ライフサイエンスコーパス: nelfinavir

1 504 participants received both efavirenz and nelfinavir).

2 ic acid proteasome inhibitors (MG-132, PS-I, nelfinavir).

3 first of which contained either efavirenz or nelfinavir.

4 otease inhibitors indinavir, saquinavir, and nelfinavir.

5 term (P=0.001) than did triple therapy with nelfinavir.

6 encing virologic failure of indinavir and/or nelfinavir.

7 nts treated with zidovudine, lamivudine, and nelfinavir.

8 e-lamivudine, combined with efavirenz and/or nelfinavir.

9 ased radiosensitivity to a similar extent as nelfinavir.

10 regrowth was detected between radiation and nelfinavir.

11 e inhibitors included saquinavir, indinavir, nelfinavir, 141W94, ritonavir (all in clinical use), and

12 Oral nelfinavir (2 x 1,250 mg) was started 3 days before and

13 were: soft-gel saquinavir, 0.54 (0.07-3.97); nelfinavir, 2.44 (1.68-3.54); indinavir/ritonavir, 1.96

14 73); hard-gel saquinavir, 3.48 (0.36-33.37); nelfinavir, 2.64 (1.37-5.08); indinavir/ritonavir, 0.32

15 induced to differentiate in the presence of nelfinavir, 3T3-L1 preadipocytes failed to accumulate cy

16 cleoside analogs (5.7%; 95% CI, 1.2%-12.9%), nelfinavir (5.9%; 95% CI, 1.2%-16.2%), saquinavir (5.9%;

17 , we have evaluated the in vitro activity of nelfinavir, a HIV PI, against human melanoma cells.

18 Our studies reveal, for the first time, that nelfinavir, a potent and cytotoxic PI, is both a substra

19 or absence of substitutions associated with nelfinavir, a protease (PR) inhibitor, and/or a reverse

20 sistance and whether this can be reversed by nelfinavir, a protease inhibitor that decreases Akt sign

21 is epistasis-type analysis suggests that the nelfinavir acts along the Akt pathway to radiosensitize

22 growth compared with radiation alone whereas nelfinavir alone had little effect on tumor regrowth.

23 ompared with 41, 34, or 45 days for control, nelfinavir alone, or radiation alone groups, respectivel

24 Nelfinavir also decreased the hypoxic induction of HIF-1

25 Nelfinavir also increased the sensitivity of U251MG cell

26 hibition analysis with ritonavir, indinavir, nelfinavir, amprenavir, saquinavir, lopinavir, and ataza

27 We examined the effect of nelfinavir, an HIV protease inhibitor that inhibits Akt

28 eutic drug for type 2 diabetes mellitus, and nelfinavir, an HIV protease inhibitor, when used alone o

29 c4/Mrp4 in mouse cells specifically enhanced nelfinavir and 9-(2-phosphonylmethoxyethyl) adenine cyto

30 Here, we show that the PIs nelfinavir and atazanavir cause cell death in various ma

31 The combination of nelfinavir and chemoradiotherapy showed acceptable toxic

32 ession reduced intracellular accumulation of nelfinavir and consequently conferred survival advantage

33 rmation on how to use established drugs like nelfinavir and efavirenz in younger children is slowly b

34 analyses of the subtype C protease bound to nelfinavir and indinavir showed that these inhibitors fo

35 with the two most commonly prescribed PRIs, nelfinavir and indinavir.

36 Western blotting in nelfinavir and its analog treated cells confirms accumul

37 Nelfinavir and its analogs are more potent inhibitors of

38 These results show nelfinavir and its analogs inhibit castration-resistant

39 Nelfinavir and its analogs inhibit human homolog M. jann

40 Nelfinavir and its analogs inhibit proliferation and ind

41 -drug group), or zidovudine for 6 weeks plus nelfinavir and lamivudine for 2 weeks (three-drug group)

42 dine, lamivudine, saquinavir, indinavir, and nelfinavir and lower-level resistance (3-fold to 5-fold)

43 m probability of 50% at 75%-80% adherence to nelfinavir and of 15% at 80%-85% adherence to lopinavir/

44 The combination of nelfinavir and radiation increased time to regrowth comp

45 ction showed a more than additive effect for nelfinavir and radiation.

46 Oral administration of the PIs nelfinavir and ritonavir significantly inhibited photore

47 ions which are usually initially selected by nelfinavir and saquinavir, D30N and L90M, respectively,

48 ith ritonavir than when it was combined with nelfinavir and were lower with adefovir-containing regim

49 avir in combination with either ritonavir or nelfinavir and, in addition, delavirdine, adefovir, or b

50 l use (indinavir, saquinavir, ritonavir, and nelfinavir) and a second-generation protease inhibitor (

51 ified in 31 children who received efavirenz, nelfinavir, and 1 or 2 nucleoside reverse-transcriptase

52 ral therapy (HAART) consisting of efavirenz, nelfinavir, and 1 or 2 nucleoside reverse-transcriptase

53 ition of AGP was the greatest for ritonavir, nelfinavir, and amprenavir and lowest for indinavir.

