ライフサイエンスコーパス: 3TC

1 3TC and FTC are taken up by cells and converted into 3TC

2 (-)3TC is the only analog containing an unnatural l(-) nucl

3 3TC-TP concentrations were on average 17-fold greater th

4 3TC/FTC-resistant mutants (M184V/I) emerged infrequently

5 ples from Burkina Faso (LPV/r group: n = 47; 3TC group: n = 48).

6 h Africa were assessed (LPV/r group: n = 92; 3TC group: n = 67) and at week 26, 95 samples from Burki

7 gic failure was associated with continuing a 3TC-containing regimen.

8 ion of HIV dynamics under the influence of a 3TC D4T Reverse Transcriptase Inhibitors (RTI) drug regi

9 ompared with those who continued receiving a 3TC-containing regimen.

10 -d4C), however, showed cross-resistance to a 3TC-resistant variant (HIV-1(M184V)).

11 ctor of 3, while replication of HIV-1 with a 3TC-resistant RT (M184V) had no significant effect on th

12 or (NRTI) backbone with lamivudine/abacavir (3TC/ABC) as a commonly used alternative.

13 ith zidovudine/lamivudine (3TC) and abacavir/3TC (except triglycerides, which were unchanged).

14 t triglycerides were unchanged with abacavir/3TC).

15 dependent changes in susceptibility to ABC, 3TC, TDF, and didanosine on titration of K65R and/or M18

16 The DTG-ABC-3TC group had a shorter median time to viral suppression

17 No participants in the DTG-ABC-3TC group had detectable antiviral resistance; one tenof

18 g to adverse events was lower in the DTG-ABC-3TC group than in the EFV-TDF-FTC group (2% vs. 10%); ra

19 iter was significantly higher in the DTG-ABC-3TC group than in the EFV-TDF-FTC group (88% vs. 81%, P=

20 plus abacavir-lamivudine once daily (DTG-ABC-3TC group) or combination therapy with efavirenz-tenofov

21 was reported more frequently in the DTG-ABC-3TC group.

22 s from baseline in spine and hip BMD for ABC-3TC versus TDF-FTC were -1.3% and -3.3% (P = .004) and -

23 xty-nine persons randomized to 4 arms of ABC-3TC or TDF-FTC with EFV or ATV/r.

24 s were randomized and blinded to receive ABC-3TC or TDF-FTC with open-label EFV or ATV/r.

25 Compared with ABC-3TC, TDF-FTC-treated participants had significantly grea

26 ABC/3TC and TDF/FTC significantly and similarly decreased fa

27 the DTG arm and 77/80 (96.3%) in the DTG/ABC/3TC arm (difference, 2.7%; 95% confidence interval [CI],

28 the DTG arm compared with 0% in the DTG/ABC/3TC arm (P = .005 by the log-rank test).

29 INSTI) class; 1 patient discontinued DTG/ABC/3TC due to an adverse event.

30 o DTG monotherapy and 80 to continue DTG/ABC/3TC.

31 standard of care: 3-drug regimen of DTG/ABC/3TC.

32 stratum, times to virologic failure for ABC/3TC or TDF/FTC were not different with EFV or ATV/r.

33 ailure rate was significantly higher for ABC/3TC than for TDF/FTC when given with either EFV or ATV/r

34 ime to virologic failure was similar for ABC/3TC vs TDF/FTC with ATV/r (hazard ratio [HR] 1.25, 95% c

35 horter times to regimen modification for ABC/3TC with EFV or ATV/r and to safety events with EFV.

36 (FTC/TDF) in P007; abacavir/lamivudine (ABC/3TC) or FTC/TDF in DRIVE-FORWARD; and 3TC/TDF for DOR an

37 r EFV combined with abacavir/lamivudine (ABC/3TC) or tenofovir/emtricitabine (TDF/FTC) in 1857 human

38 02 compared blinded abacavir/lamivudine (ABC/3TC) to tenofovir DF/emtricitabine (TDF/FTC) with efavir

39 nfected subjects to abacavir-lamivudine (ABC/3TC) versus tenofovir DF-emtricitabine (TDF/FTC) with ef

40 tabine (TDF/FTC) or abacavir/lamivudine (ABC/3TC).

