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1  compound, 42a (MTC420), displays acceptable antituberculosis activity (Mtb IC50 = 525 nM, Mtb Wayne
2 long-acting bedaquiline at 160 mg/kg exerted antituberculosis activity for 12 weeks.
3 ting formulation of bedaquiline demonstrated antituberculosis activity for up to 12 weeks after injec
4 unds in more than 50 years with demonstrated antituberculosis activity in humans.
5  discovery of novel compounds with increased antituberculosis activity in vitro and a better understa
6  ester (compound 3) with previously reported antituberculosis activity is rapidly converted to two me
7 ed that one of the compounds, 15f, possessed antituberculosis activity, with an MIC value of 3.13 mic
8 mber of compounds that exhibited significant antituberculosis activity.
9 bstituted benzyl piperazines showed the most antituberculosis activity.
10 nd of these compounds one showed significant antituberculosis activity.
11 mary cellular target was responsible for the antituberculosis activity.
12 ied as a hit in this screen, possessing good antituberculosis activity.
13 investigation of lansoprazole as a potential antituberculosis agent is warranted.
14 . tuberculosis sensitivity to the front-line antituberculosis agent isoniazid.
15 sensitivity of M. tuberculosis to the potent antituberculosis agent isoniazid.
16 ::Km(r) was more sensitive to the front-line antituberculosis agent isonicotinic acid hydrazide (INH)
17 ed the use of ethambutol (EMB), a first-line antituberculosis agent that is known to inhibit cell wal
18 culosis, there is an urgent need to discover antituberculosis agent with novel structures.
19 ir interaction with rifampicin, a first-line antituberculosis agent, has not been investigated.
20                Isoniazid (INH), a front-line antituberculosis agent, is activated by mycobacterial ca
21 he risk factors seen with antiretroviral and antituberculosis agents among others.
22 24 h after the organisms were incubated with antituberculosis agents by using fluorescein diacetate (
23 have been identified as a promising class of antituberculosis agents from phenotypic screening agains
24 f this methodology for rapidly assessing new antituberculosis agents may be limited by the relatively
25  an ongoing effort to develop new and potent antituberculosis agents, a second-generation series of n
26 alent lead series for the discovery of novel antituberculosis agents.
27 kill rates equivalent to those of first-line antituberculosis agents.
28 A1 may lead to the development of a class of antituberculosis agents.
29 boxamides represent a promising new class of antituberculosis agents.
30 plex isolates against first- and second-line antituberculosis agents.
31 sistance to an exceptionally potent class of antituberculosis agents.
32 robenzothiazinones are among the most potent antituberculosis agents.
33 sistant to isoniazid and rifampin, the major antituberculosis agents.
34 optimization of this very promising class of antituberculosis agents.
35 nd constitute targets for the development of antituberculosis agents.
36 les and 1,3,4-thiadiazoles as a new class of antituberculosis agents.
37 Ps as selective inhibitors of MtHGPRT and as antituberculosis agents.
38  essential value added in the development of antituberculosis agents.
39 rformed for both first-line and experimental antituberculosis agents.
40                                          New antituberculosis (anti-TB) drugs are urgently needed to
41 bactericidal activity of orally administered antituberculosis (anti-TB) drugs was determined in a who
42 l for the rational design and improvement of antituberculosis (anti-TB) therapeutics that target the
43 ity of isoniazid during the initial phase of antituberculosis (anti-TB) therapy has been attributed n
44 ough its peroxidase cycle, of the front line antituberculosis antibiotic isoniazid (isonicotinic acid
45 the enzyme responsible for activation of the antituberculosis antibiotic isoniazid (isonicotinic acid
46  in VPS18-knockout cells, and the first-line antituberculosis antibiotic pyrazinamide was less effect
47 lar collagen deposition did not resolve with antituberculosis antibiotics.
48 ent and selective mPTPB inhibitors as unique antituberculosis (antiTB) agents.
49 s were randomly assigned to receive standard antituberculosis care or azithromycin 250 mg orally once
50           There is an increasing flow of new antituberculosis chemical entities entering the tubercul
51  week has potent activity in mouse models of antituberculosis chemotherapy, but efficacy and safety d
52 introduction of modern rifampicin-containing antituberculosis chemotherapy.
