ライフサイエンスコーパス: EFV

24 re obtained over a period of 40 days, from 9 EFV-naive men (i.e., men about to receive EFV for the fi

25 1 RNA in SP was undetectable in 8 (89%) of 9 EFV-naive men and remained undetectable in 10 (83%) of 1

26 After EFV initiation, 2.5% (61/2435) had severe (grade 3 or hi

27 However, all EFV concentrations in SP were >/=40-fold higher than the

28 n InSTI-based, and 10,169 (64%) initiated an EFV-based, regimen.

29 The US EFV package insert recommends an EFV dose increase for patients on RIF weighing >/=50 kg.

30 /mm3) were observed between DTG (n = 29) and EFV (n = 31) arms.

31 , VAF from 190+/-83 cm2 to 107+/-44 cm2, and EFV from 137+/-37 ml to 98+/-25 ml (all p<0.0001).

32 tions conferring resistance to NVP, DLV, and EFV and several HIV-1 clades A in PBMC.

33 ed 20 weeks of tenofovir, emtricitabine, and EFV.

34 ATV+DDI+FTC and EFV+FTC-TDF were hypothesized to be non-inferior to EFV+

35 InSTI- and EFV-based initial ART regimens had similar 6-year compos

36 assay, it was remarkably superior to NVP and EFV and comparable to ETV.

37 e relationship between the degree of NVP and EFV resistance and the impairment of viral replication i

38 s) were markedly less susceptible to NVP and EFV.

39 monstrated noninferior efficacy to DRV+r and EFV as assessed by the proportion of HIV-1-infected, tre

40 The effects of ATV/r and EFV upon safety and tolerability risk did not differ sig

41 monstrated noninferior efficacy to DRV+r and EFV, with 84.1% of DOR-treated participants achieving HI

42 ates of drug-related AEs for DOR, DRV+r, and EFV were 30.9%, 32.1%, and 61.4%, respectively.

43 the TC/HDL-C ratio were similar with RPV and EFV.

44 ray absorptiometry) of rilpivirine (RPV) and EFV plus 2 nucleoside/nucleotide reverse transcriptase i

45 nificantly different between DOR/3TC/TDF and EFV/FTC/TDF (-1.6 vs +8.7 mg/dL and -3.8 vs +13.3 mg/dL,

46 fumarate/emtricitabine/EFV, and some TFV and EFV PK parameters were lower in the presence of FHT.

47 participants with virologic failure assigned EFV had more RT changes, including and excluding known r

48 The other principal differences between EFV and l-Glu in CYP46A1 activation include an apparent

49 g the dosing interval, no single SPrcolon;BP EFV-concentration ratio was significantly predictive of

50 We propose a model for CYP46A1 activation by EFV and show that EFV enhanced CYP46A1 activity and cere

51 relationship of IRE1alpha-XBP1 activation by EFV, 16 EFV analogs were employed.

52 decreasing paradigm of CYP46A1 activation by EFV.

53 in the ABC/3TC and TDF/FTC groups (combining EFV and ATV/r arms; median change, -341 [interquartile r

54 Comparing EFV+FTC-TDF to EFV+3TC-ZDV, during a median 184 wk of fo

55 be adequate in patients receiving concurrent EFV.

56 atment-naive patients on regimens containing EFV versus NVP from randomised trials and observational

57 oxil fumarate (DF)-emtricitabine once daily (EFV-TDF-FTC group).

58 citabine-tenofovir-disoproxil fumarate (DF) (EFV+FTC-TDF).

59 At such small doses, EFV may be devoid of adverse effects elicited by high dr

60 ral decay rate was also faster in the 3-drug EFV group than in the triple-nucleoside group (P=.09).

61 ntly faster in subjects receiving the 3-drug EFV regimen (0.67/day), compared with those receiving th

62 men), zidovudine/lamivudine plus EFV (3-drug EFV regimen) or zidovudine/lamivudine/abacavir plus EFV

63 ral decay in subjects randomized to a 3-drug EFV-based regimen corresponded to the overall superior e

64 Decay rates in the 4-drug EFV group were intermediate.

65 ovudine/lamivudine/abacavir plus EFV (4-drug EFV regimen).

