ライフサイエンスコーパス: indinavir

1 (63% inhibition observed with 100 micrometer indinavir).

2 mediately after a single intravenous dose of indinavir.

3 gan therapy with zidovudine, lamivudine, and indinavir.

4 ly lower therapeutic levels as compared with indinavir.

5 les to contract was also markedly reduced by indinavir.

6 imately 70% in the presence of 20 micromol/l indinavir.

7 in imaging stones that are composed of pure indinavir.

8 nts also received stavudine, lamivudine, and indinavir.

9 ost commonly prescribed PRIs, nelfinavir and indinavir.

10 on of protein kinase B were not decreased by indinavir.

11 mbined oral contraceptives, cyclosporin, and indinavir.

12 at are structurally similar to the AIDS drug Indinavir.

13 ents treated with stavudine, lamivudine, and indinavir.

14 en cultured with the combination of ATRA and indinavir.

15 r, nelfinavir, and amprenavir and lowest for indinavir.

16 combination of hydroxyurea, didanosine, and indinavir.

17 aquinavir or after a switch to nelfinavir or indinavir.

18 n HIV-1-infected patients who were not using indinavir.

19 c disorders were noted in patients receiving indinavir.

20 nfirmed that these crystals were composed of indinavir.

21 lamivudine, or that regimen with 2400 mg of indinavir.

22 of patients receiving the protease inhibitor indinavir.

23 stosterone 6B-hydroxylation by ritonavir and indinavir.

24 sterone 6beta-hydroxylation by ritonavir and indinavir.

25 t with the protease inhibitors ritonavir and indinavir.

26 and prior use of stavudine, didanosine, and indinavir.

27 could be inhibited by the HIV-1PR inhibitor, indinavir.

28 ear Met90 and an additional interaction with indinavir.

29 ntaining the zHFF sequence and was eluted by indinavir.

30 of the HIV-1 protease enzyme as compared to Indinavir.

31 Compared with this, the RRs (95% CIs) were: indinavir, 1.75 (0.82-3.73); hard-gel saquinavir, 3.48 (

32 compared efavirenz (600 mg every 24 h) plus indinavir (1000 mg every 8 h) with placebo (every 24 h)

33 Of 240 patients receiving indinavir, 142 provided urine specimens for analysis.

34 sence of nelfinavir (NFV; 47.2%, p = 0.001), indinavir (34.6%, p = 0.001), saquinavir (24.3%, p = 0.0

35 saquinavir (5.9%; 95% CI, 0.15%-28.7%), and indinavir(6.8%; 95% CI, 3.0%-13.1 %).

36 Nineteen of the 240 patients receiving indinavir (8%) developed urologic symptoms.

37 mg every 8 h) with placebo (every 24 h) plus indinavir (800 mg every 8 h) among 327 nucleoside analog

38 Patients received indinavir, 800 mg every 8 h; zidovudine, 200 mg every 8

39 d to receive 1 of 3 antiretroviral regimens: indinavir, 800 mg every 8 hours; zidovudine, 200 mg ever

40 uccess of HCMV infection was indicated using indinavir, a drug that specifically inhibits glucose upt

41 Indinavir, a protease inhibitor widely used to treat pat

42 ationalizing the rather moderate affinity of Indinavir against HTLV-1 PR and provides the basis for f

43 ontinued triple-drug therapy (106 subjects), indinavir alone (103 subjects), or a combination of zido

44 rugs than by maintenance therapy with either indinavir alone or zidovudine and lamivudine.

45 However, patients receiving indinavir also have been noted to have a significant ris

46 In this study, we tested the hypothesis that indinavir, an HIV-protease inhibitor, directly induces i

47 Notably, Indinavir; an HIV protease inhibitor, may be effective i

48 atment, 23 percent of the subjects receiving indinavir and 23 percent of those receiving zidovudine a

49 These indinavir and amprenavir troughs exceed IC(95) for most

50 triglyceride values increased after starting indinavir and correlated with VAT:TAT ratios.

51 14 intensely monitored patients treated with indinavir and efavirenz sustaining HIV RNA at <50 copies

52 In contrast, indinavir and nelfinavir, PIs that may promote or stabil

53 lly composed of indinavir or of a mixture of indinavir and other substances, such as calcium oxalate.