53 us on diagnosis, inflammatory processes, and antituberculosis chemotherapy.
54 long periods of time after the initiation of antituberculosis chemotherapy.
55 d according to whether the patients received antituberculosis chemotherapy.
56 asone or placebo in addition to 12 months of antituberculosis chemotherapy.
57 midazolium scaffold as a novel redox cycling antituberculosis chemotype with potent bactericidal acti
58                                      Six new antituberculosis compounds in 4 classes are presently in
59 e, lansoprazole sulfide (LPZS)-are potential antituberculosis compounds.
60  CD4(+) or CD8(+) T effector cells producing antituberculosis cytokine IFN-gamma in the context of im
61 studies have identified the risk factors for antituberculosis DILI; however, none have been conducted
62                    Global rollout of the new antituberculosis drug bedaquiline has been slow, in part
63  a small sample size, BTZ-043 is a promising antituberculosis drug candidate with favourable safety a
64                  Benzothiazinones (BTZs) are antituberculosis drug candidates with nanomolar bacteric
65 exploring this chemical class as a source of antituberculosis drug candidates.
66 the DDTs used for evaluating the efficacy of antituberculosis drug combinations and the gaps in the e
67 -development tools (DDTs) have been used for antituberculosis drug development over several decades.
68                         After 50 years of no antituberculosis drug development, a promising pipeline
69 thway while also identifying new targets for antituberculosis drug development.
70 l of targeting select biosynthetic steps for antituberculosis drug development.
71 of these enzymes as valid targets for future antituberculosis drug development.
72 est in the terminal respiratory oxidases for antituberculosis drug development.
73 r both industry and academia in the field of antituberculosis drug development.
74 n this Review, we discuss recent advances in antituberculosis drug discovery and development, clinica
75  synthetase (MtGS) is a promising target for antituberculosis drug discovery.
76 ycobacterium tuberculosis to the second-line antituberculosis drug ethionamide.
77        Our aim was to investigate first-line antituberculosis drug exposures under these guidelines,
78 e-peroxidase that is thought to activate the antituberculosis drug isoniazid (INH).
79 d t-BHP and to inhibitory effects due to the antituberculosis drug isoniazid (INH).
80  2-pyridylcarboxaldehyde with the first-line antituberculosis drug isoniazid [i.e., isonicotinic acid
81 s--including an InhA mutant resistant to the antituberculosis drug isoniazid and a strain overexpress
82                      The extended use of the antituberculosis drug isoniazid and the antiseptic tricl
83  However, KatG also activates the front-line antituberculosis drug isoniazid, hence rendering M. tube
84 d in increased sensitivity to the front-line antituberculosis drug isoniazid.
85 ial diazaborine compounds and the front-line antituberculosis drug isoniazid.
86 qually capable of metabolizing the important antituberculosis drug isoniazid.
87 ntibacterial diazaborines and the front-line antituberculosis drug isoniazid.
88                               The first-line antituberculosis drug isonicotinic hydrazide (INH) is a
89            Using the nitroimidazopyran-based antituberculosis drug PA-824 as a selective agent, trans
90  developed using the nitroimidazopyran-based antituberculosis drug PA-824.
91 ed to work together to strengthen the global antituberculosis drug pipeline and support the developme
92 acterium bovis is naturally resistant to the antituberculosis drug pyrazinamide (PZA).
93  have to be treated with currently available antituberculosis drug regimens for more than 20 months,
94  pipeline and support the development of new antituberculosis drug regimens.
95                 To inform efforts to prevent antituberculosis drug resistance acquired during treatme
96 notypic screen for mutations associated with antituberculosis drug resistance and for the G(1031)A po
97 id molecular tests for tuberculosis (TB) and antituberculosis drug resistance could significantly imp
98 ive genes in which mutations associated with antituberculosis drug resistance have been found.
99 stance using data from the Global Project on Antituberculosis Drug Resistance Surveillance at WHO, fr
100 wana in the 1990s have recorded low rates of antituberculosis drug resistance, despite a three-fold r
101 n immunodeficiency virus (HIV) infection and antituberculosis drug resistance.