66 Efavirenz (EFV) is a nonnucleoside reverse transcriptase inhibitor

67 Efavirenz (EFV) is an anti-HIV drug, and cytochrome P450 46A1 (CYP4

68 Efavirenz (EFV), a widely used antiretroviral drug, is associated w

69 tabine (FTC)/NVP (n = 9), TDF/3TC/efavirenz (EFV) (n = 6), and TDF/FTC/EFV (n = 19).

70 and M184V with failure of d4T/3TC/efavirenz (EFV; P < .01).

71 unavir plus ritonavir (DRV+r) and efavirenz (EFV) in 2 ongoing phase 3 trials: DRIVE-FORWARD (NCT0227

72 avir (DRV+r) in DRIVE-FORWARD and efavirenz (EFV) in P007 and DRIVE-AHEAD.

73 ), including nevirapine (NVP) and efavirenz (EFV), has been associated with severe hepatic injury.

74 , especially nevirapine (NVP) and efavirenz (EFV).

75 Compared with no ART, efavirenz (EFV) reduced exposure to all antimalarial components by

76 nges compared with those assigned efavirenz (EFV) (P >/= .13).

77 immunodeficiency virus (HIV) drug efavirenz (EFV) alters mitochondrial function in cultured neurons a

78 , we found that the anti-HIV drug efavirenz (EFV) can pharmacologically activate CYP46A1 in mice.

79 ith lamivudine or emtricitabine): efavirenz (EFV) plus zidovudine (AZT) (n = 524); EFV plus tenofovir

80 pared to historical estimates for efavirenz (EFV)- and ritonavir/lopinavir (LPV/r)-based regimens.

81 th standard of care-co-formulated efavirenz (EFV)/FTC/TDF-as initial treatment for HIV infection.

82 reatest risk was with switch from efavirenz (EFV) to rilpivirine (RPV) or elvitegravir/cobicistat and

83 udy was conducted to determine if efavirenz (EFV) or atazanavir/ritonavir (ATV/r)-based combination a

84 isoenzymes, potentially lowering efavirenz (EFV) exposure.

85 transcriptase inhibitors (NNRTI) efavirenz (EFV) and nevirapine (NVP) in first-line antiretroviral t

86 e transcriptase inhibitor (NNRTI) efavirenz (EFV) showed subunit-specific perturbation in the rate of

87 acodynamic, and dose responses of efavirenz (EFV) in SP versus those in blood plasma (BP).

88 nimals received a short course of efavirenz (EFV) monotherapy before combination ART was started.

89 were exposed to a short course of efavirenz (EFV) monotherapy.

90 The distribution of efavirenz (EFV) was then monitored in a series of hair strands coll

91 In the presence of efavirenz (EFV), a virus carrying RT-K103N together with IN-G140S a

92 r, and elvitegravir/cobicstat) or efavirenz (EFV) as an active comparator, between 2009 and 2016.

93 zanavir plus ritonavir (ATV/r) or efavirenz (EFV) in initial antiretroviral regimens among women and

94 ised 1:1 to dolutegravir (DTG) or efavirenz (EFV)-containing ART until 2 weeks post-partum (2wPP), be

95 herapy, then 50 mg once daily) or efavirenz (EFV; 600 mg daily) with 2 nucleoside reverse transcripta

96 found that four pharmaceuticals (efavirenz (EFV), acetaminophen, mirtazapine, and galantamine) presc

97 compared the effect of switching efavirenz (EFV) to raltegravir (RAL) on hepatic steatosis among HIV

98 01E+G190S are highly resistant to efavirenz (EFV) and can develop during failure of EFV-containing re

99 and delavirdine (DLV), but not to efavirenz (EFV) and etravirine (ETR), consistent with their increas

100 he noninferiority of switching to efavirenz (EFV) versus remaining on ritonavir-boosted lopinavir (LP

101 ng triple-nucleoside-based versus efavirenz (EFV)-based regimens.

