ライフサイエンスコーパス: ethionamide

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1 amic studies are needed for pyrazinamide and ethionamide.

2 ere levofloxacin, amikacin, capreomycin, and ethionamide.

3 ikacin, 97.4% for capreomycin, and 88.9% for ethionamide.

4 sis to the second-line antituberculosis drug ethionamide.

5 erculosis (Mtb) that reduces the efficacy of ethionamide, a second-line antitubercular drug used to c

6 n mshA mutants was likely due to a defect in ethionamide activation.

7 l of second-line drugs bioactivation such as ethionamide and has been shown to impair the sensitivity

8 ere resistant to the anti-tuberculosis drugs ethionamide and isoniazid were isolated and found to map

9 EthA, the bacterial monooxygenase activating ethionamide, and is thus largely responsible for the low

10 ed on a larger scale and confirmed as potent ethionamide boosters on M. tuberculosis -infected macrop

11 g design and in vitro/ex vivo evaluations of ethionamide boosters on the targeted protein EthR and on

12 nhibitors leading to the discovery of potent ethionamide boosters.

13 and high-dose L alone or in combination with ethionamide (Et), amikacin (A), and Z given for 2 or 7 m

14 Ethionamide (ETA) is an important component of second-li

15 Ethionamide (ETA), a prodrug that must undergo metabolic

16 Thioamide drugs, ethionamide (ETH) and prothionamide (PTH), are clinicall

17 ds, were tested for their resistance to INH, ethionamide (ETH) or thiolactomycin (TLM).

18 Ethionamide has been used for more than 30 years as a se

19 (i) coresistance to INH and a related drug, ethionamide; (ii) thermosensitive lethality; and (iii) a

20 Activation of the pro-drug ethionamide is regulated by the Baeyer-Villiger monooxyg

21 twork analyses on cerulenin, chlorpromazine, ethionamide, ofloxacin, thiolactomycin and triclosan.

22 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

23 [1.7-4.3]), ofloxacin (aOR: 2.3 [1.3-3.8]), ethionamide or prothionamide (aOR: 1.7 [1.4-2.1]), use o

24 binations of moxifloxacin with pyrazinamide, ethionamide, or ethambutol were more active than pyrazin

25 ciated with use of certain fluoroquinolones, ethionamide, or prothionamide, and greater total number

26 mycin, capreomycin, ofloxacin, moxifloxacin, ethionamide, para-aminosalicylic acid, cycloserine, and

27 mycin, capreomycin, ofloxacin, moxifloxacin, ethionamide, para-aminosalicylic acid, linezolid, and cy

28 nd in vivo, and provide a novel mechanism of ethionamide resistance in M. tuberculosis.

29 ical studies suggested that the mechanism of ethionamide resistance in mshA mutants was likely due to

30 We identified isoniazid and ethionamide resistance mutations on line probe assay and

31 this intergenic region, thus contributing to ethionamide resistance.

32 fective in mycothiol biosynthesis, were only ethionamide-resistant and required catalase to grow.

33 was 3.0 microg/ml, and that established for ethionamide was 5.0 microg/ml.

34 (pyrazinamide surrogate), prothionamide, or ethionamide, which were assay nonperformers.

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