102 oxacin) have previously been associated with antituberculosis drug resistance.
103 erase (RNAP) is the target of the first-line antituberculosis drug rifampin (Rif).
104 As a result, there is a need to identify new antituberculosis drug targets.
105 AT2 genotype-guided dosing may help optimize antituberculosis drug treatment and prevent treatment fa
106 ntracellular M. tuberculosis survival during antituberculosis drug treatment is not known.
107          We speculate that follow-up time in antituberculosis drug trials should take reinfection int
108 m of action of isoniazid (INH), a first-line antituberculosis drug, is complex, as mutations in at le
109    Human NAT2 acetylates and inactivates the antituberculosis drug, isoniazid (INH), and is polymorph
110                  Pyrazinamide (PZA) is a key antituberculosis drug, yet no rapid susceptibility test
111 of the prodrug isoniazid (INH), a front-line antituberculosis drug.
112           Pyrazinamide (PZA) is an important antituberculosis drug.
113 ptibility of mycobacteria to this front-line antituberculosis drug.
114 ells per kg), within 4 weeks of the start of antituberculosis-drug treatment in a specialist centre i
115                  Common suspected drugs were antituberculosis drugs (46/164, 28.1%) and beta-lactams
116                    Resistance to second-line antituberculosis drugs (SLDs) severely compromises treat
117                               The search for antituberculosis drugs active against persistent bacilli
118 ther this may be due to interactions between antituberculosis drugs and antiretrovirals needs to be i
119  be considered during the development of new antituberculosis drugs and combination regimens.
120  LM could provide targets for development of antituberculosis drugs and for derivation of attenuated
121 predict resistance to first- and second-line antituberculosis drugs and validated our predictions in
122 eous adverse reactions related to first-line antituberculosis drugs are associated with high mortalit
123         It is critical that novel classes of antituberculosis drugs are developed to combat the incre
124                  Although the key front-line antituberculosis drugs are effective in treating individ
125                             A range of novel antituberculosis drugs are in preclinical development, s
126 rch focused on drug development, several new antituberculosis drugs are in the pipeline, and the stan
127                                      Because antituberculosis drugs are prescribed as part of combina
128 tum before treatment, and all were receiving antituberculosis drugs at hospital discharge.
129 ment-naive patients to bedaquiline and other antituberculosis drugs by the 7H9 broth microdilution (B
130 of pyrazinamide (PZA), one of the first-line antituberculosis drugs currently used.
131                                   The use of antituberculosis drugs has changed tuberculosis from a d
132 ciated with increased rates of resistance to antituberculosis drugs in both the New York City area an
133 pectively assessed resistance to second-line antituberculosis drugs in eight countries.
134 azinamide and fluoroquinolones are essential antituberculosis drugs in new rifampicin-sparing regimen
135 ablets delivering higher doses of first-line antituberculosis drugs in World Health Organization-reco
136 incidence of resistance to the few available antituberculosis drugs is a significant concern, especia
137  because resistance to bedaquiline and other antituberculosis drugs is caused by mutations within a s
138 g-drug interactions involving the first-line antituberculosis drugs is reviewed in this article, alon
139 eptibility testing (DST) for the second-line antituberculosis drugs is slow, leading to diagnostic de
140         Early bactericidal activity (EBA) of antituberculosis drugs is the rate of decrease in the co
141 Mycobacterium tuberculosis by the first-line antituberculosis drugs isoniazid (INH) and ethambutol (E
142 rculosis complex were patient treatment with antituberculosis drugs prior to testing and the presence
143 arison of the early bactericidal activity of antituberculosis drugs should be evaluated using the tim
144 ates were susceptible in vitro to all of the antituberculosis drugs tested, 11 were monoresistant to
145 has also been progress in development of new antituberculosis drugs that are active against dormant o
146                               The ability of antituberculosis drugs to cross the blood-brain barrier
147 to-human translational modeling platform for antituberculosis drugs to predict phase 2A outcomes for
148 stant to at least one of the five first-line antituberculosis drugs used for treatment.