41 over time when paired with a backbone of ABC/3TC: 16% per 5 years (95% confidence interval [CI], 4%,

42 3TC/LPV/r were <3 years and all CLHIV on ABC/3TC/EFV were >=3 years.

43 More CLHIV on ABC/3TC/EFV, 47.8% (11/23), were found to have 0 or only 1 e

44 their current HIV regimen than those on ABC/3TC/EFV.

45 ls that CLHIV with detectable viremia on ABC/3TC/LPV/r are more likely to have maintained at least tw

46 All but 2 children on ABC/3TC/LPV/r were <3 years and all CLHIV on ABC/3TC/EFV wer

47 rrent regimen compared to 8.2% (4/49) on ABC/3TC/LPV/r.

48 Only ABC/3TC-containing regimens were associated with an increase

49 DRV+r (800/100 mg daily) with FTC/TDF or ABC/3TC (n = 383) or EFV/FTC/TDF (600/200/300 mg daily; n =

50 a backbone containing either TDF/FTC or ABC/3TC.

51 d ABC/3TC/LPV/r, and 23 (31.9%) received ABC/3TC/EFV.

52 lly genotyped CLHIV, 49 (68.1%) received ABC/3TC/LPV/r, and 23 (31.9%) received ABC/3TC/EFV.

53 (CI, 17.2 to 31.1) among those receiving ABC/3TC, and 20.0 (CI, 14.2 to 27.3) for those receiving oth

54 NRTI and NRTI DRMs among CLHIV receiving ABC/3TC/LPV/r suggests a lasting impact of failed PMTCT inte

55 Fat mtDNA content decreased within the ABC/3TC and TDF/FTC groups (combining EFV and ATV/r arms; me

56 Differences between the ABC/3TC and TDF/FTC groups were significant for complex I (P

57 10(3)/microg, respectively) but not the ABC/3TC group.

58 iretroviral combination were switched to ABC/3TC/DTG.

59 Due to higher virologic failure with ABC/3TC in the high HIV RNA stratum, blinded treatment was s

60 r virologic failure rates were seen with ABC/3TC with EFV (HR 2.46, 95% CI 1.20, 5.05) or ATV/r (HR 2

61 With ABC/3TC, women had a significantly higher (32%) safety risk

62 th emtricitabine [FTC]/TDF or abacavir [ABC]/3TC [n = 747]) compared with DRV+r (800/100 mg daily) wi

63 ction regimen of 3 drugs (DTG/abacavir [ABC]/3TC), followed by DTG + 3TC maintenance if virologically

64 ro against HBV, which is also active against 3TC-resistant HBV variants.

65 Discrimination against 3TC-TP is based on the slower rate of incorporation due

66 ensitivity of HIV-1 to the nucleoside analog 3TC was not affected by the level of RT per particle.

67 In contrast, a nucleoside analog (3TC-TP, triphosphate form of lamivudine) is incorporated

68 In the case of the nucleoside analogs 3TC and FTC, resistant viruses are selected with mutatio

69 are rapidly fixed in the presence of A3G and 3TC suggests that A3G-mediated editing can be an importa

70 ibited higher anti-HIV activity than AZT and 3TC against cell-free virus.

71 to the nucleoside analog inhibitors AZT and 3TC.

72 Rather, dCTP and 3TC-TP bind with nearly equal affinities, but the bindin

73 ) were determined for incorporating dCTP and 3TC-TP by wild-type and 3TC-resistant HIV-1 RT.

74 re obtained for quantification of TFV-DP and 3TC-TP using liquid chromatography-mass spectrometry.

75 16Y/Q151M)) is highly susceptible to ETV and 3TC.

76 lutamate derivative containing AZT, FLT, and 3TC (34, EC(50) = 0.9-1.4 muM) exhibited higher anti-HIV

77 e (ABC/3TC) or FTC/TDF in DRIVE-FORWARD; and 3TC/TDF for DOR and FTC/TDF for EFV in DRIVE-AHEAD.

