ライフサイエンスコーパス: raltegravir

1 , or an integrase strand transfer inhibitor (raltegravir).

2 mtricitabine with efavirenz, rilpivirine, or raltegravir.

3 here was no advantage to replacing them with raltegravir.

4 ogic failure was rare but more frequent with raltegravir.

5 after long-term exposure to dolutegravir or raltegravir.

6 repeated passage in the presence of 200 muM raltegravir.

7 r, emtricitabine, efavirenz, atazanavir, and raltegravir.

8 ing, suggesting a common mode of action with raltegravir.

9 o the target of integrase inhibitors such as raltegravir.

10 T) and tenofovir and the integrase inhibitor raltegravir.

11 tients failing treatment regimens containing raltegravir.

12 bjects failing treatment regimens containing raltegravir.

13 vely greater resistance to elvitegravir than raltegravir.

14 , severe adverse event during treatment with raltegravir.

15 tazanavir/ritonavir, darunavir/ritonavir, or raltegravir.

16 Administration (US FDA) approved MK-0518, or raltegravir ( 1), as the first IN inhibitor for HIV/AIDS

17 ir (odds ratio [OR] 1.27, 95% CI 1.17-1.38), raltegravir (1.37, 1.20-1.56), and tenofovir alafenamide

18 roM), L-731,988 (34 nM), L-870,810 (2.4 nM), raltegravir (10 nM), elvitegravir (4.0 nM), and GSK36473

19 interactive voice and web response system to raltegravir 1200 mg (two 600 mg tablets) orally once dai

20 These results support the use of raltegravir 1200 mg once daily for first-line therapy.

21 INTERPRETATION: A once daily raltegravir 1200 mg regimen was non-inferior compared wi

22 cluded in the primary efficacy analysis (153 raltegravir, 154 efavirenz).

23 2 efavirenz) and 394 delivered on-study (200 raltegravir, 194 efavirenz); 307 were included in the pr

24 o Dec 11, 2018, 408 women were enrolled (206 raltegravir, 202 efavirenz) and 394 delivered on-study (

25 allocated to treatment, of whom 281 received raltegravir, 282 received efavirenz, and three were neve

26 gained more weight at 18 months compared to raltegravir (3.4 kg) and PIs (4.1 kg), though these diff

27 130 nM vs 9 nM), L-870,810 (130 nM vs 4 nM), raltegravir (300 nM vs 9 nM), elvitegravir (90 nM vs 6 n

28 mg (two 600 mg tablets) orally once daily or raltegravir 400 mg (one tablet) orally twice daily, each

29 ery 8 hours for 9 days plus a single dose of raltegravir 400 mg on day 10 followed by a washout perio

30 wed by a washout period and a single dose of raltegravir 400 mg on day 38, or the same medication in

31 00 mg regimen was non-inferior compared with raltegravir 400 mg twice daily for initial treatment of

32 >/=1 year were randomly assigned to receive raltegravir 400 mg twice daily or placebo for 24 weeks.

33 Patients were randomly assigned (2:1) to raltegravir 400 mg twice daily or placebo, both with opt

34 udy in HIV-infected pregnant women receiving raltegravir 400 mg twice daily was performed (Pharmacoki

35 to antiretroviral regimens containing either raltegravir (400 mg twice daily) or efavirenz (600 mg ea

36 ession for >/= 1 year were randomized to add raltegravir (400 mg twice daily) or matching placebo for

37 ratio to switch from lopinavir-ritonavir to raltegravir (400 mg twice daily; n=353) or to remain on

38 ritonavir (100 mg once per day) plus either raltegravir (400 mg twice per day; NtRTI-sparing regimen

39 or plus NRTI group), protease inhibitor plus raltegravir (400 mg twice per day; protease inhibitor pl

40 zanavir, 300 mg/d, with ritonavir, 100 mg/d; raltegravir, 400 mg twice daily; or darunavir, 800 mg/d,

41 favirenz) and infants (25% in each group; 50 raltegravir, 48 efavirenz), with no treatment-related de

42 similar among mothers (30% in each group; 61 raltegravir, 59 efavirenz) and infants (25% in each grou

43 (135 dolutegravir, 153 elvitegravir, and 63 raltegravir), 86% were male, and 49% were white.