149 articipating laboratories for the first-line antituberculosis drugs used in the United States-isoniaz
150 s, while no cross-resistance to conventional antituberculosis drugs was observed.
151 s, those who started fewer than three active antituberculosis drugs were at a higher risk of tubercul
152 binary phenotypic AST results for up to nine antituberculosis drugs were determined and correlated wi
153 osure to isoniazid or ethambutol, front-line antituberculosis drugs which also target the cell envelo
154 C M. tuberculosis BioC presents a target for antituberculosis drugs which thus far have been directed
155 on of efavirenz and weeks 22 (efavirenz plus antituberculosis drugs) and 50 (efavirenz alone) after i
156 t with rIFN-gamma aerosol in addition to the antituberculosis drugs, 10 of 10 patients had increased
157 ty of IFN-gamma ELISpot for other first-line antituberculosis drugs, additional optimization is neede
158 rculosis health services, development of new antituberculosis drugs, adjunct therapies and vaccines,
159 pic viruses, herbal and dietary supplements, antituberculosis drugs, and autoimmune hepatitis.
160 rifampin (RIF) are two of the most important antituberculosis drugs, and resistance to both of these
161  disease, the metabolism and distribution of antituberculosis drugs, and the toxicity experienced.
162 compounds, MTB became even more sensitive to antituberculosis drugs, in vitro and in vivo, in a mouse
163 s and found that tolerance developed to most antituberculosis drugs, including the newer agents moxif
164                                              Antituberculosis drugs, mostly developed over 60 years a
165 started a regimen with at least three active antituberculosis drugs, those who started fewer than thr
166                               In the case of antituberculosis drugs, which are frequently administere
167 stablished for the majority of commonly used antituberculosis drugs, with a convenient 7H9 broth micr
168       Isoniazid is one of the most effective antituberculosis drugs, yet its precise mechanism of act
169 cacy would facilitate clinical trials of new antituberculosis drugs.
170 henotypic DST for first-line and second-line antituberculosis drugs.
171 tb synergistically with oxidants and several antituberculosis drugs.
172 6S rRNA gene after 3 days of incubation with antituberculosis drugs.
173 ility of this important class of second-line antituberculosis drugs.
174 berculosis represents a potential target for antituberculosis drugs.
175 arget MmpL3, and their development as future antituberculosis drugs.
176 t during infections as well as for resisting antituberculosis drugs.
177  and influences resistance to two first-line antituberculosis drugs.
178 are important in the rapid evaluation of new antituberculosis drugs.
179 important targets for the development of new antituberculosis drugs.
180 0.75-1.5 microg/mL, comparable to first-line antituberculosis drugs.
181  treatment and promote the assessment of new antituberculosis drugs.
182 obacteria necessitate the development of new antituberculosis drugs.
183 transferase (PptT) is a potential target for antituberculosis drugs.
184 ficacy comparable to that of clinically used antituberculosis drugs.
185 erminants of resistance to the full range of antituberculosis drugs.
186 luate resistance to the principal first-line antituberculosis drugs.
187 placebo concomitant with standard first-line antituberculosis drugs.
188  all conventional first-line and second-line antituberculosis drugs.
189 od for a panel of first-line and second-line antituberculosis drugs.
190 in seven genes associated with resistance to antituberculosis drugs: katG, the inhA promoter, and the
191 ions that a DDT should answer with regard to antituberculosis drugs: What combination(s) of drugs wil
192 ended given the lower potency of second-line antituberculosis drugs; and strategies to improve treatm
193 ted a specific function of the sst1 locus in antituberculosis immunity in vivo, especially its role i
194 t NKT cells may be an important component of antituberculosis immunity.
195 otentially important implications for global antituberculosis immunization policies and future tuberc
196  and guiding experimental searches for novel antituberculosis interventions.
197 -dihydro-imidazooxazole derivative, is a new antituberculosis medication that inhibits mycolic acid s
198  may be protective against DILI while taking antituberculosis medication.
