ライフサイエンスコーパス: abacavir

1 nked to cellular reversion of the prodrug to abacavir.

2 receiving efavirenz and 285 spent receiving abacavir.

3 plaque was only found in patients exposed to abacavir.

4 100,000 copies/mL who were naive for 3TC and abacavir.

5 (1.19 [0.50 to 2.83]; p=0.70) compared with abacavir.

6 events of grade 3 or higher were related to abacavir.

7 es exposed to HIV receiving a single dose of abacavir.

8 termine hypersensitivity versus tolerance to abacavir.

9 nteraction with the antiviral small molecule abacavir.

10 n Jurkat T cells, making them susceptible to abacavir.

11 to stavudine, 159 to zidovudine, and 165 to abacavir.

12 her ritonavir-boosted protease inhibitors or abacavir.

13 er ritonavir-boosted protease inhibitors, or abacavir.

14 nce to zidovudine, lamivudine, tenofovir, or abacavir.

15 /mixed plaque was positively associated with abacavir (1.46, 95% CI 1.08-1.98) and negatively associa

16 0.89% tenofovir/tenofovir alafenamide, 1.74% abacavir, 1.07% lamivudine/emtricitabine).

17 .23-1.80); nevirapine, 1.65 (0.90-3.02); and abacavir, 1.82 (0.73-4.52).

18 Abacavir (1592U89, or Ziagen) is a powerful and selectiv

19 t of K65R, reducing resistance to tenofovir, abacavir, 2',3'-dideoxycytidine, dideoxyinosine, and sta

20 .58-2.59); nevirapine, 1.53 (1.11-2.10); and abacavir, 2.03 (1.26-3.25).

21 se inhibitor (NRTI) backbone with lamivudine/abacavir (3TC/ABC) as a commonly used alternative.

22 creased with zidovudine/lamivudine (3TC) and abacavir/3TC (except triglycerides, which were unchanged

23 up (except triglycerides were unchanged with abacavir/3TC).

24 y entry, 984 (12.6%) participants were using abacavir, 4743 (61.0%) were using tenofovir disoproxil f

25 se weighing 6 kg to less than 25 kg received abacavir (60 mg), dolutegravir (5 mg), and lamivudine (3

26 group) or co-formulated dolutegravir 50 mg, abacavir 600 mg, and lamivudine 300 mg (the dolutegravir

27 e 25 mg, or coformulated dolutegravir 50 mg, abacavir 600 mg, and lamivudine 300 mg once daily.

28 de 25 mg or coformulated dolutegravir 50 mg, abacavir 600 mg, and lamivudine 300 mg, with matching pl

29 herapy with daily oral dolutegravir (50 mg), abacavir (600 mg), and lamivudine (300 mg) for 20 weeks.

30 e weighing 25 kg to less than 40 kg received abacavir (600 mg), dolutegravir (50 mg), and lamivudine

31 9 participants reported previous exposure to abacavir, 6681 (86.0%) to tenofovir disoproxil fumarate,

32 were synthesized and cytokine secretion from abacavir/abacavir analogue-responsive CD8(+) T-cell clon

33 line viral load >100,000 copies/mL receiving abacavir (ABC) as part of the nucleoside-backbone compon

34 One randomized trial compared abacavir (ABC) plus lamivudine (3TC) and ZDV+3TC as part

35 line regimens consisting of tenofovir (TDF), abacavir (ABC), and lamivudine (3TC); (2) lower fold res

36 Abacavir (ABC)-induced hypersensitivity is associated wi

37 Long-term effects of abacavir (ABC)-lamivudine (3TC), compared with tenofovir

38 repurposing potential of the antiviral drug abacavir (ABC).

39 for >=12 months, and stable regimen with DTG/abacavir (ABC)/lamivudine (3TC) were 1:1 randomized to c

40 bine (FTC), tenofovir alafenamide (TAF)/FTC, abacavir (ABC)/lamivudine (3TC), and others were estimat

41 ioning in this population after switching to abacavir (ABC)/lamivudine (3TC)/DTG over 6 months.