102 rom the excitotoxic insult, while efavirenz (EFV) did not contrast the neurotoxic effect of glutamate

103 ir (TDF)-emtricitabine (FTC) with efavirenz (EFV) or atazanavir plus ritonavir (ATV/r), on bone miner

104 r DF-emtricitabine (TDF/FTC) with efavirenz (EFV) or atazanavir-ritonavir (ATV/r).

105 r DF/emtricitabine (TDF/FTC) with efavirenz (EFV) or atazanavir/ritonavir (ATV/r) in human immunodefi

106 lamivudine [3TC]/zidovudine [ZDV]/efavirenz [EFV], 3TC/ZDV/nelfinavir [NFV], or other regimens) and s

107 /3TC than for TDF/FTC when given with either EFV or ATV/r.

108 ART (TFV disoproxil fumarate/emtricitabine/EFV at 300/200/600 mg) was initiated at week 3.

109 nce of TFV disoproxil fumarate/emtricitabine/EFV, and some TFV and EFV PK parameters were lower in th

110 onducted a pharmacokinetic study to evaluate EFV trough concentrations (Cmin) and human immunodeficie

111 occurred more frequently among those failing EFV, the clinical relevance of which warrants further in

112 reduced susceptibility to NVP (8.9-13-fold), EFV (4-56-fold), etravirine (ETV; 1.9-4.7-fold) and decr

113 Following EFV exposure, XBP1 splicing (indicating activation) was

114 Virologic failure following EFV-containing treatment was associated with more HIV-1

115 ) for DTG and 82% (36/44, 95% CI 70-93%) for EFV.

116 and -4.0% (P = .024), respectively; and for EFV versus ATV/r were -1.7% and -3.1% (P = .035) and -3.

117 0.610/day), significantly slower than d1 for EFV-based regimens [P < .001]).

118 zation and a customized D-optimal design for EFV encapsulation modeling.

119 cells/mm3 for DRV+r, and 188.4 cells/mm3 for EFV/FTC/TDF.

120 th a median CD4+ count of 208 cells/mm3; for EFV (n = 44), 55% of participants had HIV-1 RNA >100 000

121 FORWARD; and 3TC/TDF for DOR and FTC/TDF for EFV in DRIVE-AHEAD.

122 the mechanisms responsible for the frequent EFV-associated neurotoxicity.

123 ith NAFLD were randomized 1:1 to switch from EFV to RAL (400 mg twice daily), maintaining nucleoside

124 isoproxil fumarate (TDF)/emtricitabine (FTC)/EFV 600 mg with a viral load (VL) <50 copies/mL switched

125 ants exposed to ART from conception, TDF-FTC-EFV was associated with a lower risk for adverse birth o

126 arate, emtricitabine, and efavirenz (TDF-FTC-EFV) (901 of 2472 [36.4%]) compared with TDF-FTC and nev

127 Compared with TDF-FTC-EFV, all other regimens were associated with higher risk

128 TDF/3TC/efavirenz (EFV) (n = 6), and TDF/FTC/EFV (n = 19).

129 TDF/FTC/EFV was equivalent or superior to its comparator arms.

130 emtricitabine/tenofovir disoproxil fumarate (EFV/FTC/TDF).

131 se of protein phosphorylation are central in EFV effects and explain behavioral improvements in EFV-t

132 aecalibacterium prausnitzii were depleted in EFV and PI compared to HIV SN and negatively correlated

133 fects and explain behavioral improvements in EFV-treated 5XFAD mice.

134 The loss in EFV was limited (-27+/-11%) compared to VAF diminution (

135 o cART and 10 each taking cART that included EFV or ATV/r.

136 (NRTI) regimen versus regimens that included EFV plus an NRTI.