44 er inhibitor (dolutegravir, elvitegravir, or raltegravir), a nonnucleoside reverse transcriptase inhi

45 Similarly, raltegravir, a pharmacologic integrase inhibitor, abolis

46 Previous reports showed that raltegravir, a recently approved antiviral compound that

47 The end-stage LIVER disease and RALtegravir-Agence Nationale de Recherche sur le Sida et

48 ); each PI had greater increases relative to raltegravir (all P </= .001 at week 96).

49 ) and C(max) for raltegravir + boceprevir vs raltegravir alone were 1.04 (90% CI, .88-1.22) and 1.11

50 ion (C(max)) for raltegravir + boceprevir vs raltegravir alone were 4.27 (95% confidence interval [CI

51 on the crystal structure of ALDOA identified raltegravir, an antiretroviral agent that targets HIV in

52 drug-drug interaction between boceprevir and raltegravir, an HIV integrase inhibitor.

53 RK-2-investigated the efficacy and safety of raltegravir, an HIV-1 integrase strand-transfer inhibito

54 AMD3100, a CXCR4 entry inhibitor, but not by raltegravir, an integrase, indicating that only early li

55 the limits of quantification at 1 pg/mL for raltegravir and 2 pg/mL for four proprietary compounds.

56 462 were treated with raltegravir and 237 with placebo.

57 ach variant was tested for susceptibility to raltegravir and dolutegravir using a single-cycle indica

58 viral intensification therapy (standard dose raltegravir and dose-adjusted maraviroc based on baselin

59 Raltegravir and efavirenz-based initial antiretroviral t

60 ns that determine the resistance pathways to raltegravir and elvitegravir (N155H, Q148K/R/H, and E92Q

61 grase inhibitors are in clinical trials, and raltegravir and elvitegravir are likely to be the first

62 Our findings demonstrate that both raltegravir and elvitegravir are potent IN inhibitors an

63 rugs with IN, consistent with the binding of raltegravir and elvitegravir at the IN-DNA interface.

64 (3) to determine the resistance profile for raltegravir and elvitegravir in those IN mutants.

65 1) to investigate and compare the effects of raltegravir and elvitegravir on the three IN-mediated re

66 ertion rendered isolates highly resistant to raltegravir and elvitegravir, and moderately resistant t

67 ts harboring resistance to the other INSTIs, raltegravir and elvitegravir.

68 sted lopinavir, and the integrase inhibitors raltegravir and elvitegravir.

69 fect of pregnancy on the pharmacokinetics of raltegravir and its safety and efficacy in HIV-infected

70 (42%) of all patients initially assigned to raltegravir and less than 400 copies per mL in 210 (45%)

71 703 randomized patients (462 and 237 in the raltegravir and placebo groups, respectively) received t

72 g-related adverse events were similar in the raltegravir and placebo groups.

73 going close to those of the clinically used raltegravir and retained potencies against a panel of IN

74 Raltegravir and ritonavir-boosted darunavir were equival

75 cidence of tolerability discontinuation than raltegravir and ritonavir-boosted darunavir, respectivel

76 l modeling to visualize interactions between raltegravir and the imputed HLA molecule.

77 nt resistance to APV, an integrase inhibitor raltegravir, and a GRL-09510 congener (GRL-09610), no va

78 etravirine; B3, ritonavir-boosted darunavir, raltegravir, and either tenofovir plus emtricitabine or

79 arious levels of resistance to dolutegravir, raltegravir, and elvitegravir.

80 l use of recently approved drugs (maraviroc, raltegravir, and etravirine) in treatment-experienced pa

81 rd prophylaxis, adjunctive raltegravir or no raltegravir, and supplementary food or no supplementary

82 L54 mutant viruses were fully susceptible to raltegravir, any virus bearing the UL42 mutation was as

83 The geometric mean (GM) of raltegravir area under the concentration-time curve (AUC

84 Raltegravir as a film-coated tablet 400 mg twice daily (

85 recommend a boosted protease inhibitor plus raltegravir as an alternative second-line combination.