78 Incorporation of FTC and 3TC monophosphate varied up to 10-fold opposite 7 differ

79 me greater later in the dosing interval, and 3TC SP concentrations were substantially greater than BP

80 logic failure accumulated additional Nvp and 3TC mutations plus Rtv and Nfv mutations.

81 Nvp and 3TC mutations were detected frequently at virologic fail

82 e supporting the use of coformulated TDF and 3TC/FTC as preferred backbone drugs for PEP.

83 (DXG-TP), 3'-azido-3'-deoxythymidine-TP, and 3TC-TP by using steady state kinetic analysis and the in

84 corporating dCTP and 3TC-TP by wild-type and 3TC-resistant HIV-1 RT.

85 ell as DNA replication of both wild-type and 3TC-resistant virus.

86 Infants received ZDV and 3TC for 6 weeks and a single dose of oral d4T at weeks 1

87 deoxy-CTP), (+)3TC-triphosphate (TP), and (-)3TC-TP on the polymerase and exonuclease activities of r

88 ase (RT) inhibitor lamivudine (also known as 3TC) is associated with a substitution of valine for met

89 y resistant RT and several drugs (i.e., AZT, 3TC, hydroxyurea, and thymidine) and led to increases in

90 sical mixture containing FLT-succinate, AZT, 3TC, and glutamic acid exhibited 115-fold less activity

91 ART regimens were TDF/3TC/EFV (39%) and AZT/3TC/NVP (34%); 49% of pregnancies had prenatal TDF expos

92 ffect was observed with AZT-resistant or AZT/3TC dually resistant RT and several drugs (i.e., AZT, 3T

93 nificantly more virological failure than AZT/3TC/NVP; a third study was terminated prematurely becaus

94 Pol gamma were similar (0.01 s(-)1) for both 3TC analogs.

95 V) was used to select for resistance to both 3TC and PMPA by serial passage in the presence of increa

96 -TP also demonstrated that the loosely bound 3TC-TP is misaligned at the active site to prevent a ste

97 Moreover, chain termination by 3TC and FTC was strongly influenced by template sequence

98 ry rat hepatocytes and normal rats comparing 3TC and the corresponding HepDirect prodrug demonstrated

99 No effect of prior or concomitant 3TC/FTC was shown.

100 ng that Lys154 may play a role in conferring 3TC sensitivity to HIV-1 RT.

101 ratory toxicities than were those containing 3TC (adjusted HR, 0.78; P = .04).

102 c/mL >/=3 months were randomized to continue 3TC/ABC or switch to FTC/TDF.

103 TC/TDF was noninferior compared to continued 3TC/ABC (86.4% vs 83.3%, treatment difference 3.0% (95%

104 by comparing the effects of dideoxy-CTP), (+)3TC-triphosphate (TP), and (-)3TC-TP on the polymerase a

105 In cell culture (-)3TC is less toxic than its d(+) isomer, (+)3TC, containi

106 (3TC), ZDV/didanosine (ddI), stavudine (d4T)/3TC, d4T/ddI, and ddI/3TC.

107 proved for antiviral therapy: AZT, ddC, D4T, 3TC and carbovir.

108 D4T/3TC, d4T/ddI, and ddI/3TC have similar toxicity rates an

109 lure of stavudine-lamivudine-nevirapine (d4T/3TC/NVP; P < .01), and K103N, V106M, and M184V with fail

110 K103N, V106M, and M184V with failure of d4T/3TC/efavirenz (EFV; P < .01).

111 wer rate of clinical toxicities than was d4T/3TC.

112 istered with AZT (Zidovudine 100 mg/kg/day), 3TC (Lamivudine 50 mg/kg/day) or D4T (Stavudine 10 mg/kg

113 tructure of Pollambda-DNA-D-dCTP, L-dCTP, (-)3TC-TP, and (-)FTC-TP all have their ribose rotated by 1

114 or Zdv, zalcitabine (ddC), didanosine (ddI), 3TC, and stavudine (d4T) were determined, using an enzym

115 se transcriptase enzyme inhibitors AZT, ddI, 3TC, d4T, foscarnet, and nevirapine, as well as the prot

116 linical toxicities than were d4T/ddI and ddI/3TC and with a higher rate of laboratory toxicities than

117 D4T/3TC, d4T/ddI, and ddI/3TC have similar toxicity rates and are appropriate for

118 (ddI), stavudine (d4T)/3TC, d4T/ddI, and ddI/3TC.