42 vudine (300 mg) combination tablet (COM) and abacavir (ABC; 300 mg) in 87 antiretroviral therapy-expe

43 00 mg daily] with emtricitabine [FTC]/TDF or abacavir [ABC]/3TC [n = 747]) compared with DRV+r (800/1

44 e: 48-week induction regimen of 3 drugs (DTG/abacavir [ABC]/3TC), followed by DTG + 3TC maintenance i

45 study, the removal of five antiviral drugs (abacavir, acyclovir, emtricitabine, lamivudine and zidov

46 Abacavir adverse reactions were recently shown to be dri

47 Hypersensitivity to abacavir affects about 4% of patients who receive the dr

48 month in the base case or >0.5% per month if abacavir also confers low virological suppression probab

49 We recently reported that abacavir, an anti-HIV-1 drug, potently and selectively k

50 Here we analyzed whether abacavir, an HIV-1 reverse transcriptase inhibitor often

51 In parallel, the effect of selected abacavir analogues on the repertoire of self-peptides pr

52 Seventeen abacavir analogues were synthesized and cytokine secreti

53 to assess the predicted binding poses of the abacavir analogues within the HLA-B*57:01 peptide bindin

54 were higher at 6-14 days (51.7 mg x h/L for abacavir and 17.2 mg x h/L for lamivudine) than at 19-24

55 In contrast the anti-HBV potency of both abacavir and carbovir were improved (10- and 20-fold, re

56 Abacavir and didanosine increased rolling, adhesion and

57 Our results support the association of abacavir and didanosine with CV diseases.

58 human leukocyte antigen (HLA) associations: abacavir and HLA-B*57:01, carbamazepine and HLA-B*15:02,

59 n tenofovir and emtricitabine or combination abacavir and lamivudine background treatment.

60 Geometric mean abacavir and lamivudine exposures (AUC(0-24)) were highe

61 a single-tablet regimen of dolutegravir plus abacavir and lamivudine once a day (dolutegravir group)

62 vir disoproxil fumarate and emtricitabine or abacavir and lamivudine) and with no resistance were ran

63 itabine and tenofovir disoproxil fumarate or abacavir and lamivudine.

64 Abacavir and ten analogues stimulated CD8(+) T-cell IFN-

65 s that are presented only in the presence of abacavir and that were recognized by T cells of hypersen

66 substantially on the comparative outcomes of abacavir and zidovudine after switching to dolutegravir-

67 For abacavir and zidovudine, rapid transformation was attrib

68 ART drugs (ritonavir, indinavir, lamivudine, abacavir, and AZT) significantly decreased endothelial n

69 Subjects received nelfinavir, saquinavir, abacavir, and either another nucleoside analog (n=10) or

70 lafenamide than in those given dolutegravir, abacavir, and lamivudine (10% [n=32] vs 23% [n=72]; p<0.

71 enofovir alafenamide than with dolutegravir, abacavir, and lamivudine (26% [n=82] vs 40% [n=127]), th

72 namide (n=316) or coformulated dolutegravir, abacavir, and lamivudine (n=315), of whom 314 and 315 pa

73 nofovir alafenamide (n=316) or dolutegravir, abacavir, and lamivudine (n=315).

74 de compared with co-formulated dolutegravir, abacavir, and lamivudine at week 96.

75 of drug-related nausea in the dolutegravir, abacavir, and lamivudine group (5% [n=17] vs 17% [n=55];

76 patients (n=293 of 315) in the dolutegravir, abacavir, and lamivudine group (difference -0.6%, 95.002

77 up and 265 (84%) of 315 in the dolutegravir, abacavir, and lamivudine group (difference -2.6%, 95% CI

78 versus five (2%) of 315 in the dolutegravir, abacavir, and lamivudine group (study 1), and six (2%) o

79 irine is non-inferior to daily dolutegravir, abacavir, and lamivudine in virologically suppressed adu

80 ofovir alafenamide, and 315 to dolutegravir, abacavir, and lamivudine) and 645 in study 2 (327 to bic

81 y to group 2 drugs (didanosine, zalcitabine, abacavir, and lamivudine) decreased.