86 earing the UL42 mutation was as resistant to raltegravir as clone 7.

87 gions to evaluate the safety and efficacy of raltegravir, as compared with placebo, in combination wi

88 abotegravir, dolutegravir, elvitegravir, and raltegravir) at the virological failure of an INSTI-base

89 GM ratio estimates of raltegravir AUC(0-12h) and C(max) for raltegravir + boce

90 NRTIs] plus ritonavir-boosted darunavir plus raltegravir; B2, ritonavir-boosted darunavir plus ralteg

91 itonavir-boosted atazanavir or darunavir, or raltegravir-based cART.

92 Raltegravir-based combination treatment had rapid and po

93 A raltegravir-based regimen was associated with significan

94 prior peg-IFN/RBV standard therapy and on a raltegravir-based regimen with HIV RNA <400 copies/mL.

95 ed antiretroviral therapy (ART) regimen to a raltegravir-based regimen.

96 n 6 patients at the virological failure of a raltegravir-based regimen.

97 In 2007, raltegravir became the first integrase inhibitor approve

98 references of HIV integrase and to (2) study raltegravir binding in the context of these dynamic mode

99 Raltegravir binds to IN and blocks the integration of th

100 tes of raltegravir AUC(0-12h) and C(max) for raltegravir + boceprevir vs raltegravir alone were 1.04

101 nd maximum plasma concentration (C(max)) for raltegravir + boceprevir vs raltegravir alone were 4.27

102 Elvitegravir was more potent than raltegravir, but neither drug could block disintegration

103 was seen following switch to elvitegravir or raltegravir, but not dolutegravir.

104 f a clinically significant drug interaction, raltegravir can be recommended for combined HIV/HCV trea

105 Raltegravir can be used in standard dosages in HIV-infec

106 Dolutegravir and raltegravir can directly impact adipocytes and adipose t

107 A total of 21 different raltegravir-chelator derivative (RCD) compounds were pre

108 RT recipients, IHS was associated with lower raltegravir concentrations in blood and semen, compared

109 Those patients had adequate raltegravir concentrations, but harbored multiresistant

110 ents before and 48 weeks after initiation of raltegravir-containing combination antiretroviral therap

111 V-1-infected patients, who started a salvage raltegravir-containing regimen, were investigated.

112 tients who are not consistent in following a raltegravir-containing treatment regimen.

113 The median ratio of raltegravir cord to maternal blood was 1.21 (interquarti

114 lipid changes noted with the PIs relative to raltegravir deserves further evaluation.

115 he primary analysis, protease inhibitor plus raltegravir did not meet non-inferiority criteria.

116 At low nanomolar concentrations (<50 nM), raltegravir displayed a time-dependent inhibition of con

117 Results of the study indicate that raltegravir displayed linear pharmacokinetics between a

118 ART regimen, containing either InSTI (i.e., raltegravir, dolutegravir, and elvitegravir/cobicstat) o

119 patients were included, of which 68% started raltegravir during pregnancy.

120 The observed mean decrease in exposure to raltegravir during third trimester compared to postpartu

121 combination of tenofovir, emtricitabine, and raltegravir effectively suppresses peripheral and system

122 NTD reports for 4 integrase inhibitors (DTG, raltegravir, elvitegravir, bictegravir), 2 protease inhi

123 The results show raltegravir, elvitegravir, MK-2048, RDS 1997, and RDS 21

124 rimary objective was to use antiretrovirals (raltegravir, etravirine, and ritonavir-boosted darunavir

125 rformed on plasma samples at baseline and at raltegravir failure.