54 However, from March, 1996 (when indinavir and ritonavir were approved by the FDA for mar

55 eater degree of phenotypic susceptibility to indinavir and saquinavir at baseline were significantly

56 Indinavir and saquinavir exhibited slight anti-P. carini

57 redicted to two current protease inhibitors, Indinavir and Saquinavir.

58 The work with indinavir and YPFP-NH(2) also argues that room should be

59 m patients experiencing virologic failure of indinavir and/or nelfinavir.

60 mbination therapy with a protease inhibitor (indinavir) and a nonnucleoside reverse transcriptase inh

61 and 11 receiving zidovudine, lamivudine, and indinavir) and in 38 uninfected adults.

62 ifferent HIV protease inhibitors (ritonavir, indinavir, and atazanavir) induce endoplasmic reticulum

63 d for recent abacavir, cumulative lopinavir, indinavir, and darunavir exposure was OR = 1.82 (95% CI,

64 d for recent abacavir, cumulative lopinavir, indinavir, and darunavir exposure was OR=1.82 (1.27-2.59

65 Ketoconazole, clotrimazole, ritonavir, indinavir, and itraconazole are strong inhibitors; analy

66 fold) to zidovudine, lamivudine, saquinavir, indinavir, and nelfinavir and lower-level resistance (3-

67 in inhibitor-binding strength to ritonavir, indinavir, and nelfinavir when compared to LAI and V6.

68 Drug Administration (saquinavir, ritonavir, indinavir, and nelfinavir) as AIDS therapeutics.

69 -fold weaker inhibition by the clinical drug indinavir, and reduced dimer stability, while the inhibi

70 G48V, and L90M with three drugs, amprenavir, indinavir, and saquinavir, yield good agreements with ex

71 ul HIV-1 PR inhibitors, including ritonavir, indinavir, and saquinavir.

72 s with the Mdr1a P-gp substrates loperamide, indinavir, and talinolol indicated that Mdr1a was functi

73 ated either with tenofovir or tenofovir plus indinavir, and were assessed for the development of Vgam

74 nalogues of the Merck HIV protease inhibitor indinavir, are described.

75 tease inhibitors, ritonavir, saquinavir, and indinavir, are very effective in inhibiting HIV-1 replic

76 a sevenfold difference among the subjects in indinavir area under the curve (AUC), and there was a si

77 Within the indinavir arm of the study, we found that positive cultu

78 on of indinavir, zidovudine, and lamivudine (indinavir arm) to that of a combination of zidovudine an

79 Using indinavir as a model drug, a substructure similarity sea

80 Indinavir at 100 microm had no effect on Glut1 transport

81 there was a significant correlation between indinavir AUC (r2=0.378, P=.019), minimum plasma concent

82 ral therapy [ART]) with a ritonavir-boosted, indinavir-based, twice-daily regimen maintained suppress

83 However, saquinavir, amprenavir, and indinavir blood levels are increased substantially when

84 ecognized stone types, that is, melamine and indinavir calculi.

85 Resistance to indinavir can emerge during treatment failure in nucleos

86 These data demonstrate that indinavir causes acute and reversible changes in whole-b

87 Nevirapine significantly reduced median indinavir Cmin (47.5%) and AUC (27.4%) and, to a lesser

88 Doxorubicin clearance and indinavir concentration curves were similar among patien

89 Mean random plasma indinavir concentrations in the 2 groups with rebound we

90 ired to maintain euglycemia by 18 and 49% at indinavir concentrations of 14 and 27 micromol/l, respec

91 ents who experienced virologic failure on an indinavir-containing regimen suppressed virus load level

92 t isolate, the combination of saquinavir and indinavir demonstrated antagonism at all doses.

93 Amprenavir and indinavir did not affect adipogenesis or lipolysis.

94 Indinavir did not alter the suppression of hepatic gluco

95 These data suggest that indinavir dosing should be dependent on drug exposure an

96 demonstrate that the HIV protease inhibitor, indinavir, dramatically inhibits insulin-stimulated gluc

97 Intravenous infusion of indinavir during hyperglycemic clamps on rats significan

98 indinavir (indinavir group), efavirenz plus indinavir (efavirenz + indinavir group), or nelfinavir p

99 tudy was conducted to assess the response to indinavir, efavirenz, and adefovir in human immunodefici

100 d dideoxyinosine with the protease inhibitor indinavir effectively inhibits MLV-derived RCR replicati

101 ectively labeled GLUT4 in rat adipocytes and indinavir effectively protected against photolabeling.

