ライフサイエンスコーパス: abacavir

1 receiving efavirenz and 285 spent receiving abacavir.

2 100,000 copies/mL who were naive for 3TC and abacavir.

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

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

5 her ritonavir-boosted protease inhibitors or abacavir.

6 er ritonavir-boosted protease inhibitors, or abacavir.

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

8 nked to cellular reversion of the prodrug to abacavir.

9 .23-1.80); nevirapine, 1.65 (0.90-3.02); and abacavir, 1.82 (0.73-4.52).

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

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

12 .58-2.59); nevirapine, 1.53 (1.11-2.10); and abacavir, 2.03 (1.26-3.25).

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

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

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

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

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

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

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

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

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

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

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

24 Abacavir adverse reactions were recently shown to be dri

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

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

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

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

29 Abacavir and didanosine increased rolling, adhesion and

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

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

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

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

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

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

36 For abacavir and zidovudine, rapid transformation was attrib

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

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

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

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

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

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

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

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

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

46 ombination versus coformulated dolutegravir, abacavir, and lamivudine.

47 rointestinal tolerability than dolutegravir, abacavir, and lamivudine.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

66 he abacavir ProTide compared with the parent abacavir compound.

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

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

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

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

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

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

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

74 158 in the zidovudine group, and 164 in the abacavir group, and followed for median 2.3 years (5% lo

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

76 Abacavir has been shown to select for multiple resistant

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

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

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

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

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

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

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

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

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

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

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

88 Abacavir is metabolized to the active compound carbovir

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

110 regimens relative to oral cabotegravir plus abacavir-lamivudine.

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

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

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

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

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

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

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

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

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

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

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

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

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

124 3TC) > tenofovir (PMPA) > zidovudine (AZT) > abacavir (metabolized to carbovir, CBV).

125 nsitivity reactions among patients receiving abacavir must remain unchanged.

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

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

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

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

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

131 , 103 (65%) on zidovudine, and 105 (64%), on abacavir (p=0.63; zidovudine vs stavudine: hazard ratio

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

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

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

135 3-drug EFV regimen) or zidovudine/lamivudine/abacavir plus EFV (4-drug EFV regimen).

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

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

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

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

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

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

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

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

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

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

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

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

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

149 has been observed clinically in response to abacavir treatment.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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