126 We compared substitution of raltegravir for lopinavir-ritonavir with continuation of

127 th some (34.7%) also receiving maraviroc and raltegravir for the first 24 weeks (hereafter, "ART plus

128 fety, tolerability, and efficacy of multiple raltegravir formulations in human immunodeficiency virus

129 Emergent resistance was associated with the raltegravir group (OR 2.47, 95% CI 1.02-5.99; p=0.05), b

130 (81%) of 383 in the protease inhibitor plus raltegravir group (p=0.07; lower 95% confidence limit fo

131 roup, 64% of the patients (mean, 277) in the raltegravir group (P=0.21 for the comparison with the NR

132 6% of patients in the NRTI group, 86% in the raltegravir group (P=0.97), and 61% in the monotherapy g

133 viral load measurements at 96 weeks; in the raltegravir group 236 had baseline sequence data and 255

134 l failure was 10.3% (95% CI 6.5-14.0) in the raltegravir group and 12.4% (8.3-16.5) in the NRTI group

135 144 (94%) women in the raltegravir group and 129 (84%) in the efavirenz group m

136 ndomly assigned 515 participants: 260 to the raltegravir group and 255 to the NRTI group; two partici

137 After week 156, 251 patients (54%) from the raltegravir group and 47 (20%) from the placebo group en

138 ticipants had virological failure (46 in the raltegravir group and 50 in the NRTI group).

139 62 (24%) participants in the raltegravir group and 81 (32%) in the NRTI group had gra

140 e) showed that 86.1% (n=241 patients) of the raltegravir group and 81.9% (n=230) of the efavirenz gro

141 5 to the NRTI group; two participants in the raltegravir group and one in the NRTI group were exclude

142 f 383 patients in the protease inhibitor and raltegravir group at week 144 (p=0.02) and 233 (61%) of

143 er than expected virological efficacy in the raltegravir group compared with the lopinavir-ritonavir

144 The raltegravir group had a significant increase in the leve

145 4%, 95% CI 80.2-88.1) of 347 patients in the raltegravir group had vRNA concentration less than 50 co

146 were significantly greater (p<0.0001) in the raltegravir group than in the lopinavir-ritonavir group

147 At week 156, 51% in the raltegravir group versus 22% in the placebo group (non-c

148 inavir) plus 400 mg raltegravir twice a day (raltegravir group) or to ritonavir-boosted lopinavir plu

149 00 mg twice per day; protease inhibitor plus raltegravir group), or protease inhibitor monotherapy (p

150 lus raltegravir in a superiority comparison (raltegravir group, 433 patients), or protease-inhibitor

151 -ritonavir group (3%) and no patients in the raltegravir group.

152 in the NtRTI group and 3.0 (1.0-4.3) in the raltegravir group.

153 cluded in the NtRTI group and and 270 in the raltegravir group.

154 ritonavir-boosted lopinavir and raltegravir (raltegravir-group) provided non-inferior efficacy to rit

155 Raltegravir has a favourable long-term efficacy and safe

156 ce susceptibility to the integrase inhibitor raltegravir have been identified in patients failing tre

157 t clinical trials of the integrase inhibitor raltegravir have demonstrated more rapid viral decay tha

158 This effect was most pronounced for raltegravir- (HR=1.42 [1.06-1.91]) vs. NNRTI-initiators.

159 apy after 12 weeks of induction therapy with raltegravir in a noninferiority comparison (monotherapy

160 up, 426 patients), a protease inhibitor plus raltegravir in a superiority comparison (raltegravir gro

161 at was intensified (iART) with maraviroc and raltegravir in an open-label fashion.

162 The use of raltegravir in human immunodeficiency virus (HIV)-infect

163 Resistance to raltegravir in integrase strand transfer inhibitor-naive

164 pressed while taking a stable atazanavir- or raltegravir-inclusive antiretroviral regimen.

165 tients previously reported to have developed raltegravir-induced DRESS syndrome and in 1 previously u

166 Five of the 6 patients who developed raltegravir-induced DRESS syndrome were African, and 1 w

167 tween carriage of the HLA-B*53:01 allele and raltegravir-induced DRESS syndrome, and the potential ut

168 ele HLA-B*53:01 in the immunopathogenesis of raltegravir-induced DRESS syndrome.