119 sis of RT(Y115F/F116Y/Q151M/F160M/M184V):DNA:3TC-TP also demonstrated that the loosely bound 3TC-TP i

120 DOR/3TC/TDF recipients had significantly lower rates of dizz

121 In HIV-1 treatment-naive adults, DOR/3TC/TDF demonstrated non-inferior efficacy to EFV/FTC/TD

122 -C) were significantly different between DOR/3TC/TDF and EFV/FTC/TDF (-1.6 vs +8.7 mg/dL and -3.8 vs

123 agents) and as a fixed-dose combination (DOR/3TC/TDF), demonstrated noninferior efficacy to DRV+r and

124 vir disoproxil fumarate (TDF) at 300 mg (DOR/3TC/TDF) or to efavirenz at 600 mg, emtricitabine at 200

125 At week 48, 84.3% (307/364) of DOR/3TC/TDF recipients and 80.8% (294/364) of EFV/FTC/TDF re

126 (DTG/abacavir [ABC]/3TC), followed by DTG + 3TC maintenance if virologically suppressed; and (4) sta

127 ost-effectiveness and budget impact of DTG + 3TC regimens in the United States.

128 rison); (2) 2-drug: initial regimen of DTG + 3TC; (3) induction-maintenance: 48-week induction regime

129 Should DTG + 3TC demonstrate high rates of virologic suppression, thi

130 y suppressed patients were switched to DTG + 3TC maintenance.

131 g was the preferred strategy only when DTG + 3TC 48-week virologic suppression rate exceeded 90%.

132 DTG/3TC was noninferior in maintaining virologic suppression

133 es/mL to switch to once-daily fixed-dose DTG/3TC or remain on a tenofovir alafenamide (TAF)-based reg

134 ed; 741 received >=1 dose of study drug (DTG/3TC, N = 369; TAF-based regimen, N = 372).

135 No participants receiving DTG/3TC and 1 receiving a TAF-based regimen met confirmed vi

136 with HIV-1 RNA >=50 copies/mL receiving DTG/3TC was 0.3% (1/369) vs 0.5% (2/372) with a TAF-based re

137 sent efficacy and safety of switching to DTG/3TC in virologically suppressed individuals.

138 7 (4.6%) and 13 (3.5%) participants with DTG/3TC and 3 (0.8%) and 2 (0.5%) with a TAF-based regimen,

139 ure or emergent resistance reported with DTG/3TC, supporting it as a simplification strategy for viro

140 d emergence of M184V mutants of HIV-1 during 3TC therapy of human patients.

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

142 (15%) among 519 participants assigned to EFV+3TC-ZDV (HR 1.51, CI 1.12-2.04; p = 0.007).

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

144 DF had similar high efficacy compared to EFV+3TC-ZDV in this trial population, recruited in diverse m

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

146 Comparing ATV+DDI+FTC to EFV+3TC-ZDV, during a median follow-up of 81 wk there were 1

147 th efavirenz plus lamivudine-zidovudine (EFV+3TC-ZDV), atazanavir plus didanosine-EC plus emtricitabi

148 dine [3TC]/zidovudine [ZDV]/efavirenz [EFV], 3TC/ZDV/nelfinavir [NFV], or other regimens) and studied

149 cumulation and/or inhibition of elimination (3TC) are responsible for SP concentrations of these agen

150 rimentally simulated previously reported ETV/3TC resistance for HBV using HIV(Y115F/F116Y/Q151M) with

151 This model can also explain 3TC resistance in feline immunodeficiency virus and huma

152 TP substrate but increasing its affinity for 3TC-triphosphate.

153 ted proviruses via recombination allowed for 3TC escape under culture conditions prohibitive for any

154 00 and <100,000 copies/mL who were naive for 3TC and abacavir.

