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1  4- and 5-nitroimidazoles and explored their antitubercular activities.
2 ied, CyC 17 exhibited the best extracellular antitubercular activity (MIC50 = 500 nM).
3 azolopyridine ureas as a novel scaffold with antitubercular activity acting through inhibition of DNA
4 esulted in compounds with moderate to potent antitubercular activity and improved physicochemical pro
5               New prospective scaffolds with antitubercular activity derived from homo-piperazine, ph
6  Mycobacterium tuberculosis RNAP but lowered antitubercular activity in cell culture under both aerob
7 A inhibitors disclosed here display in vitro antitubercular activity superior to most current first l
8 ructure-activity relationships lining up the antitubercular activity were exploited for the rational
9 derivative 26 exhibited exceptionally potent antitubercular activity with an MIC99 under iron-deficie
10 assessed for biochemical potency, whole-cell antitubercular activity, and in vivo pharmacokinetic par
11 -phenoxypropyl)-1H-benzo[d]imidazole for its antitubercular activity.
12 xhibits exceptionally potent biochemical and antitubercular activity.
13 1) as the primary target responsible for the antitubercular activity.
14 mal inhibition and excellent narrow-spectrum antitubercular activity.
15 of mycobactin biosynthesis, exhibited potent antitubercular activity.
16 soniazid-NADH adduct that ultimately confers antitubercular activity.
17 of basic cyclic peptides that exhibit potent antitubercular activity.
18 ing a nitroimidazopyran nucleus that possess antitubercular activity.
19 s (Mtb) in order to identify novel hits with antitubercular activity.
20                                          The antitubercular agent isoniazid can be activated by Mycob
21 icals found with KatG, while the less potent antitubercular agent nicotinic acid hydrazide produced t
22 -carboxamide analogue, 3, as a highly potent antitubercular agent, and the subsequent chemical modifi
23            This makes the discovery of novel antitubercular agents a cogent priority.
24 alues lower than those of the most prominent antitubercular agents currently in use.
25  (Sal-AMS) is a prototype for a new class of antitubercular agents that inhibit the aryl acid adenyla
26 red the discovery of a novel class of potent antitubercular agents that unexpectedly possessed notabl
27 re a promising class of potent and selective antitubercular agents, if the metabolic liability can be
28 rotein and a validated target to develop new antitubercular agents, particularly for the treatment of
29 rotein and a validated target to develop new antitubercular agents, particularly for the treatment of
30 ntify small molecule inhibitors as potential antitubercular agents.
31 igase) is a key target for the design of new antitubercular agents.
32 tency greater than that of many conventional antitubercular agents.
33 suggesting that it can be developed as a new antitubercular aimed at the acute infection.
34                Lesions responded to combined antitubercular and steroid therapy, usually spared fovea
35 vely explored for their potential use as new antituberculars based on their excellent bactericidal pr
36 unction with isoniazid, but removed from the antitubercular chemotherapeutic arsenal due to toxic sid
37  biosynthesis, DNA repair, and activation of antitubercular compounds.
38 afish larvae for in vivo characterization of antitubercular drug activity and tolerance.
39   MbtA is a validated therapeutic target for antitubercular drug development.
40 dy tuberculosis pathogenesis, as well as for antitubercular drug discovery.
41 tuberculosis, is the target of the frontline antitubercular drug isoniazid (INH).
42                                The preferred antitubercular drug isoniazid specifically targets a lon
43 obacterium tuberculosis and a target for the antitubercular drug isoniazid.
44 sis is responsible for the activation of the antitubercular drug isonicotinic acid hydrazide (INH) an
45 s is inhibited by isoniazid, a key frontline antitubercular drug that is inactivated by mycobacterial
46 s the efficacy of ethionamide, a second-line antitubercular drug used to combat multidrug-resistant M
47                 Isoniazid (INH), a frontline antitubercular drug, inhibits InhA, the enoyl reductase
48 erium marinum to thiacetazone, a second line antitubercular drug, is associated with a severe decreas
49 ponsible for activation of the commonly used antitubercular drug, isoniazid (INH).
50 e for increased resistance to the front-line antitubercular drug, isoniazid, by acetylating and hence
51 losis, is important in the activation of the antitubercular drug, isoniazid.
52 e originally been designed as hybrids of the antitubercular drugs BM212 (1) and SQ109 (2), which show
53 g pocket of Eis is a potential target of new antitubercular drugs expected to overcome aminoglycoside
54      One challenge to the development of new antitubercular drugs is the existence of multiple virule
55 ween these two components was provided using antitubercular drugs such as ethambutol or isoniazid kno
56 osis highlights the need for identifying new antitubercular drugs that can treat these infections.
57                                 However, new antitubercular drugs with new mechanisms of action have
58 ly) TB; hence the quest for highly effective antitubercular drugs with novel modes of action is imper
59 ation issues, including interactions between antitubercular drugs, antiretroviral drugs, and medicine
60       The mechanisms of action of the unique antitubercular drugs, including isoniazid, ethambutol, a
61                       In contrast to current antitubercular drugs, nitroimidazopyrans exhibited bacte
62 otential target for the development of novel antitubercular drugs.
63 AGP is also regarded as a target for several antitubercular drugs.
64 the development of a novel chemical class of antitubercular drugs.
65 otential to be developed into a new class of antitubercular drugs.
66 otential target to develop antibacterial and antitubercular drugs.
67 um tuberculosis and is the target of several antitubercular drugs.
68 rculosis (M. tb) emphasizes the need for new antitubercular drugs.
69 M/LM balance might represent targets for new antitubercular drugs.
70  the oxidative activation of other thioamide antitubercular drugs.
71 ation of an aromatic nitro group to exert an antitubercular effect.
72                                          The antitubercular efficacy of spectinamides demonstrates th
73 s an enzymatic defense against an element of antitubercular immunity.
74                            Activation of the antitubercular isoniazid (INH) by the Mycobacterium tube
75 s of structure 1, previously assigned to the antitubercular marine natural product pseudopteroxazole,
76 acene-6,11,13-trione (1), proposed to be the antitubercular natural product eucapsitrione, has been s
77              A formal total synthesis of the antitubercular natural product was accomplished.
78 wed with good enzymatic potency but with low antitubercular potency.
79  by in vitro and in vivo evaluation of their antitubercular potential against Mtb.
80 tive stress management and activation of the antitubercular pro-drug isoniazid.
81                          Key to their potent antitubercular properties was their structural modificat
82 rculosis emphasize the necessity to find new antitubercular targets and drugs.
83            Resistance against currently used antitubercular therapeutics increasingly undermines effo
84 d as a possible target for the design of new antitubercular therapeutics.
85 p from initiation of treatment that included antitubercular therapy (ATT) with oral corticosteroids (
86 veitis and the associations with response to antitubercular therapy (ATT).
87 y virus (HIV)-infected patients on RIF-based antitubercular therapy in the French National Agency for
88 s in well-validated biosynthetic pathways in antitubercular therapy is a powerful strategy that remov
89  specific efflux pump inhibitors to standard antitubercular therapy should shorten the duration of cu
90                                              Antitubercular therapy significantly reduced recurrences
91  confirmed rifampin monoresistance following antitubercular therapy.
92 lu-Natal, South Africa, who received minimal antitubercular treatment and most of whom were HIV serop

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