137 Nucleoside Reverse Transcriptase Inhibitors (EFV) or ritonavir-boosted Protease Inhibitors (PI) with

138 tions related to the requirement to initiate EFV-ART prior to randomisation, and to continue DTG for

139 Among 3576 women, 2435 (68%) initiated EFV at a median 121.1 weeks post delivery.

140 Six years after treatment initiation, EFV plus AZT showed the highest cumulative resistance in

141 o receive ABC-3TC or TDF-FTC with open-label EFV or ATV/r.

142 ted Cox regression confirmed that first-line EFV plus AZT (reference) was associated with a higher me

143 /C genotype had significantly lower mean log EFV MR.

144 ompared to <60 kg, was associated with lower EFV Cmin (1.68 vs 2.02, P = .021).

145 iated with a trend toward higher, not lower, EFV Cmin compared to EFV alone.

146 Patients weighing >/=60 kg had lower median EFV Cmin versus those <60 kg, but there was no associati

147 Overall, median EFV exposure in SP was 3.4% (range, 2.0%-5.0%) of that i

148 We then evaluated the anti-HIV medication EFV for the mode of interaction with CYP46A1 and the eff

149 emtricitabine at 200 mg, and TDF at 300 mg (EFV/FTC/TDF) for 96 weeks.

150 Moreover, EFV and l-Glu synergistically activated CYP46A1.

151 infection and reduces susceptibility to NVP, EFV, ETV, and AZT.

152 OR/3TC/TDF recipients and 80.8% (294/364) of EFV/FTC/TDF recipients achieved <50 HIV-1 RNA copies/mL

153 escribed EFV, but only 32% of NVP and 50% of EFV-associated episodes were detected during the first 1

154 achieved by 77.5% of DOR/3TC/TDF vs 73.6% of EFV/FTC/TDF participants, with a treatment difference of

155 gs include the greater antiviral activity of EFV versus NVP and longer intracellular half-life of FTC

156 After three doses over 4 days of EFV monotherapy, 103N mutations (AAC and AAT) rapidly em

157 The doses of EFV administered to mice and required for the stimulatio

158 e data do not support weight-based dosing of EFV with RIF.

159 V-1-infected women, and once-daily dosing of EFV+FTC-TDF are advantageous for use of this regimen for

160 renz (EFV) and can develop during failure of EFV-containing regimens in patients.

161 es in 50% inhibitory concentration (IC50) of EFV than viruses carrying a single NNRTI mutation.

162 y, incubation with the primary metabolite of EFV, 8-hydroxyefavirenz (8-OHEFV), only resulted in 10.3

163 eight gain; participants who switched off of EFV and TDF had the greatest weight gain.

164 rations with cholesterol, in the presence of EFV or l-Glu, suggest that water displacement from the h

165 eplicate more efficiently in the presence of EFV than in its absence.

166 Similarly, in the presence of EFV, the RT-E138K plus IN-G140S/Q148H mutant virus was f

167 characteristics, ART regimens, and timing of EFV initiation.

168 This finding supports the use of EFV as the preferred NNRTI in first-line treatment regim

169 The ratio of %EFV to %VAF loss decreased with sleep apnea syndrome (1.

170 mefantrine were 10-fold lower in children on EFV vs LPV/r-based ART, changes that were associated wit

171 he IN-G140S/Q148H mutations had no effect on EFV or RPV susceptibility.

172 ) patients on RAL and 3 (15%) individuals on EFV (P = .029).

173 cy of adverse events (two on DTG-ART, one on EFV-ART, all considered unrelated to drug).

174 s (HIV) virologic suppression in patients on EFV (600 mg) and RIF-based tuberculosis treatment in the

175 HIV-infected patients on EFV plus tenofovir/emtricitabine or abacavir/lamivudine

176 erienced neuropsychiatric AEs on DOR than on EFV (25.0% vs 55.9%, respectively), and fewer experience

177 and lower for those on DOR than for those on EFV (2.5% vs 6.6%, respectively).

178 s of recurrent malaria by day 28 in those on EFV vs LPV/r-based ART.