102 Moreover, indinavir enhanced the ability of ATRA to induce express

103 vity and safety of a 4-drug regimen: 1000 mg indinavir every 8 h with 200 mg nevirapine, 40 mg stavud

104 de or no therapy were treated with 800 mg of indinavir every 8 h.

105 ree treatments for up to 52 weeks: 800 mg of indinavir every eight hours; 200 mg of zidovudine every

106 human immunodeficiency virus (HIV)-infected, indinavir-experienced patients, was designed to study th

107 ther with delavirdine, adefovir, or both, in indinavir-experienced persons.

108 d to the identification of 18 metabolites of indinavir following incubation of the drug with human he

109 type 1-infected children treated first with indinavir for 16 weeks and then with combination antiret

110 12 nmol/l) and 0, 1, 5, 20, or 40 micromol/l indinavir for 4 h.

111 ition constants (K(i)) of the antiviral drug indinavir for the reaction catalyzed by the mutant enzym

112 Indinavir forms characteristic crystals in the urine.

113 group (90 percent), 12 of 28 patients in the indinavir group (43 percent), and none of 30 patients in

114 group (P=.04) and higher in the nelfinavir + indinavir group (P=.006), compared with that in the indi

115 rologic failure was lower in the efavirenz + indinavir group (P=.04) and higher in the nelfinavir + i

116 toward an increased rate in the nelfinavir + indinavir group (P=.07), compared with the indinavir gro

117 or 4 adverse event rates in the efavirenz + indinavir group (P=.97) and a trend toward an increased

118 , or nelfinavir plus indinavir (nelfinavir + indinavir group) and were monitored for 2.1 years.

119 ed lamivudine plus zidovudine and indinavir (indinavir group), efavirenz plus indinavir (efavirenz +

120 roup), efavirenz plus indinavir (efavirenz + indinavir group), or nelfinavir plus indinavir (nelfinav

121 idovudine-lamivudine group, 3% and 2% in the indinavir group, and 0% in the zidovudine-lamivudine gro

122 ovudine-lamivudine group and 13 of 29 in the indinavir group, respectively) had a sustained reduction

123 + indinavir group (P=.07), compared with the indinavir group, were noted.

124 ir group (P=.006), compared with that in the indinavir group.

125 groups was similar, and patients in the two indinavir groups did not gain a significant amount of we

126 ive to nonnucleoside analogues who had taken indinavir >6 months.

127 ata were examined from five studies in which indinavir had been administered as monotherapy or as a c

128 In contrast, indinavir had only a slight effect on DC induced T-cell

129 Indinavir has a high urinary excretion with poor solubil

130 Nevirapine and indinavir have the potential of affecting the pharmacoki

131 Indinavir (IDV) (also called CRIXIVAN, MK-639, or L-735,

132 paring 2 formulations of saquinavir (SQV) to indinavir (IDV) in patients with extensive hard-gel SQV

133 Indinavir (IDV) is a potent and selective human immunode

134 ART was prepared using indinavir (IDV) nanoparticles (NP, nanoART) loaded into

135 om saquinavir (SQV) hard capsules (SQVhc) to indinavir (IDV) or saquinavir soft-gel capsules (SQVsgc)

136 ding zidovudine (ZDV), lamivudine (3TC), and indinavir (IDV), and found a significant increase in the

137 nfected subjects who received 36-52 weeks of indinavir (IDV)/zidovudine (ZDV)/lamivudine (3TC), IDV,

138 mpared treatment with the protease inhibitor indinavir in addition to zidovudine and lamivudine with

139 Although oral indinavir increased plasma bilirubin levels in wild-type

140 ects received lamivudine plus zidovudine and indinavir (indinavir group), efavirenz plus indinavir (e

141 anavir, atazanavir/ritonavir, fosamprenavir, indinavir, indinavir/ritonavir, and lopinavir/ritonavir

142 Indinavir induced a similar reduction in maximally insul

143 y was observed within 4 h after stopping the indinavir infusion.