82 lafenamide was non-inferior to dolutegravir, abacavir, and lamivudine, with 276 (88%) of 314 particip

83 s non-inferior to coformulated dolutegravir, abacavir, and lamivudine, with no treatment-emergent res

84 rointestinal tolerability than dolutegravir, abacavir, and lamivudine.

85 , and tenofovir alafenamide to dolutegravir, abacavir, and lamivudine.

86 ombination versus coformulated dolutegravir, abacavir, and lamivudine.

87 cular mechanism of resistance in response to abacavir, and nucleoside analogs in general, a set of re

88 Carbovir, abacavir, and their 2'-methyl derivatives as well as hex

89 to emtricitabine, tenofovir, lamivudine, and abacavir; and an estimated glomerular filtration rate of

90 pression while receiving regimens containing abacavir appear more likely to experience virological an

91 initial treatment of HIV-1 infection; adding abacavir as a fourth drug provided no additional benefit

92 Our data identify abacavir as a novel inflammasome-stimulating drug allerg

93 everse transcriptase inhibitors, identifying abacavir as a specific inflammasome activator.

94 e aimed to compare stavudine, zidovudine, or abacavir as dual or triple fixed-dose-combination paedia

95 ving either tenofovir disoproxil fumarate or abacavir as part of their antiretroviral therapy regimen

96 lation controls in a genome-wide analysis of abacavir-associated hypersensitivity reaction.

97 se was dependent on the enantiomeric form of abacavir at both cyclopropyl and cyclopentyl regions.

98 .35 mug/mL (95.5%), and 0.98 mug/mL (27.9%); abacavir AUC(0-24 h) was 17.7 h.mug/mL (38.8%), 19.8 h.m

99 ve other HAART drugs (indinavir, lamivudine, abacavir, AZT, and ddI) and the 3-plex significantly als

100 nti-HIV potency was noted for the ProTide of abacavir but not for that of carbovir.

101 cross-resistance with TAMs to lamivudine and abacavir, but not stavudine or didanosine.

102 Here we show that abacavir can bind within the F pocket of the peptide-bin

103 agents (6-mercaptopurine, 6-thioguanine, and Abacavir) can inhibit human telomerase activity, and it

104 ivity for dGTP over the active metabolite of abacavir (carbovir triphosphate).

105 Our model predicted a slow abacavir clearance of 2.51 mL/min per kg at birth, which

106 virological failure and therapy failure for abacavir, compared with those for efavirenz, were 2.17 (

107 he abacavir ProTide compared with the parent abacavir compound.

108 45 infants contributed 308 abacavir concentrations; 21 neonates were younger than 1

109 ipidemia OR=1.92 (1.41-2.63), and for recent abacavir, cumulative lopinavir, indinavir, and darunavir

110 R = 1.92 (95% CI, 1.41-2.63), and for recent abacavir, cumulative lopinavir, indinavir, and darunavir

111 umulated DRMs to drugs not received, such as abacavir, didanosine, tenofovir, etravirine, and rilpivi

112 grade 3 or higher adverse events related to abacavir, dolutegravir, and lamivudine and no discontinu

113 , non-comparative dose-confirmation study of abacavir, dolutegravir, and lamivudine in children young

114 ity of dispersible and immediate-release FDC abacavir, dolutegravir, and lamivudine taken once per da

115 al efforts to expand the availability of FDC abacavir, dolutegravir, and lamivudine to children with

116 within each weight band, and thus dosing of abacavir, dolutegravir, and lamivudine was confirmed at

117 Dosing of abacavir, dolutegravir, and lamivudine was confirmed in

118 icistat/emtricitabine/tenofovir alafenamide, abacavir/dolutegravir/lamivudine, raltegravir, rilpiviri

119 Ten neonates administered a single abacavir dose of 8 mg/kg before 15 days of life had subs

120 Therapeutic targets were achieved with exact abacavir doses of 2.0 mg/kg twice daily from 0 weeks to

121 m neonates and infants to determine an exact abacavir dosing strategy (mg/kg) for infants aged 0-3 mo

122 y (n = 157); in combination with amprenavir, abacavir, efavirenz, and adefovir dipivoxil.

