberculosis.
53 ical studies suggested that the mechanism of ethionamide resistance in mshA mutants was likely due to
54 ying mutations in the ethA gene, which cause ethionamide resistance in the clinic.
55                  We identified isoniazid and ethionamide resistance mutations on line probe assay and
56 this intergenic region, thus contributing to ethionamide resistance.
57 fective in mycothiol biosynthesis, were only ethionamide-resistant and required catalase to grow.
58 compared to phenotypic DST, ranging from 33 (ethionamide) to 94% (rifampicin), while specificity rema
59  was 3.0 microg/ml, and that established for ethionamide was 5.0 microg/ml.
60  (pyrazinamide surrogate), prothionamide, or ethionamide, which were assay nonperformers.
61  South African tuberculosis program replaced ethionamide with linezolid as part of an all-oral 9-mont