144 finavir, and saquinavir but not ritonavir or indinavir) inhibited Akt phosphorylation at Ser473 at se

145 at PIs, including ritonavir, saquinavir, and indinavir, inhibited the growth of DU145 and PC-3 androg

146 y transform GLUT1 into GLUT4 with respect to indinavir inhibition of 2-DOG uptake and ATB-BMPA bindin

147 These results provide evidence that indinavir inhibits the translocation or intrinsic activi

148 urprisingly, we find that ritonavir, but not indinavir, inhibits osteoclast differentiation in a reve

149 Indinavir is a viral protease inhibitor used for the tre

150 Indinavir is an antiviral agent that has a significant r

151 es for the inhibitors nelfinavir, ritonavir, indinavir, KNI272, and AG1776 as well as the catalytic e

152 regimens were compared, the group receiving indinavir + lamivudine + zidovudine had a significantly

153 Five HAART drugs (ritonavir, indinavir, lamivudine, abacavir, and AZT) significantly

154 Five other HAART drugs (indinavir, lamivudine, abacavir, AZT, and ddI) and the 3

155 experienced patients for whom treatment with indinavir, lamivudine, and zidovudine failed, for indina

156 dinavir-resistant variants on treatment with indinavir, lamivudine, and zidovudine may occur slowly,

157 cubic millimeter, who had been treated with indinavir, lamivudine, and zidovudine, and who had less

158 hus, in patients treated with efavirenz plus indinavir, levels of residual viremia were established b

159 incubated with eight HAART drugs [ritonavir, indinavir, lopinavir, zidovudine (AZT), abacavir, stavud

160 dies indicated one binding site for the drug indinavir (M(r) 614), a known substrate and inhibitor.

161 To determine whether indinavir may be directly affecting the intrinsic transp

162 e postulated that this side-effect is due to indinavir-mediated impairment of bilirubin UDP-glucurono

163 eam of glucose transport mostly reversed the indinavir-mediated inhibition of insulin release in MIN6

164 in the 9 subjects with viral rebound during indinavir monotherapy or in the 17 subjects with rebound

165 weeks in a phase 1/2 protocol of 16 weeks of indinavir monotherapy, followed by the addition of zidov

166 prior PI exposure) to saquinavir (n = 116); indinavir (n = 69); nelfinavir (n = 139); or placebo twi

167 irenz + indinavir group), or nelfinavir plus indinavir (nelfinavir + indinavir group) and were monito

168 The inhibitors included saquinavir, indinavir, nelfinavir, 141W94, ritonavir (all in clinica

169 Inhibition analysis with ritonavir, indinavir, nelfinavir, amprenavir, saquinavir, lopinavir

170 r, and >60% showed resistance to saquinavir, indinavir, nelfinavir, and fosamprenavir.

171 load below 200 copies/mL in the saquinavir, indinavir, nelfinavir, and placebo arms were 34% (40/116

172 d the vectorial transport characteristics of indinavir, nelfinavir, and saquinavir in vitro using the

173 rotease was seen with saquinavir, ritonavir, indinavir, nelfinavir, or amprenavir at concentrations >

174 ANAM-11 lowers the binding affinity of indinavir, nelfinavir, saquinavir, and ritonavir by fact

175 nt mutant of the HIV-1 protease that affects indinavir, nelfinavir, saquinavir, ritonavir, amprenavir

176 Of 40 patients who were not receiving indinavir, none had similar crystals (P < 0.001).

177 To address these problems, a nanoparticle indinavir (NP-IDV) formulation packaged into carrier bon

178 To determine the acute in vivo effects of indinavir on whole-body glucose homeostasis, glucose tol

179 impact of two common HIV PIs, ritonavir and indinavir, on osteoclast formation and function.

180 z, tenofovir, emtricitabine, lamivudine, and indinavir), only efavirenz increased ER stress via upreg

181 avir, ritonavir, amprenavir, saquinavir, and indinavir), only nelfinavir both effectively stimulated

182 drug reactions about twice as frequently as indinavir or nelfinavir, and women experienced significa

183 Ritonavir, but not the HIV PIs indinavir or nelfinavir, up-regulated the production of

184 nary stones that are principally composed of indinavir or of a mixture of indinavir and other substan

185 Use of indinavir or other protease inhibitors is advised when t

186 salvage therapy regimens after failure of an indinavir or ritonavir regimen.

187 protease, particularly in patients receiving indinavir or ritonavir treatment, is V82A, which comprom

188 on stable antiretroviral regimens, including indinavir or ritonavir, received sargramostim or placebo

189 ced crystalline nephropathy (e.g., caused by indinavir or triamterene).

190 ceiving the triple-drug therapy after either indinavir or zidovudine-lamivudine treatment had similar

191 Patients treated with ritonavir, indinavir, or nelfinavir experience similar reductions i

192 d PR(G73S) were determined in complexes with indinavir, or the p2/NC substrate analog at resolutions

193 atients experiencing virologic failure of an indinavir- or ritonavir-containing treatment regimen wer

194 stronauts, cystinuric individuals, older and indinavir patients achieve importance.