179 For those on EFV, close clinical follow-up for recurrent malaria foll

180 (85% [605/713], P < 0.001), and for those on EFV-based treatment (60% [12/20] vs 86% [214/248], P = 0

181 95% confidence interval [CI] 0.76, 2.05) or EFV (HR 1.23, 95% CI 0.77, 1.96), with significantly sho

182 daily) with FTC/TDF or ABC/3TC (n = 383) or EFV/FTC/TDF (600/200/300 mg daily; n = 364).

183 ed with the WHO approach (362 800 deaths) or EFV (367 300 deaths).

184 receiving failing regimens containing NVP or EFV, respectively.

185 ed a randomized trial of open-label ATV/r or EFV combined with abacavir/lamivudine (ABC/3TC) or tenof

186 n a 1:1 ratio to receive EVG/COBI/FTC/TDF or EFV/FTC/TDF, once daily, plus matching placebo.

187 d protease inhibitors are often favored over EFV in women of childbearing potential.

188 proximately 2.5 microM for both p66- and p51-EFV complexes, 250 nM for the p66/p66-EFV complex, and 7

189 66/p66-EFV complex, and 7 nM for the p51/p51-EFV complex.

190 ssociation constant of 92 nM for the p66/p51-EFV complex was calculated from the thermodynamic linkag

191 In the crystal structure of the p66/p51-EFV complex, the drug is bound to the p66 subunit.

192 nd p51-EFV complexes, 250 nM for the p66/p66-EFV complex, and 7 nM for the p51/p51-EFV complex.

193 imen) or zidovudine/lamivudine/abacavir plus EFV (4-drug EFV regimen).

194 leoside regimen), zidovudine/lamivudine plus EFV (3-drug EFV regimen) or zidovudine/lamivudine/abacav

195 EFV Cmin was measured 20-28 hours post-EFV dose at weeks 4, 8, 16, 24 on-RIF and weeks 4, 8 off

196 y, including 312 and 256 patients prescribed EFV and NVP, respectively.

197 prescribed NVP and 8.0% of those prescribed EFV, but only 32% of NVP and 50% of EFV-associated episo

198 9 EFV-naive men (i.e., men about to receive EFV for the first time) and from 12 EFV-experienced men

199 Seven hundred eighty patients received EFV; 543 provided >/=1 EFV Cmin.

200 experienced men (i.e., men already receiving EFV as part of an antiretroviral regimen).

201 oholic fatty liver disease (NAFLD) receiving EFV plus 2 nucleoside analogues.

202 at TE in HIV-infected patients not receiving EFV.

203 eiving ATV/r, and 2 of 10 subjects receiving EFV in combination with atovaquone 750 mg BID achieved a

204 Subjects receiving EFV-based cART had 47% and 44% lower atovaquone AUCtau t

205 Only 5 of 10 subjects receiving EFV-based cART plus atovaquone 750 mg BID had an atovaqu

206 Compared with RPV, EFV significantly (P < .001) increased lipid levels.

207 with previously published results and the RT-EFV cocrystal structure.

208 isms in the CYP2B6 gene associated with slow EFV metabolism.

209 In SP, EFV reaches concentrations above the HIV-1 IC(90)(WT) th

210 48 weeks, HIV-infected individuals switching EFV to RAL showed decreases in the degree of hepatic ste

211 ), and altered sensorium (4.4% vs 8.2%) than EFV/FTC/TDF recipients.

212 d parameters and fewer dyslipidemia AEs than EFV-based treatment.

213 icant losses in spine, but not hip, BMD than EFV.

214 Fewer (P < .001) RPV-treated patients than EFV-treated patients had TC, LDL-C, and triglyceride lev

215 More RPV- than EFV-treated patients had HDL-C values below these cutoff

216 These data demonstrate that EFV and compounds sharing the EFV scaffold can activate

217 Here we demonstrate that EFV stimulates the activation in primary hepatocytes of

218 We determined that EFV stimulates K101E+G190S virus during early infection

219 Previously, we discovered that EFV activates CYP46A1 and improves behavioral performanc

220 r (PXR)-null mouse hepatocytes revealed that EFV-mediated XBP1 splicing and hepatocyte death were not