199  in which (i) specimens from patients taking antituberculosis medications are excluded from testing a
200 at host factors such as poor compliance with antituberculosis medications or decreased absorption of
201 th submicromolar IC(50) values and promising antituberculosis MIC values.
202                              Isoniazid is an antituberculosis prodrug that requires activation by the
203 ycobacterium bovis BCG, induced considerable antituberculosis protective immunity in immune-deficient
204 t to Mycobacterium bovis BCG vaccine-induced antituberculosis protective immunity.
205                              The substantial antituberculosis protective responses induced by Sin85B
206 ntrolled trial comparing a standard, 9-month antituberculosis regimen (containing rifampicin 10 mg/kg
207              We compared a standard, 9-month antituberculosis regimen (which included 10 mg of rifamp
208 th tuberculosis treated with a thrice-weekly antituberculosis regimen are at a higher risk of ARR, co
209                                          New antituberculosis regimens are urgently needed to shorten
210                  Treatment with standardized antituberculosis regimens dosed daily throughout, high u
211 nt nonadherence occurs on the forgiveness of antituberculosis regimens.
212 e in support of selection and development of antituberculosis regimens.
213 ch needed to support equitable access to new antituberculosis regimens.
214 s indirectly on immune cells to modulate the antituberculosis response and bacterial control.
215 ntribution of CD4+ T cells to the protective antituberculosis response involves the production of Th1
216 not currently be used for blood specimens or antituberculosis susceptibility testing.
217 otics or combinations of the four first-line antituberculosis (TB) drugs.
218 tiretroviral therapy (ART) initiation during antituberculosis (TB) treatment.
219 , the mechanisms of action of the front-line antituberculosis therapeutic agent isoniazid (INH) remai
220  a target for structure-based development of antituberculosis therapeutics.
221  further facilitate the development of novel antituberculosis therapies are discussed.
222  per year underscore the urgent need for new antituberculosis therapies.
223 opportunity for further investigation of new antituberculosis therapies.
224 ent supplementation in children treated with antituberculosis therapy (ATT).
225                                              Antituberculosis therapy (rifampicin, isoniazid, ethambu
226               Participants received standard antituberculosis therapy (rifampicin, isoniazid, pyrazin
227 umen is still needed to decide when to start antituberculosis therapy and continued research for bett
228  a promising tool for monitoring response to antituberculosis therapy and evaluating the efficacy of
229 sociation between weight gain or loss during antituberculosis therapy and relapse has not been well s
230  three patients (nine specimens) who were on antituberculosis therapy before the study began were exc
231       There was no difference in efficacy of antituberculosis therapy delivered for either 6 months o
232 ine ART interrupted, and on rifampicin-based antituberculosis therapy for less than 3 months.
233 plicates combined antiretroviral therapy and antituberculosis therapy in HIV-1-coinfected tuberculosi
234  to identify clinical studies performed with antituberculosis therapy in which PK/PD data and/or para
235 ed with high morbidity and mortality even if antituberculosis therapy is administered.
236 ricidal activity during the initial phase of antituberculosis therapy is due to the depletion of Myco
237 erculosis exposure, previous active disease, antituberculosis therapy status, etc., were considered i
238 uggest the potential for host-based, adjunct antituberculosis therapy targeting lipid metabolism.
239 ed trial to compare 6 months and 9 months of antituberculosis therapy using DOTs.
240 e 6 months (n = 104) or 9 months (n = 93) of antituberculosis therapy using intermittent directly obs
241 vity in culture-negative children started on antituberculosis therapy was 2% (1-3) for expectorated o
242                                              Antituberculosis therapy was initiated in 566/576 (98.3%
243                   Patients already receiving antituberculosis therapy were excluded.
244 s bacteraemia who were not already receiving antituberculosis therapy, 13 (45%) had an abnormal chest
245                         Before initiation of antituberculosis therapy, measures of AFB, M. tuberculos
246 of linezolid or fluoroquinolones to standard antituberculosis therapy, or treatment with adjunctive a
247 in of M. tuberculosis that could be used for antituberculosis therapy.
248 nodeficiency virus and in patients receiving antituberculosis therapy.
249 components and represents a novel target for antituberculosis therapy.