123 Current exposure to abacavir, efavirenz, lamivudine, and zidovudine was sign

124 intracellular phosphorylated metabolites of abacavir, emtricitabine, tenofovir disoproxil fumarate,

125 AD-OR for dyslipidemia, diabetes, and recent abacavir exposure were 1.58 (1.29-1.93), 2.19 (1.59-3.03

126 c model and performed simulations to achieve abacavir exposures (area under the curve for 0-12 h) wit

127 c model and performed simulations to achieve abacavir exposures (area under the curve for 0-12 h) wit

128 We show that abacavir fails to generate direct innate immune activati

129 stance profile and once-daily dosing favours abacavir for African children, supporting WHO 2013 guide

130 Alteration of the chemical constitution of abacavir generates analogues that retain a degree of pha

131 In contrast, abacavir generates polyclonal T-cell response by interac

132 Abacavir geometric mean AUC0-24 crossed the upper refere

133 158 in the zidovudine group, and 164 in the abacavir group, and followed for median 2.3 years (5% lo

134 e children in the stavudine, zidovudine, and abacavir groups, respectively, had viral load less than

135 Abacavir has been shown to select for multiple resistant

136 As tenofovir and abacavir have replaced zidovudine and stavudine in antir

137 The associations between abacavir hypersensitivity and HLA-B*57:01 and carbamazep

138 ch has successfully reduced the incidence of abacavir hypersensitivity reactions.

139 Diarrhoea, nausea, and abacavir hypersensitivity were the most frequent drug-re

140 f HLA-B57 for predicting hypersensitivity to abacavir identified in this study compared with a previo

141 the triple mutant's increased resistance to abacavir in cell culture is perhaps due to a fitness adv

142 er prodrugs of cabotegravir, lamivudine, and abacavir in combination with native rilpivirine was foll

143 de of resistance observed in cell culture to abacavir in previous studies was less than that observed

144 on of the P-gp substrate and antiviral agent abacavir, in conjunction with a traceless tether.

145 Previous and current use of abacavir increases the hazard of MACE among people with

146 epletion of cardiolipin synthase 1 abolished abacavir-induced IL-1beta secretion, suggesting that mit

147 itochondrial cardiolipin release may trigger abacavir-induced inflammasome activation.

148 tion and inhibition of K(+) efflux mitigated abacavir-induced mitochondrial reactive oxygen species p

149 ir function; however, the mechanism by which abacavir induces this pathologic T-cell response remains

150 Abacavir is a potential option for prophylaxis and early

151 Abacavir is associated with hypersensitivity reactions i

152 Abacavir is metabolized to the active compound carbovir

153 nucleoside reverse transcriptase inhibitors (Abacavir + Lamivudine (32.4%), Emtricitabine + Tenofovir

154 erse transcriptase inhibitors (2NRTI, mainly abacavir+lamivudine) with a non-nucleoside reverse trans

155 ere to assess pharmacokinetics and safety of abacavir, lamivudine, and lopinavir.

156 LV-I replication was inhibited by tenofovir, abacavir, lamivudine, zalcitabine, stavudine, and zidovu

157 2, pharmacokinetic and safety trial, generic abacavir- lamivudine (120:60 mg) double-scored dispersib

158 egy selected in stage 2 was a quarter of the abacavir-lamivudine (30:15 mg) fixed-dose dispersible ta

159 Neonates received a single dose of abacavir-lamivudine (30:15 mg, a quarter of a tablet) an

160 g once-daily treatment with DTG (50 mg) plus abacavir-lamivudine (600/300 mg).