169 up), or protease inhibitor monotherapy (plus raltegravir induction for first 12 weeks, re-intensified

170 receive lopinavir monotherapy (after initial raltegravir induction) in the Europe-Africa Research Net

171 blotting and quantitative PCR revealed that raltegravir inhibits DNA replication of HSV-1 rather tha

172 Raltegravir intensification did not have a significant e

173 , placebo-controlled study to assess whether raltegravir intensification reduces low-level viral repl

174 Raltegravir intensification resulted in a rapid increase

175 Raltegravir is a recently, Food and Drug Administration-

176 Raltegravir is a well tolerated alternative to efavirenz

177 Raltegravir is an alternative for treatment-experienced

178 Ritonavir-boosted lopinavir plus raltegravir is an appropriate alternative, especially if

179 Raltegravir is an FDA approved inhibitor directed agains

180 , and MK-0536 are equally effective, whereas raltegravir is approximately 70% as effective.

181 b to autoimmune disease, are not affected by raltegravir, lupus-prone (NZBxNZW) F(1) mice die of glom

182 Overall, these results suggest that raltegravir may be a valuable therapeutic agent against

183 re, the anti-HIV-1 drugs AZT, tenofovir, and raltegravir may be useful for treatment of XMRV infectio

184 ntly unknown, virtual modeling suggests that raltegravir may bind within the antigen binding cleft of

185 Removing the NRTIs or replacing them with raltegravir may provide a benefit.

186 se of antiviral agents (i.e., zidovudine and raltegravir) may be of benefit.

187 tion, previously identified with MK-2048 and raltegravir, may represent the initial substitution in a

188 Raltegravir (MK-0518) is an inhibitor of human immunodef

189 target of the newly approved anti-AIDS drug raltegravir (MK-0518, Isentress) while elvitegravir (GS-

190 nical adverse events occurred in patients on raltegravir (n=124 [44.1%]) than those on efavirenz (n=2

191 and safety analyses for the combined trials (raltegravir, n=350; lopinavir-ritonavir, n=352).

192 mparison with the NRTI group; superiority of raltegravir not shown), and 55% of the patients (mean, 2

193 INTERPRETATION: Protease inhibitor plus raltegravir offered no advantage over protease inhibitor

194 We report here that the activity profile of raltegravir on the replication of murine leukemia virus

195 virus specifically blocked at integration by raltegravir or catalytic site mutations (IN(D64N/D116N/E

196 ighest risk for red-flag DDI, and the use of raltegravir or dolutegravir-based antiretroviral therapy

197 or regimens including darunavir, atazanavir, raltegravir or dolutegravir.

198 ficacy of antiretroviral therapy with either raltegravir or efavirenz in late pregnancy.

199 atients, 471 patients had viruses with >/= 1 raltegravir or elvitegravir resistance mutation (15.6%).

200 le continuing their failing regimen (without raltegravir or elvitegravir) through day 7, after which

201 east 1 ritonavir-boosted protease inhibitor, raltegravir or etravirine.

202 phylaxis or standard prophylaxis, adjunctive raltegravir or no raltegravir, and supplementary food or

203 Patients were randomly assigned to raltegravir or placebo in a 2:1 ratio.

204 Tolerability of regimens containing raltegravir or ritonavir-boosted darunavir was superior

205 ed resting CD4(+) T cells in the presence of raltegravir or with integrase active-site mutant HIV-1 y

206 e, defined as discontinuation of atazanavir, raltegravir, or darunavir for toxicity.

207 egimens that included darunavir, atazanavir, raltegravir, or dolutegravir.

208 ighest risk for red-flag DDI, and the use of raltegravir- or dolutegravir-based antiretroviral therap

209 stance was predicted in 12% of patients with raltegravir- or elvitegravir-resistant viruses (2% of al

210 lected, without resistance testing); or with raltegravir; or alone as protease inhibitor monotherapy

211 of dolutegravir, tenofovir alafenamide, and raltegravir, particularly given the potential consequenc

212 ere dolutegravir plus lamivudine (22.8%) and raltegravir plus boosted darunavir (19.8%); the most com

213 gravir; B2, ritonavir-boosted darunavir plus raltegravir plus etravirine; B3, ritonavir-boosted darun

214 ted patients with limited treatment options, raltegravir plus optimized background therapy provided b

215 vudine), C (ritonavir-boosted darunavir plus raltegravir plus tenofovir-emtricitabine or tenofovir pl

216 Raltegravir produced the most favorable lipid profile.

217 Merck's Raltegravir (RAL) (October 2007) and Gilead's Elvitegrav

218 were evaluated here for susceptibilities to raltegravir (RAL) and elvitegravir (EVG).