155 in incorporation efficiency was observed for 3TC-MP incorporation by M184V RT for DNA- and RNA-depend

156 Switching to FTC/TDF from 3TC/ABC maintained virologic suppression, had fewer VFs,

157 Prior to treatment, variants with genotypic 3TC resistance (RT-M184I/V) were detected at low levels

158 Myristoyl-Glu(3TC)-FLT (46, EC(50) = 0.3-0.6 muM) and myristoyl-Glu(FT

159 .06 to 0.0004 s(-1) for the series FIAU > (+)3TC approximately equal to (-)3TC > CBV > AZT > PMPA app

160 didehydro-2',3'-dideoxythymidine (d4T) >> (+)3TC >> (-)3TC > PMPA > azidothymidine (AZT) >> Carbovir

161 2',3'-dideoxythymidine (d4T) >> (+)3TC >> (-)3TC > PMPA > azidothymidine (AZT) >> Carbovir (CBV).

162 and the side chains of Val184 of M184V RT in 3TC-resistant mutant HIV strains destabilizes the RT-nuc

163 lysis reveals that Pol gamma incorporates (-)3TC-triphosphate 16-fold less efficiently than the corre

164 ent with the reverse transcriptase inhibitor 3TC resulted in decreased TE transposition as well as in

165 -)3TC is less toxic than its d(+) isomer, (+)3TC, containing the natural nucleoside configuration, an

166 Virologic outcome among 104 lamivudine (3TC)-experienced individuals infected with human immunod

167 g-term effects of abacavir (ABC)-lamivudine (3TC), compared with tenofovir (TDF)-emtricitabine (FTC)

168 regimen with DTG/abacavir (ABC)/lamivudine (3TC) were 1:1 randomized to continue their regimen or to

169 namide (TAF)/FTC, abacavir (ABC)/lamivudine (3TC), and others were estimated through Poisson regressi

170 fter switching to abacavir (ABC)/lamivudine (3TC)/DTG over 6 months.

171 bility to the nucleoside analogs lamivudine (3TC) and tenofovir at both the virus and enzyme levels.

172 , 100, and 200 mg once daily and lamivudine (3TC) 150 mg 2 times/day in 82 human immunodeficiency vir

173 Women received d4T and lamivudine (3TC) from enrollment until labor.

174 ine (d4T), didanosine (ddI), and lamivudine (3TC), and the nucleotide RTI inhibitor tenofovir (TDF),

175 ors, such as entecavir (ETV) and lamivudine (3TC), serve as crucial anti-HBV drugs.

176 rapy with dolutegravir (DTG) and lamivudine (3TC).

177 fovir (TDF), abacavir (ABC), and lamivudine (3TC); (2) lower fold resistance associated with mixtures

178 rug regimen dolutegravir (DTG) + lamivudine (3TC) is indicated for treatment-naive adults with human

179 zed to ddA) > stavudine (d4T) >> lamivudine (3TC) > tenofovir (PMPA) > zidovudine (AZT) > abacavir (m

180 T) inhibitors (NRTIs), including lamivudine (3TC) and zidovudine (Zdv), are being evaluated for the t

181 rse transcriptase (RT) inhibitor lamivudine (3TC).

182 M184V/I cause high-level lamivudine (3TC) and emtricitabine (FTC) resistance and increased te

183 M184V/I cause high-level lamivudine (3TC) and emtricitabine (FTC) resistance, and increased t

184 based-on tenofovir (TDF) and/or lamivudine (3TC) in a real-world setting.

185 ife to prophylaxis with LPV/r or lamivudine (3TC) to prevent transmission during breastfeeding.

186 ial compared abacavir (ABC) plus lamivudine (3TC) and ZDV+3TC as part of a dual or triple first-line

187 dren given zidovudine (ZDV) plus lamivudine (3TC) as a 2-drug PEP regimen.

188 erent combinations of stavudine, lamivudine (3TC), nevirapine (Nvp), nelfinavir (Nfv), and ritonavir

189 ore TDF-containing regimens: TDF/lamivudine (3TC)/nevirapine (NVP) (n = 3), TDF/ emtricitabine (FTC)/

190 5'-monophosphates of vidarabine, lamivudine (3TC), and cytarabine as well as the phosphonic acid adef

191 he appearance of proviruses with lamivudine (3TC) drug resistance-associated mutations before any dru

192 rus (SIVmac251) and treated with lamivudine (3TC) or emtricitabine [(-)-FTC] (two animals per drug).