195 No difference in indinavir pharmacokinetics was observed before or after

196 Ten patients were subsequently switched to indinavir plus nevirapine and 2 NRTIs, resulting in a me

197 develops in up to 25% of patients receiving indinavir, prompting drug discontinuation and further cl

198 Incubation of muscles with 5 micromol/l indinavir reduced the insulin-stimulated increase in 3MG

199 3MG transport by 40%, whereas 20 micromol/l indinavir reduced the insulin-stimulated increase in 3MG

200 Indinavir resistance was not detected in the 9 subjects

201 on and subsequent rebound, 6 without primary indinavir-resistance mutations underwent clonal analysis

202 avir, lamivudine, and zidovudine failed, for indinavir-resistant minority variants.

203 Selection for indinavir-resistant variants on treatment with indinavir

204 al potency, and selection of a predominantly indinavir-resistant virus population may be delayed for

205 that focal lymphadenitis after initiation of indinavir resulted from unsuspected local or disseminate

206 A 4-drug regimen containing efavirenz plus indinavir resulted in a superior virologic response, whe

207 onse, whereas one containing nelfinavir plus indinavir resulted in an inferior response and a greater

208 or positions in three complexes with that of Indinavir revealed displacements of the protease backbon

209 her four currently approved PRIs-saquinavir, indinavir, ritonavir, and nelfinavir-has failed.

210 mbination with the HIV-1 protease inhibitors indinavir, ritonavir, and saquinavir.

211 -level resistance to amprenavir, nelfinavir, indinavir, ritonavir, saquinavir, and lopinavir, includi

212 Indinavir, ritonavir, saquinavir, and nelfinavir inhibit

213 ng thermodynamics of the protease inhibitors indinavir, ritonavir, saquinavir, and nelfinavir to the

214 This suggests that twice-daily indinavir-ritonavir and, to a lesser extent, amprenavir-

215 (0.36-33.37); nelfinavir, 2.64 (1.37-5.08); indinavir/ritonavir, 0.32 (0.04-2.49); saquinavir/ritona

216 4 (0.07-3.97); nelfinavir, 2.44 (1.68-3.54); indinavir/ritonavir, 1.96 (1.02-3.77); saquinavir/ritona

217 zanavir/ritonavir, fosamprenavir, indinavir, indinavir/ritonavir, and lopinavir/ritonavir were associ

218 virapine, as well as the protease inhibitors indinavir, saquinavir, and nelfinavir.

219 30%, 37%, 37%, and 42% loss of activity for indinavir, saquinavir, nelfinavir, ritonavir, and ampren

220 es involved four inhibitors in clinical use (indinavir, saquinavir, ritonavir, and nelfinavir) and a

221 Multiply substituted indinavir-selected mutants M46I/L63P/V82T/I84V and L10R/

222 e subtype C protease bound to nelfinavir and indinavir showed that these inhibitors form similar inte

223 the V6(54/84) variant bound to ritonavir and indinavir shows structural changes in the 80's loops and

224 r in combination [three HAART drugs (3-plex; indinavir, stavudine, and ddI)] at their clinical plasma

225 animal models (rats, dogs, and monkeys) than indinavir sulfate and is currently in advanced human cli

226 Indinavir sulfate is a protease inhibitor that has been

227 y using the antiretroviral drugs zidovudine, indinavir sulfate, and didanosine, demonstrating that th

228 vailable are saquinavir mesylate, ritonavir, indinavir sulfate, and nelfinavir mesylate.

229 resulted in the identification of Crixivan (indinavir sulfate, MK-639, L-735,524), has now yielded M

230 with the preparation of an intermediate for Indinavir synthesis and the stereoselective synthesis of

231 eeks was greater in the two groups receiving indinavir than in the zidovudine-lamivudine group (P< or

232 % of patients ultimately need to discontinue indinavir therapy altogether.

233 The initiation of indinavir therapy in patients with CD4 counts of less th

234 d for months even in the presence of ongoing indinavir therapy.

235 fold to 19-fold increases after 1-3 weeks of indinavir therapy.

236 ode enlargement within 1-3 weeks of starting indinavir therapy.