221 for CYP46A1 activation by EFV and show that EFV enhanced CYP46A1 activity and cerebral cholesterol t

222 We show that EFV promotes inducible nitric oxide synthase (iNOS) expr

223 We also showed that EFV stimulates K101E+Y188L and K101E+V106I virus, but no

224 The EFV variation was not correlated with percentage of body

225 edian time to viral suppression than did the EFV-TDF-FTC group (28 vs. 84 days, P<0.001), as well as

226 L arm and 30 (Q1-Q3, -17 to 49) dB/m for the EFV group (P = .011).

227 14.6% for the InSTI group and 14.3% for the EFV group, corresponding with a RD of 0.3 percentage poi

228 12.2% for the InSTI group and 11.9% for the EFV group, corresponding with a RD was 0.3 percentage po

229 the CYP46A1 surface, which differs from the EFV-binding site.

230 ies/mL by 48 months was 0.07 and 0.12 in the EFV and LPV/r groups, respectively (P = .21).

231 w-up, 440 in the InSTI group and 1097 in the EFV group incurred the composite outcome.

232 pies/mL were less frequently observed in the EFV group than the LPV/r group (odds ratio [OR] 0.67, 95

233 s lower in the DTG-ABC-3TC group than in the EFV-TDF-FTC group (2% vs. 10%); rash and neuropsychiatri

234 higher in the DTG-ABC-3TC group than in the EFV-TDF-FTC group (88% vs. 81%, P=0.003), thus meeting t

235 lence) were significantly more common in the EFV-TDF-FTC group, whereas insomnia was reported more fr

236 n participants with virologic failure in the EFV-TDF-FTC group.

237 48 in the EVG/COBI/FTC/TDF group than in the EFV/FTC/TDF group (median 13 mumol/L, IQR 5 to 20 vs 1 m

238 cholesterol (HDL-C) levels increased in the EFV/FTC/TDF group but not in the DOR/3TC/TDF group; the

239 the EVG/COBI/FTC/TDF group vs 18/352 in the EFV/FTC/TDF group).

240 -up, 440 of the InSTI group and 1,097 of the EFV group incurred the composite outcome.

241 red with 79.9% of the DRV+r and 80.8% of the EFV groups.

242 monstrate that EFV and compounds sharing the EFV scaffold can activate IRE1alpha-XBP1 across human, m

243 AF, 215 to the DTG + FTC/TDF, and 211 to the EFV/FTC/TDF arm.

244 Of these, an analog in which the EFV alkyne is replaced with an alkene and an analog in w

245 Compared with the EFV group, the DTG group showed greater increments of CD

246 to EFV+FTC-TDF versus 313 (60%) assigned to EFV+3TC-ZDV (HR 0.64, CI 0.54-0.76; p<0.001) and there w

247 76 (15%) among 519 participants assigned to EFV+3TC-ZDV (HR 1.51, CI 1.12-2.04; p = 0.007).

248 curred in 243 (46%) participants assigned to EFV+FTC-TDF versus 313 (60%) assigned to EFV+3TC-ZDV (HR

249 se inhibitor backbone than women assigned to EFV, or men assigned to ATV/r.

250 ward higher, not lower, EFV Cmin compared to EFV alone.

251 TC-TDF had similar high efficacy compared to EFV+3TC-ZDV in this trial population, recruited in diver

252 es/mL was twice as fast with DTG compared to EFV, suggesting DTG has potential to reduce risk of vert

253 TC/TDF demonstrated non-inferior efficacy to EFV/FTC/TDF at week 48 and was well tolerated, with sign

254 Comparing ATV+DDI+FTC to EFV+3TC-ZDV, during a median follow-up of 81 wk there we

255 -TDF were hypothesized to be non-inferior to EFV+3TC-ZDV if the upper one-sided 95% confidence bound

256 EVG/COBI/FTC/TDF was non-inferior to EFV/FTC/TDF; 305/348 (87.6%) versus 296/352 (84.1%) of p

257 The data obtained pointed to EFV effects at the synaptic level, plasmin-depended amyl

258 in 2 of 2 RT-SHIV-infected macaques prior to EFV exposure.