193 Treatment of patients with lamivudine (3TC) results in loss of detectable levels of hepatitis B

194 penetration of zidovudine (ZDV), lamivudine (3TC), and amprenavir (APV), given alone and in combinati

195 l treated with zidovudine (ZDV), lamivudine (3TC), and lopinavir-ritonavir (LPV/r), were followed up

196 mon NRTI pairs: zidovudine (ZDV)/lamivudine (3TC), ZDV/didanosine (ddI), stavudine (d4T)/3TC, d4T/ddI

197 levels increased with zidovudine/lamivudine (3TC) and abacavir/3TC (except triglycerides, which were

198 eive sdNVP and either zidovudine/lamivudine (3TC), tenofovir/emtricitabine (FTC), or lopinavir/ritona

199 hate forms of antiviral drugs lamivudine ((-)3TC-TP) and emtricitabine ((-)FTC-TP) provide little str

200 n-terminating antiviral drugs lamivudine ((-)3TC-TP) and emtricitabine ((-)FTC-TP), we structurally r

201 CTP), or the triphosphates of lamivudine ((-)3TC-TP) and emtricitabine ((-)FTC-TP) with four ternary

202 is B (interferon [IFN]-alpha and lamivudine [3TC]) have limited long-term utility because of side eff

203 E-AHEAD from the DOR groups (DOR/lamivudine [3TC]/tenofovir disoproxil fumarate [TDF] or DOR [100 mg

204 antiretroviral therapy regimens (lamivudine [3TC]/zidovudine [ZDV]/efavirenz [EFV], 3TC/ZDV/nelfinavi

205 90.2%-97.7%) and lowest for ZDV+ lamivudine [3TC]+LPV/r (59.1%; 95% CI, 36.2%-82.0%).

206 L-2',3'-dideoxy-3'-thiacytidine (lamivudine, 3TC)] for the treatment of Herpes B virus (HBV) infectio

207 )-2',3'-dideoxy-3'-thiacytidine (lamivudine, 3TC, 1) were synthesized and evaluated for their anti-HI

208 Nonetheless, 3TC and FTC (collectively referred to as XTC) appear to

209 Nonetheless, 3TC and FTC (collectively referred to as XTC) appear to

210 compared to that of HIV-WT in the absence of 3TC treatment.

211 Structural and biochemical analysis of 3TC-resistant HIV-1 reverse transcriptase (RT) led to a

212 mergence of resistance to the combination of 3TC plus PMPA.

213 an atypically tight binding conformation of 3TC-TP, where the Met184 side-chain is pushed away by th

214 nosubstituted 5'-O-fatty acyl derivatives of 3TC (EC(50) = 0.2-2.3 muM) were more potent than the cor

215 account for the strong antiviral efficacy of 3TC versus that of ddC.

216 Emergence of 3TC-resistant variants and nucleotide diversity were det

217 cal use of Zdv, ddC, ddI, and d4T but not of 3TC for the antiretroviral treatment of HTLV-1-associate

218 e-chain is pushed away by the oxathiolane of 3TC-TP and exocyclic methylene of ETV-TP.

219 -7-fold resistant to the 5'-triphosphates of 3TC, FTC, and AZT.

220 onversely, the more effective excision of (-)3TC, CBV, and AZT may contribute to lower toxicity.

221 conformation, following incorporation of (-)3TC-MP, with a second (-)3TC-TP molecule bound to the ac

222 h HIV-1 CRF02_AG, 8 treatment-naive and 4 on 3TC-AZT-NVP] showed 3 to 4 mutations in the Gag P2/NC CS

223 of FTC than with the lower FTC doses and/or 3TC (P=.02, P=.04, and P=.04, respectively).