54 ug regimen containing didanosine, stavudine, nelfinavir, and efavirenz and the groups that received t

55 g regimen containing zidovudine, lamivudine, nelfinavir, and efavirenz and the groups that received t

56 adherence, receiving the 4-drug regimen with nelfinavir, and female sex; older age was associated wit

57 showed resistance to saquinavir, indinavir, nelfinavir, and fosamprenavir.

58 se inhibitors, the combination of efavirenz, nelfinavir, and nucleoside reverse-transcriptase inhibit

59 a novel combination consisting of efavirenz, nelfinavir, and one or more nucleoside reverse-transcrip

60 200 copies/mL in the saquinavir, indinavir, nelfinavir, and placebo arms were 34% (40/116), 36% (25/

61 ly tested and three of the five (amprenavir, nelfinavir, and saquinavir but not ritonavir or indinavi

62 he HIV protease inhibitors (HPI) amprenavir, nelfinavir, and saquinavir have previously been shown to

63 rial transport characteristics of indinavir, nelfinavir, and saquinavir in vitro using the model P-gl

64 nts predict plasma exposure to efavirenz and nelfinavir, and they may predict virologic failure and/o

65 ns about twice as frequently as indinavir or nelfinavir, and women experienced significantly more adv

66 not zidovudine and lamivudine combined with nelfinavir) appeared to delay the failure of the second

67 Efavirenz and nelfinavir are metabolized by cytochrome P-450 (CYP) 2B6

68 response was compared in patients receiving nelfinavir as monotherapy (16 weeks) or in combination w

69 creen identified the HIV1-protease inhibitor nelfinavir as potent suppressor of PAX3 and MITF express

70 ation (saquinavir, ritonavir, indinavir, and nelfinavir) as AIDS therapeutics.

71 Nelfinavir attenuated apoptosis as well as mitochondrial

72 Nelfinavir belongs to the protease inhibitor class of dr

73 4 pharmacophore model, which showed that the nelfinavir binding site is shared with chemotherapeutic

74 Nelfinavir blocked Mrp4-mediated export, which is consis

75 amprenavir, saquinavir, and indinavir), only nelfinavir both effectively stimulated MRP4 ATPase activ

76 We determined the toxicity of nelfinavir chemoradiotherapy in borderline resectable an

77 In addition, in vivo, doses of amprenavir or nelfinavir comparable with the therapeutic levels achiev

78 g viral rebound while receiving therapy with nelfinavir-containing regimens, to determine whether the

79 r the area under the curve for efavirenz and nelfinavir corresponded to expected values.

80 consequently conferred survival advantage to nelfinavir cytotoxicity.

81 Nelfinavir decreased Akt phosphorylation and enhanced ra

82 Nelfinavir decreased Sp1 phosphorylation and decreased S

83 Our results suggest that nelfinavir decreases HIF-1alpha/VEGF expression and tumo

84 Here we show that the HIV-PI Nelfinavir decreases translation rates and promotes a tr

85 Nelfinavir decreases VEGF expression under normoxia via

86 failing a therapy regimen containing the PI nelfinavir developed mutations at position 88 in the pro

87 Mice treated with Nelfinavir display hallmarks of this stress response in

88 ntrolled study of lopinavir/ritonavir versus nelfinavir, each administered with stavudine and lamivud

89 study that compared lopinavir/ritonavir with nelfinavir, each coadministered with stavudine and lamiv

90 ve, in addition to two nucleoside analogues, nelfinavir, efavirenz, or nelfinavir plus efavirenz.

91 One protease inhibitor, nelfinavir, elicited both of these effects strongly.

92 tients treated with ritonavir, indinavir, or nelfinavir experience similar reductions in viral load a

93 lternate PIs, may be relatively common after nelfinavir failure.

94 Genotyping from 29 nelfinavir failures revealed D30N in 17 (59%) and L90M i

95 time to reach 1,000 mm(3) in the radiation + nelfinavir group was 71 days, as compared with 41, 34, o

96 group, and 64 percent and 35 percent in the nelfinavir group.

97 r significantly between pooled ritonavir and nelfinavir groups (28% vs. 33%; P=.50) or between pooled

98 eived stavudine, lamivudine, nevirapine, and nelfinavir had plasma HIV-1 RNA levels of less than 400

99 ible explanation for the discordance is that nelfinavir has an effect on tumor oxygenation.

100 d PRIs-saquinavir, indinavir, ritonavir, and nelfinavir-has failed.