237 avir) or unable to activate SXR (nelfinavir, indinavir) thus defining analogs that fail to induce SXR

238 After the addition of the protease inhibitor indinavir to combination drug regimens for HIV-1 infecti

239 tor azidothymidine or the protease inhibitor indinavir to the culture prevented HIV spread and inhibi

240 l (consisting of zidovudine, lamivudine, and indinavir) to determine optimum dosage and sampling time

241 termined in complex with the antiviral drug, indinavir, to gain insight into the molecular basis of d

242 lirubin increased by a mean of 0.34 mg/dl in indinavir-treated HIV patients lacking the Gilbert's pol

243 nsulin levels were significantly elevated in indinavir-treated versus control rats (P < 0.05) during

244 suggest that some HIV-1-infected patients on indinavir treatment accumulate intra-abdominal fat that

245 glycemic- hyperinsulinemic clamp conditions, indinavir treatment acutely reduced the glucose infusion

246 lower rates of positive HIV cultures in the indinavir treatment arm than in the dual-nucleoside trea

247 Indinavir treatment did not affect early insulin signali

248 serum-unconjugated bilirubin associated with indinavir treatment result from direct inhibition of bil

249 Published reports of indinavir urolithiasis estimate its incidence at between

250 Indinavir urolithiasis generally responds to a conservat

251 Indinavir urolithiasis is unique in that computed tomogr

252 Rather, physicians need to know more about indinavir urolithiasis to help their patients cope with

253 in and hematuria are the typical symptoms of indinavir urolithiasis.

254 he VAT:TAT ratio correlated with duration of indinavir use (r=0.47, p=0.01).

255 urolithiasis is a significant side effect of indinavir use, limiting its clinical application is not

256 nd whether such changes were associated with indinavir use.

257 for the three groups-non-users, symptom-free indinavir users, and symptomatic indinavir users-were 0.

258 ymptom-free indinavir users, and symptomatic indinavir users-were 0.40 (SD 0.15), 0.59 (0.18), and 0.

259 h this, the rebound rate for those receiving indinavir was 1.52 times higher (rate ratio [RR], 1.52 [

260 e well-known and approved HIV-1 PR inhibitor Indinavir was determined at 2.40 A resolution.

261 the HIV-1 protease inhibitors saquinavir and indinavir was determined.

262 Indinavir was found to competitively inhibit UGT enzymat

263 immunodeficiency, stavudine, didanosine, and indinavir were associated with larger pericardial adipos

264 d both in the presence and in the absence of Indinavir when combined with mutations in the gag p7/p1

265 Thus, efavirenz plus indinavir with concomitant NRTIs is effective therapy fo

266 islets was significantly inhibited by the PI indinavir with IC(50) values of 1.1 and 2.1 micro mol/l,

267 n HIV-1-infected patients who had been using indinavir without abdominal symptoms for at least 6 mont

268 eceived triple combination drug therapy with indinavir, zidovudine and lamivudine or zidovudine plus

269 e progressed to AIDS or death was lower with indinavir, zidovudine, and lamivudine (6 percent) than w

270 efficacy of treatment with a combination of indinavir, zidovudine, and lamivudine (indinavir arm) to

271 Treatment with indinavir, zidovudine, and lamivudine as compared with z

272 Combination antiretroviral therapy with indinavir, zidovudine, and lamivudine can suppress the l

273 a HIV RNA after six months of treatment with indinavir, zidovudine, and lamivudine is better sustaine

274 r antiretroviral therapy, the combination of indinavir, zidovudine, and lamivudine reduces levels of

275 A 3-drug combination of indinavir, zidovudine, and lamivudine started simultaneo

276 Simultaneous initiation of indinavir, zidovudine, and lamivudine suppressed HIV RNA

277 A three-drug regimen of indinavir, zidovudine, and lamivudine suppressed viremia

278 ndomized, double-blind, multicenter study of indinavir, zidovudine, and lamivudine was conducted in 3

279 1 infection benefit from triple therapy with indinavir, zidovudine, and lamivudine, although the prop

280 is systematic procedure on three HIV drugs, (Indinavir, Zidovudine, and Nevirapine), discovered uniqu

281 nts receiving initial combination therapy of indinavir-zidovudine-lamivudine (ACTG 343 and Merck 035)

282 ectively, at week 24 were 56% and 45% in the indinavir-zidovudine-lamivudine group, 3% and 2% in the

283 Prolonged indinavir-zidovudine-lamivudine treatment has significan