224 cquisition, but whether they alter TFV-DP or 3TC-TP exposure, and therefore compromise prevention eff

225 Low-frequency NVP- or 3TC/FTC-resistant mutants at codons 103, 181, and 184 we

226 During labor, women received oral 3TC and either intravenous or oral d4T.

227 essed on a boosted protease inhibitor (PI) + 3TC/ABC regimen, the merits of switching to FTC/TDF as t

228 Individuals who received 3TC/ZDV/EFV had a more rapid phase 1 viral decay rate th

229 e 1 viral decay rate than those who received 3TC/ZDV/NFV or other regimens.

230 Subjects receiving 3TC/ABC + PI + ritonavir (RTV) with HIV-1 RNA < 200 c/mL

231 155 to PI + RTV + FTC/TDF, 156 to PI + RTV + 3TC/ABC).

232 incorporation of (-)3TC-MP, with a second (-)3TC-TP molecule bound to the active site in the absence

233 At baseline, all patients were taking 3TC or FTC and were hepatitis B surface antigen and hepa

234 TDF/3TC/EFV was equivalent to its comparator arms.

235 TDF/3TC/NVP was the least well-studied and appeared the leas

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

237 Further study of TDF/3TC/NVP is required before it is widely deployed for ini

238 In 2 comparative studies, TDF/3TC/NVP was associated with significantly more virologic

239 The most frequent ART regimens were TDF/3TC/EFV (39%) and AZT/3TC/NVP (34%); 49% of pregnancies

240 In contrast, removal of 3'-terminal 3TC residues was 50% as efficient as natural 3' termini.

241 3TC/ZDV/EFV regimen may be more potent than 3TC/ZDV/NFV or other regimens and that early viral dynam

242 P by two orders of magnitude better than (-)-3TC-TP.

243 rosterone (DHEA) level than infants from the 3TC arm: 3.91 versus 1.48 ng/mL (P < .001).

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

245 in, (-)beta-L-2',3'-dideoxy-3'-thiacytidine (3TC [lamivudine]), and famciclovir (oral prodrug of penc

246 and (-)beta-L-2',3'-dideoxy-3'-thiacytidine (3TC) (M184V) remain sensitive to DXG.

247 eoside analog 2',3'-dideoxy-3'-thiacytidine (3TC) is a potent inhibitor of wild-type human immunodefi

248 isition of (-)2',3'-dideoxy-3'-thiacytidine (3TC) resistance in vitro.

249 addition, (-)2',3'-dideoxy-3'-thiacytidine (3TC) was also found to increase the mutation rate of HIV

250 ug beta-l-(-)-2',3'-dideoxy-3'-thiacytidine (3TC) was difficult to remove by pyrophosphorolysis, in c

251 s of (-)-beta-2',3'-dideoxy-3'-thiacytidine (3TC), (-)-beta-2',3'-dideoxy-5-fluoro-3'-thiacytidine (F

252 ine (AZT), (-)2',3'-dideoxy-3'-thiacytidine (3TC), and AZT-resistant HIV-1 reverse transcriptase (RT)

253 nalog inhibitor, 3'-dideoxy 3'-thiacytidine (3TC), implying that Lys154 may play a role in conferring

254 evirapine and 2',3'-dideoxy-3'-thiacytidine (3TC), respectively.

255 ides (-)-beta-2',3'-dideoxy-3'-thiacytidine (3TC)--an approved anti-human immunodeficiency virus (HIV

256 t to create a 2',3'-dideoxy-3'-thiacytidine (3TC)-sensitive virus, the second residue in the highly c

257 (D4T-TP), (-)-2',3'-dideoxy-3'-thiacytidine (3TC-TP), and carbocyclic 2',3'-didehydro-ddGTP (CBV-TP)

258 resistance to (-)-2'-deoxy-3'-thiacytidine (3TC; lamivudine) and increased sensitivity to 9-[2-(phos

259 beta-d-(+)-2',3'-dideoxy-3'-thiacytidine ((-)3TC])).

260 beta-L-(-)-2',3'-dideoxy-3'-thiacytidine (-)3TC, and (R)-9-(2-phosphonylmethoxypropyl)adenine (PMPA)

261 dine, [(-)-2,3'-dideoxy-3'-thiacytidine, (-)-3TC] are both potent RT inhibitors, but Pol gamma discri

262 omplex, which causes the cross-resistance to 3TC (M184V mutant).