219 tegrase strand transfer inhibitors (INSTIs), raltegravir (RAL) and elvitegravir (EVG).

220 e inhibitor, has limited cross-resistance to raltegravir (RAL) and elvitegravir in vitro.

221 protease inhibitor (PI) regimen, a switch to raltegravir (RAL) can be an option in case of comorbidit

222 (RIF) induces UGT1A1, an enzyme involved in raltegravir (RAL) elimination, thereby potentially lower

223 , dolutegravir (DTG), elvitegravir (EVG), or raltegravir (RAL) from any prior regimen were eligible.

224 vir (ATV/r), darunavir-ritonavir (DRV/r), or raltegravir (RAL) in ACTG A5260s, a substudy of A5257.

225 efficacy, and pharmacokinetic parameters of raltegravir (RAL) in human immunodeficiency virus (HIV)-

226 antiretroviral therapy (cART) incorporating raltegravir (RAL) is highly effective for virologic supp

227 d the effect of switching efavirenz (EFV) to raltegravir (RAL) on hepatic steatosis among HIV-infecte

228 t is unclear whether the integrase inhibitor raltegravir (RAL) reduces inflammation and immune activa

229 ave shown that all three FDA-approved drugs, raltegravir (RAL), elvitegravir and dolutegravir (DTG),

230 In the presence of raltegravir (RAL), MK-2048, and L-841,411, IN incorporat

231 Resistance to raltegravir (RAL), the first HIV-1 integrase (IN) inhibi

232 to define viral kinetics after initiation of raltegravir (RAL)-based antiretroviral therapy (ART).

233 mary resistance pathways in subjects failing raltegravir (RAL)-containing treatments.

234 vir (ATV/r), darunavir/ritonavir (DRV/r), or raltegravir (RAL).

235 ure frequently lead to cross-resistance with raltegravir (RAL).

236 tazanavir/ritonavir, darunavir/ritonavir, or raltegravir (RAL).

237 -G140S/Q148H mutant virus in the presence of raltegravir (RAL); the RT-K103N mutation had no effect.

238 ll culture system with viral replication and raltegravir (RAL; an integrase inhibitor) suppression, m

239 [LPV/r], 71.1%; 95% CI, 43.6%-98.6%; TDF+FTC+raltegravir [RAL], 74.7%; 95% CI, 41.4%-100%; TDF+FTC+ b

240 ing ART with ritonavir-boosted lopinavir and raltegravir (raltegravir-group) provided non-inferior ef

241 when compared to an abbreviated analogue of raltegravir (RCD-1).

242 patients experiencing virological failure to raltegravir received dolutegravir with optimized backgro

243 ent in 13 of these 17 patients: 7 of the 462 raltegravir recipients (1.5%) and 6 of the 237 placebo r

244 Virological failure occurred in 166 raltegravir recipients (36%) during the double-blind pha

245 ncompletion as treatment failure, 355 of 458 raltegravir recipients (77.5%) had HIV-1 RNA levels belo

246 follow-up, cancers were detected in 3.5% of raltegravir recipients and in 1.7% of placebo recipients

247 iter was achieved at week 16 in 61.8% of the raltegravir recipients, as compared with 34.7% of placeb

248 revention of perinatal HIV transmission with raltegravir recommended as a preferred or alternative in

249 ontaining efavirenz, darunavir/ritonavir, or raltegravir regardless of pretreatment viral load.

250 ause mortality among 415 patients starting a raltegravir regimen compared to 2646 starting an efavire

251 c pathways to resistance in subjects failing raltegravir regimens and defines the effects of primary

252 and the recombinant viruses were tested for raltegravir resistance.