250 emia; five of these patients were already on antituberculosis therapy.
251 the development of DIH in patients receiving antituberculosis therapy.
252 nduced hepatitis (DIH) in patients receiving antituberculosis therapy.
253  the host and pathogen are novel targets for antituberculosis therapy.
254 tify PK/PD studies that have been applied to antituberculosis therapy.
255 eased plasma efavirenz concentrations during antituberculosis therapy.
256 T on ARR among patients taking thrice-weekly antituberculosis therapy.
257 are urgently needed to improve diagnosis and antituberculosis treatment (ATT) initiation in children
258                                        Early antituberculosis treatment and adjunctive treatment with
259     The addition of azithromycin to standard antituberculosis treatment appears to diminish excess ne
260 e alone was sufficient to make most clinical antituberculosis treatment decisions.
261 sis (TB) patients who move before completing antituberculosis treatment have not been described.
262 tiretroviral therapy (ART) initiation during antituberculosis treatment in co-infected patients.
263 usceptibility testing and suboptimal initial antituberculosis treatment in settings with a high preva
264 n-susceptible tuberculosis were recruited at antituberculosis treatment initiation in Khayelitsha, So
265                                    Effective antituberculosis treatment monitoring is difficult as th
266 icentre randomised clinical trial REMoxTB of antituberculosis treatment on a weekly basis (weeks 0 to
267              Shortening the interval between antituberculosis treatment onset and initiation of antir
268 ns had been collected less than 10 days into antituberculosis treatment was 60.0%.
269                                              Antituberculosis treatment was completed in 32 patients;
270 arance in patients taking both efavirenz and antituberculosis treatment was highly dependent on NAT2
271                               Four months of antituberculosis treatment was noninferior to 6 months o
272                                  Intensified antituberculosis treatment was not associated with a hig
273 r 6 months (24 weeks) of standard first-line antituberculosis treatment with pediatric fixed-dose com
274             We hypothesized that intensified antituberculosis treatment would enhance the killing of
275     Ocular inflammation reacted favorably to antituberculosis treatment, although only a small minori
276  the end of (6 months) and after (12 months) antituberculosis treatment, and compared to individuals
277                    After receiving empirical antituberculosis treatment, he was treated with broad-sp
278 ne were administered in addition to standard antituberculosis treatment, including rifampicin and iso
279  10 tuberculosis patients 10 +/- 2 days post-antituberculosis treatment, there was no detectable STAT
280 CrI: 82; 98) of CPTB-positive cases received antituberculosis treatment, which indicates substantial
281  or placebo (n = 200) during intensive-phase antituberculosis treatment.
282  treated with either standard or intensified antituberculosis treatment.
283 -043 is a promising novel drug candidate for antituberculosis treatment.
284 ph nodes or bronchial wash and received full antituberculosis treatment.
285 was reported as unrelated to tuberculosis or antituberculosis treatment.
286 tance-conferring mutations during inadequate antituberculosis treatment.
287 and 50 (efavirenz alone) after initiation of antituberculosis treatment.
288  The diagnosis was a paradoxical reaction to antituberculosis treatment; after 6 more months of treat
289  HIV infection, immunosuppressive therapies, antituberculosis treatments, and other poorly understood
290 ic that is an essential component of current antituberculosis treatments, particularly in the case of
291                                          The antituberculosis vaccine bacillus Calmette-Guerin (BCG)
292 memory, also termed trained immunity, by the antituberculosis vaccine bacillus Calmette-Guerin (BCG)
293                                BACKGROUNDThe antituberculosis vaccine bacillus Calmette-Guerin (BCG)
294          Bacillus Calmette-Guerin (BCG), the antituberculosis vaccine, localizes within immature phag
295 ogression in the lungs and the efficiency of antituberculosis vaccine.
296 cellent candidate for inclusion in a subunit antituberculosis vaccine.
297                                   Hence, new antituberculosis vaccines are needed.
298 employed to assess the efficacy of candidate antituberculosis vaccines.
299  interfere with the development of effective antituberculosis vaccines.
300 on and 227 (65%) of the control participants antituberculosis was initiated treatment at baseline.

 
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