263 ral mechanism of HBV and HIV-1 resistance to 3TC and ETV and should aid in the design of new agents t

264 of new agents to overcome drug resistance to 3TC and ETV.

265 ce involves enhanced excision, resistance to 3TC involves a block to incorporation of the analog.

266 In contrast, high-level resistance to 3TC was found in all HTLV-1 isolates.

267 type 1 (HIV-1) is selected for resistance to 3TC, the methionine normally present at position 184 is

268 F-4'Sd4FC 35 showed high cross-resistance to 3TC-resistant mutant (M184V) RT.

269 sily detected the evolution of resistance to 3TC.

270 MLV RT confer a high level of resistance to 3TC.

271 site, leads to a high level of resistance to 3TC.

272 3M mutant RT is also relatively resistant to 3TC.

273 ition of the YXDD motif are all resistant to 3TC.

274 3 mutants of MLV RT were highly resistant to 3TC.

275 ries FIAU > (+)3TC approximately equal to (-)3TC > CBV > AZT > PMPA approximately equal to d4T >> ddA

276 as natural deoxynucleotides, whereas AZT-TP, 3TC-TP, and CBV-TP were only moderate inhibitors of DNA

277 Similar to reports of FTC-TP, 3TC-TP exposure was significantly greater than TFV-DP in

278 /Q151M):DNA complexed with 3TC-triphosphate (3TC-TP)/ETV-triphosphate (ETV-TP)/dCTP/dGTP.

279 pread use, however, lamivudine triphosphate (3TC-TP) exposure in the FGT is unknown.

280 e and the superior antiviral activity versus 3TC of the 200 mg/day FTC dose confirmed the results of

281 ellular half-life of FTC-triphosphate versus 3TC-triphosphate.

282 copies/mL, 86% were HBeAg positive, 94% were 3TC resistant, median serum ALT was 52 IU/L, and 98% had

283 We sought to determine whether 3TC can inhibit the replication of wild-type murine leuk

284 cohort of 6 HIV coinfected subjects for whom 3TC and IFN therapy had previously failed.

285 V-1 RT(Y115F/F116Y/Q151M):DNA complexed with 3TC-triphosphate (3TC-TP)/ETV-triphosphate (ETV-TP)/dCTP

286 acillus in vaginal swabs was correlated with 3TC-TP concentrations in cervical tissues.

287 emonstrate that the combination of PMPA with 3TC or (-)-FTC selects for the K65R mutation and against

288 Prior treatment with 3TC/FTC does not compromise efficacy of TDF treatment.

289 The use of combination treatment with 3TC/FTC offers no significant benefit over TDF alone.

290 d4T with or without 3TC is a potential alternative to ZDV for HIV-infected p

291 abacavir (ABC) plus lamivudine (3TC) and ZDV+3TC as part of a dual or triple first-line antiretrovira

292 (1.9%; 95% CI, 0%-3.8%) and highest for ZDV+3TC+boosted atazanavir (21.2%; 95% CI, 13.5%-30.0%).

293 This review supports ZDV+3TC+LPV/r as the preferred 3-drug regimen for PEP in chi

294 We conclude that the combination of ZDV, 3TC, and LPV/r is able to provide efficient and durable

295 y preterm birth, and neonatal death; and ZDV-3TC-LPV-R was associated with higher risk for preterm bi

296 -1.52); zidovudine, lamivudine, and NPV (ZDV-3TC-NVP) (647 of 1365 [47.4%]; ARR, 1.30; 95% CI, 1.20-1

297 7.4%]; ARR, 1.30; 95% CI, 1.20-1.41); or ZDV-3TC-LPV-R (75 of 167 [44.9%]; ARR, 1.21; 95% CI, 1.01-1.

298 ere associated with higher risk for SGA; ZDV-3TC-NVP was associated with higher risk of stillbirth, v

299 ZDV/3TC was associated with a lower rate of clinical toxicit

300 At week 96, patients receiving zidovudine/3TC had lost limb fat, and those receiving emtricitabine