259 , indicating that they were present prior to EFV exposure.

260 ted children >/=3 years of age from LPV/r to EFV are sustained long-term.

261 Children randomized to EFV had a reduced risk of elevated total cholesterol (OR

262 equencing, including 289 (33%) randomized to EFV-based therapy and 585 (67%) randomized to DTG-based

263 zed to ATV/r compared to women randomized to EFV.

264 ring the early steps of infection similar to EFV, but that the newest NNRTI, etravirine (ETR), did no

265 =3 years of age were randomized to switch to EFV or remain on LPV/r in Johannesburg, South Africa.

266 Comparing EFV+FTC-TDF to EFV+3TC-ZDV, during a median 184 wk of follow-up there w

267 There were 2 discontinuations for toxicity (EFV).

268 e emergence, compared with other treatments: EFV plus TDF (hazard ratio [HR], 0.57; range, 0.42-0.76)

269 The US EFV package insert recommends an EFV dose increase for p

270 In an analysis of DOR versus EFV, the treatment difference for discontinuations due t

271 te was 3% higher in the DTG + FTC/TAF versus EFV/FTC/TDF arm (1.03 [95% confidence interval {CI}, 1.0

272 nce imaging to assess epicardial fat volume (EFV), cardiac function, and computed tomography visceral

273 g a single-cycle cell culture assay in which EFV was added either during the infection or the virus p

274 With EFV, lipid levels increased in each N[t]RTI subgroup (ex

275 similar extent (by 12% with RPV and 11% with EFV).

276 rease in limb fat (16% with RPV and 17% with EFV).

277 treated (348 with EVG/COBI/FTC/TDF, 352 with EFV/FTC/TDF).

278 ic failure rates were seen with ABC/3TC with EFV (HR 2.46, 95% CI 1.20, 5.05) or ATV/r (HR 2.22, 95%

279 mes to regimen modification for ABC/3TC with EFV or ATV/r and to safety events with EFV.

280 ith DTG exceeded pediatric deaths added with EFV unless dolutegravir-associated NTD risk was 1.5% or

281 had a favorable safety profile compared with EFV or DRV+r and a favorable tolerability profile compar

282 approach offered some benefits compared with EFV, averting 4900 women's deaths and 20 500 sexual tran

283 Compared with EFV, DTG averted 13 700 women's deaths (0.44% decrease)

284 favorable tolerability profile compared with EFV.

285 14, hsCRP, and Lp-PLA2 levels, compared with EFV/FTC/TDF.

286 changes in LDL-C and non-HDL-C compared with EFV/FTC/TDF.

287 ide analogues unchanged, or to continue with EFV plus 2 nucleoside analogues.

288 by CAP, compared with those continuing with EFV.

289 r ABC/3TC or TDF/FTC were not different with EFV or ATV/r.

290 with EFV or ATV/r and to safety events with EFV.

291 domized to 4 arms of ABC-3TC or TDF-FTC with EFV or ATV/r.

292 Of note, with EFV treatment, 47.2% of mouse hepatocytes were apoptotic

293 emia AEs were less common with RPV than with EFV.

294 transition at lower viremia levels than with EFV.

295 more common with EVG/COBI/FTC/TDF than with EFV/FTC/TDF (72/348 vs 48/352) and dizziness (23/348 vs

296 amivudine or emtricitabine/efavirenz TDF/XTC/EFV (TLE).

297 different between TDF/XTC/DTG versus TDF/XTC/EFV in utero ARV exposure and between AZT versus NVP new

298 Individuals who received 3TC/ZDV/EFV had a more rapid phase 1 viral decay rate than those

299 Our findings indicate that the 3TC/ZDV/EFV regimen may be more potent than 3TC/ZDV/NFV or other

300 y with efavirenz plus lamivudine-zidovudine (EFV+3TC-ZDV), atazanavir plus didanosine-EC plus emtrici