253 IN inhibitors, and may help overcome rising raltegravir resistance.

254 Extended antiviral testing against a few raltegravir-resistant HIV-1 clones revealed a resistance

255 A raltegravir-resistant HSV-1 mutant was generated by repe

256 8 is equally potent against wild-type IN and raltegravir-resistant IN mutant N155H, suggesting this i

257 Studies of raltegravir-resistant IN mutants N155H and Q148H without

258 l loads of 42 raltegravir-susceptible and 40 raltegravir-resistant specimens were determined using Re

259 The dynamics of raltegravir-resistant variants and their impact on virol

260 afenamide, abacavir/dolutegravir/lamivudine, raltegravir, rilpivirine, atazanavir/ritonavir, darunavi

261 g that the RealTime HIV-1 assay can tolerate raltegravir-selected mutations.

262 tion of PF74 against the integrase inhibitor raltegravir showed an additive antiviral effect that is

263 The pharmacokinetics of raltegravir showed extensive variability.

264 ese important questions, we investigated the raltegravir susceptibility and replication capacity of v

265 rimary and secondary resistance mutations on raltegravir susceptibility and replication capacity.

266 y mutations and other secondary mutations on raltegravir susceptibility and viral replication capacit

267 ion generally displayed larger reductions in raltegravir susceptibility than viruses with an N155H mu

268 Viral loads of 42 raltegravir-susceptible and 40 raltegravir-resistant spe

269 resulted in a higher level of resistance to raltegravir than N155H alone.

270 of Q148H showed a higher cross-resistance to raltegravir than observed with N155H, providing evidence

271 iral suppression was shorter for patients on raltegravir than on efavirenz (log-rank test p<0.0001).

272 ing G140S and Q148K were more susceptible to raltegravir than viruses containing a Q148K mutation alo

273 with a G140S mutation were more resistant to raltegravir than viruses containing a Q148R(H) mutation

274 This paper shows that raltegravir, the antiretrovirus drug targeting integrase

275 results did not establish non-inferiority of raltegravir to lopinavir-ritonavir.

276 We compared a new once daily formulation of raltegravir to the currently marketed twice daily formul

277 Raltegravir-treated NZB mice, which share the H-2 haplot

278 he potential utility of HLA screening before raltegravir treatment.

279 mg ritonavir, 400 mg lopinavir) plus 400 mg raltegravir twice a day (raltegravir group) or to ritona

280 f ritonavir once daily), each with 400 mg of raltegravir twice daily and 300 mg of tenofovir disoprox

281 ratio (double-blind) to receive 400 mg oral raltegravir twice daily or 600 mg oral efavirenz once da

282 ratio to receive oral treatment with 400 mg raltegravir twice daily plus 800 mg darunavir and 100 mg

283 r which all patients were offered open-label raltegravir until week 240.

284 The discovery of raltegravir validated the existence of the IN, which is

285 ratio was 5.7-fold higher (P = .023) in the raltegravir vs. placebo group.

286 Although switching to raltegravir was associated with greater reductions in se

287 Exposure to raltegravir was highly variable.

288 ence of -3.4% (-8.4 to 1.5), indicating that raltegravir was non-inferior, but not superior, to NRTIs

289 uperior to ritonavir-boosted atazanavir, and raltegravir was superior to both protease inhibitors.

290 Raltegravir was well tolerated during pregnancy.

291 cause nonautoimmune mice are not affected by raltegravir, we consider off-target effects unlikely and

292 ed after treatment with a suboptimal dose of raltegravir were aberrant.

293 vitro, dolutegravir and, to a lesser extent, raltegravir were associated with greater extracellular m

294 Atazanavir-ritonavir and raltegravir were associated with less frequent viral sup

295 In this study, subtoxic levels of raltegravir were shown to inhibit the replication of fou

296 NRTIs plus ritonavir-boosted darunavir plus raltegravir) were defined by increasing levels of resist

297 f maximum effective concentration (EC50) for raltegravir when introduced into 1 or more mutational ba

298 We compared the safety and efficacy of raltegravir with efavirenz as part of combination antire

299 Use of raltegravir with optimum background therapy is effective

300 med to assess whether boosted lopinavir plus raltegravir would be non-inferior to boosted lopinavir p