161 immunodeficiency virus-infected subjects to abacavir-lamivudine (ABC/3TC) versus tenofovir DF-emtric

162 twice daily, each with the co-formulation of abacavir-lamivudine 600 mg/300 mg once daily.

163 tially received oral cabotegravir 30 mg plus abacavir-lamivudine 600-300 mg once daily.

164 ge, and a second dose of a quarter tablet of abacavir-lamivudine and lopinavir boosted with ritonavir

165 ritonavir than in those given efavirenz with abacavir-lamivudine but not with tenofovir DF-emtricitab

166 Abacavir-lamivudine dispersible tablets and ritonavir-bo

167 sumed 50% of children who had viraemia after abacavir-lamivudine exposure had NRTI resistance; with r

168 he pharmacokinetics and safety of paediatric abacavir-lamivudine fixed-dose dispersible tablets and r

169 first adverse event was also shorter in the abacavir-lamivudine group (P<0.001).

170 gic failure was significantly shorter in the abacavir-lamivudine group than in the tenofovir DF-emtri

171 01), with 57 virologic failures (14%) in the abacavir-lamivudine group versus 26 (7%) in the tenofovi

172 Dolutegravir plus abacavir-lamivudine had a better safety profile and was

173 gned to dolutegravir at a dose of 50 mg plus abacavir-lamivudine once daily (DTG-ABC-3TC group) or co

174 renz and did not differ according to whether abacavir-lamivudine or tenofovir DF-emtricitabine was al

175 ve similar antiviral activity when used with abacavir-lamivudine or tenofovir DF-emtricitabine.

176 enz, each given with with placebo-controlled abacavir-lamivudine or tenofovir disoproxil fumarate (DF

177 mens as initial therapy for HIV-1 infection: abacavir-lamivudine or tenofovir disoproxil fumarate (DF

178 tly shorter in patients randomly assigned to abacavir-lamivudine than in those assigned to tenofovir

179 oninferior to oral therapy with dolutegravir-abacavir-lamivudine with regard to maintaining HIV-1 sup

180 Dolutegravir, in combination with abacavir-lamivudine, may provide a simplified regimen.

181 k induction period on oral cabotegravir plus abacavir-lamivudine, patients with viral suppression (pl

182 gravir, keeping current NRTIs (dolutegravir; abacavir-lamivudine-dolutegravir); or (3) transition to

183 g current NRTIs if virologically suppressed (abacavir-lamivudine-dolutegravir, 70% of cohort) or swit

184 ivudine-dolutegravir was more effective than abacavir-lamivudine-dolutegravir.

185 : (1) continue current ART (no dolutegravir; abacavir-lamivudine-efavirenz); (2) transition all child

186 can children aged 8 years with HIV receiving abacavir-lamivudine-efavirenz: (1) continue current ART

187 opinavir-ritonavir, each in combination with abacavir-lamivudine.

188 virine or continuing with daily dolutegravir-abacavir-lamivudine.

189 ily oral induction therapy with dolutegravir-abacavir-lamivudine.

190 ections) or continued oral cabotegravir plus abacavir-lamivudine.

191 regimens relative to oral cabotegravir plus abacavir-lamivudine.

192 stigator-selected tenofovir-emtricitabine or abacavir-lamivudine.

193 ere assigned to receive efavirenz, both with abacavir-lamivudine; 322 (70%) and 324 (70%), respective

194 Subjects received DTG (50 mg) plus abacavir/lamivudine (600/300 mg) once daily.

195 fovir disoproxil fumarate (FTC/TDF) in P007; abacavir/lamivudine (ABC/3TC) or FTC/TDF in DRIVE-FORWAR

196 ial of open-label ATV/r or EFV combined with abacavir/lamivudine (ABC/3TC) or tenofovir/emtricitabine

197 Clinical Trials Group A5202 compared blinded abacavir/lamivudine (ABC/3TC) to tenofovir DF/emtricitab

198 bone of tenofovir/emtricitabine (TDF/FTC) or abacavir/lamivudine (ABC/3TC).

199 irenz, both administered once daily with the abacavir/lamivudine fixed-dose combination in treatment-

200 ide reverse transcriptase inhibitors (NRTIs; abacavir/lamivudine or tenofovir disoproxil fumarate/emt

201 The tenofovir disoproxil fumarate/abacavir/lamivudine regimen resulted in an unexpected an

202 ients on EFV plus tenofovir/emtricitabine or abacavir/lamivudine with NAFLD were randomized 1:1 to sw

203 ptase inhibitors (tenofovir/emtricitabine or abacavir/lamivudine) plus a nonnucleoside reverse transc

204 ptase inhibitors (tenofovir/emtricitabine or abacavir/lamivudine).

205 r efavirenz, with tenofovir/emtricitabine or abacavir/lamivudine.

206 Patients were randomized 1:1 to continue abacavir/lamivudine/dolutegravir or switch to dolutegrav

207 sed optimal dosing guidance is available for abacavir liquid formulation use from birth.

208 ational and international guidelines for the abacavir liquid formulation will expand antiretroviral o

209 cal vascular disease, while prolonged use of abacavir may increase it.

210 3TC) > tenofovir (PMPA) > zidovudine (AZT) > abacavir (metabolized to carbovir, CBV).

211 nsitivity reactions among patients receiving abacavir must remain unchanged.

212 other aromatic antiepileptic drugs (n = 24), abacavir (n = 11), nevirapine (n = 14), trimethoprim-sul

213 y-one compounds inhibited uridine uptake and abacavir, nevirapine, ticagrelor, and uridine triacetate

214 renz as the third drug (in addition to 2 non-abacavir nucleosides) in combination antiretroviral ther

215 nd and therapy failure in patients receiving abacavir or efavirenz as the third drug (in addition to

216 lin, cloxacillin, and dicloxacillin, but not abacavir or nitroso sulfamethoxazole.

217 ll stimulation may be due to presentation of abacavir or of altered peptides.

218 osis who are not suitable for NtRTIs such as abacavir or tenofovir alafenamide.

219 g second-line dolutegravir-based ART with an abacavir or tenofovir backbone were at lower risk of vir

220 marate (TAF)-emtricitabine or standard care (abacavir or zidovudine, plus lamivudine) as the backbone

221 , 95%CI 5.1-74.3) or dolutegravir+lamivudine+abacavir (OR=5.4, 95%CI 1.1-25.8), compared to dolutegra

222 ght gain than tenofovir disoproxil fumarate, abacavir, or zidovudine.

223 001), but not those receiving efavirenz with abacavir (P = .65).

224 , 103 (65%) on zidovudine, and 105 (64%), on abacavir (p=0.63; zidovudine vs stavudine: hazard ratio

225 .001) but not those receiving efavirenz with abacavir (p=0.65).

226 Presentation of these HLA-abacavir-peptide complexes to T-cells is hypothesized to

227 Abacavir pharmacokinetic and safety data were pooled fro

228 We used abacavir pharmacokinetic data from neonates and infants

229 tion, the pharmacokinetic disposition of the abacavir phenylethoxyalaninyl phosphoramidate was evalua

230 nz (3-drug regimen) vs zidovudine/lamivudine/abacavir plus efavirenz (4-drug regimen).

231 ne plus efavirenz, and zidovudine-lamivudine-abacavir plus efavirenz.

232 3-drug EFV regimen) or zidovudine/lamivudine/abacavir plus EFV (4-drug EFV regimen).

233 mtricitabine, zidovudine plus lamivudine, or abacavir plus lamivudine).

234 kbones (zidovudine, stavudine, tenofovir, or abacavir, plus lamivudine or emtricitabine) with either

235 Abacavir (prodrug of CBV) and PMPA are two new drugs tha

236 are formed in CEM cells upon response to the abacavir ProTide compared with the parent abacavir compo

237 As in CEM cells, the abacavir ProTide provided significantly enhanced carbovi

238 wer metabolic effects, such as tenofovir and abacavir, remain widely unavailable.

239 ne dolutegravir and abacavir with high-level abacavir resistance at baseline compared with those with

240 at low-to-moderate CVD risk, suggesting that abacavir should be avoided and previous exposure conside

241 ent with our previous observations of NRTIs, abacavir, stavudine, and zalcitabine increased HIV-1 mut

242 vir, indinavir, lopinavir, zidovudine (AZT), abacavir, stavudine, didanosine (ddI), and lamivudine] i

243 evels declined rapidly after the addition of abacavir, suggesting that productive infection contribut

244 arate [300 mg] and emtricitabine [200 mg] or abacavir sulfate [600 mg] and lamivudine [300 mg]).

245 lls were pretreated with the antiretrovirals abacavir sulphate (ABC), tenofovir disoproxil fumarate,

246 nd several anti-viral drugs (e.g. Maraviroc, Abacavir, Telbivudine, and Cidofovir) may inhibit Ebola

247 etic screening tests, such as HLA-B*57:01 in abacavir therapy, which has successfully reduced the inc

248 Switch from abacavir to TAF was associated with less weight gain tha

249 e patients with detectable viremia who added abacavir to their regimen after 5 years, HIV RNA levels

250 ne-dolutegravir, 70% of cohort) or switching abacavir to zidovudine (zidovudine) if viraemic (zidovud

251 (OR = 1.36; 95% CI, 1.06-1.73), and current abacavir treatment (OR = 1.56; 95% CI, 1.17-2.07).

252 thnicities and testing for HLA-B*5701 before abacavir treatment are recommended.

253 has been observed clinically in response to abacavir treatment.

254 randomized to receive zidovudine/lamivudine/abacavir (triple-nucleoside regimen), zidovudine/lamivud

255 2-3 kg), 10 mg (3-4 kg), and 12 mg (4-5 kg) abacavir twice daily achieved target exposures throughou

256 w evidence regarding the association between abacavir use and risk of cardiovascular events was incon

257 5% confidence interval, -.008 to .003]), and abacavir use with greater IMT (beta = .043 [.012-.074]).

258 dices were not associated, aside from recent abacavir use.

259 : hazard ratio [HR] 0.99 [95% CI 0.75-1.29]; abacavir vs stavudine: HR 0.88 [0.67-1.15]).

260 Abacavir was added to the regimen of eight patients at y

261 0) and current exposure (1.41, 1.01-1.96) to abacavir was associated with a higher hazard of MACE tha

262 The phenylmethoxyalaninyl phosphoramidate of abacavir was prepared in good yield in one step.

263 Dimeric prodrugs of abacavir were designed to have two functions: inhibit P-

264 ations found has been for the antiviral drug abacavir, which causes severe adverse reactions exclusiv

265 pants receiving second-line dolutegravir and abacavir with high-level abacavir resistance at baseline

266 re the relationship between the structure of abacavir with HLA-B*57:01 binding and the CD8(+) T-cell

267 In a randomized comparison of nevirapine or abacavir with zidovudine plus lamivudine, routine viral

268 (ProTide) technology to the antiviral agent abacavir (Ziagen), used for the treatment of HIV infecti

269 formation was the main removal mechanism for abacavir, zidovudine, and emtricitabine, with half-lives

270 er cubic millimeter) to receive coformulated abacavir, zidovudine, and lamivudine (the nucleoside rev

271 ection, the triple-nucleoside combination of abacavir, zidovudine, and lamivudine was virologically i

272 Lamivudine, abacavir, zidovudine, emtricitabine, and tenofovir signi

273 ombined GSS for lamivudine or emtricitabine, abacavir, zidovudine, stavudine, didanosine, and tenofov

274 s infected with HIV-1: zidovudine-lamivudine-abacavir, zidovudine-lamivudine plus efavirenz, and zido

275 itonavir/zidovudine/lamivudine (PI group) or abacavir/zidovudine/lamivudine (NRTI group) in a clinica