101 gimens containing didanosine, stavudine, and nelfinavir (hazard ratio for a first regimen failure, 0.

102 ared with starting with a regimen containing nelfinavir (hazard ratio for failure of the second regim

103 ns beginning with didanosine, stavudine, and nelfinavir (hazard ratio for regimen failure, 1.24) or d

104 ratio, 0.63); or zidovudine, lamivudine, and nelfinavir (hazard ratio, 0.49), but not the three-drug

105 s beginning with zidovudine, lamivudine, and nelfinavir (hazard ratio, 1.06) or zidovudine, lamivudin

106 Receiving the 4-drug regimen with nelfinavir, higher stress scores, older age, and higher

107 We found that Nelfinavir impaired the maturation of lamin A, a structu

108 s suggest that clinical use of metformin and nelfinavir in combination is expected to have synergisti

109 Food and Drug Administration-approved agent Nelfinavir in combination with DR5 agonists to induce ap

110 four-drug regimens containing efavirenz and nelfinavir in combination with either didanosine and sta

111 esults support the clinical investigation of nelfinavir in combination with radiation and temozolomid

112 These data support the use of nelfinavir in combination with radiation in future clini

113 patient received saquinavir, ritonavir, and nelfinavir in conjunction with tacrolimus.

114 Plasma exposure to efavirenz and nelfinavir in each population was significantly associat

115 + indinavir group (P=.04) and higher in the nelfinavir + indinavir group (P=.006), compared with tha

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

117 inavir group), or nelfinavir plus indinavir (nelfinavir + indinavir group) and were monitored for 2.1

118 aker (saquinavir) or unable to activate SXR (nelfinavir, indinavir) thus defining analogs that fail t

119 ed with high-level resistance to amprenavir, nelfinavir, indinavir, ritonavir, saquinavir, and lopina

120 dipocyte phenotype promote susceptibility to nelfinavir-induced cell death.

121 We provide evidence that Nelfinavir-induced ER stress modulates DR5 expression in

122 Indinavir, ritonavir, saquinavir, and nelfinavir inhibit the A and C subtype proteases with 2.

123 We further show that nelfinavir inhibits CDK2 through proteasome-dependent de

124 Nelfinavir inhibits the growth of melanoma cell lines at

125 kes place in the in vivo setting as well, as nelfinavir inhibits the growth of xenografted human mali

126 Because nelfinavir is a new MRP4/ABCC4 substrate, we developed a

127 Our results suggest that nelfinavir is a promising candidate chemotherapeutic age

128 Nelfinavir is a substrate for P-glycoprotein, which is e

129 The HIV1 protease inhibitor nelfinavir is being investigated as a cancer therapeutic

130 These results suggest that nelfinavir is both an inhibitor and substrate of MRP4.

131 Moreover, nelfinavir is effective in BRAF and NRAS mutant melanoma

132 cell lines demonstrate a close similarity of nelfinavir, its analogs, and 1,10-phenanthroline.

133 s with the hypoxia marker EF5 and found that nelfinavir leads to increased oxygenation within tumor x

134 These results suggest that nelfinavir may have limited utility after saquinavir fai

135 sidered together, these results suggest that nelfinavir may promote adipose tissue atrophy by comprom

136 Food and Drug Administration-approved drug, nelfinavir, may be an effective radiosensitizer in the c

137 cy of the cytosolic DNA-sensor AIM2 impaired Nelfinavir-mediated inflammasome activation.

138 Mechanistically, Nelfinavir-mediated ISR bypassed direct activation of th

139 pharmacokinetics, and antiviral activity of nelfinavir mesylate (Viracept), an inhibitor of human im

140 cs and antiviral activity, AG1343 (Viracept, nelfinavir mesylate), a nonpeptidic inhibitor of HIV-1 p

141 mesylate, ritonavir, indinavir sulfate, and nelfinavir mesylate.

142 that HIV-infected cancer patients receiving nelfinavir might experience both enhanced antitumor effi

143 of all inhibitors tested, with ritonavir and nelfinavir most affected.

144 to saquinavir (n = 116); indinavir (n = 69); nelfinavir (n = 139); or placebo twice per day (n = 157)

145 However, nelfinavir neither decreased Akt phosphorylation in immo

146 Nelfinavir (NFV) is a clinically important antiviral dru

147 Nelfinavir (NFV) is an HIV-1 protease inhibitor with dem

148 tion at the Gag p1-p6 cleavage site with the nelfinavir (NFV) resistance D30N/N88D protease mutations

149 volution of the p1-p6 cleavage site with the nelfinavir (NFV) resistance D30N/N88D protease mutations

150 nonactive-site N88S mutation in response to nelfinavir (NFV) therapy, whereas clade B protease devel

151 avudine, lamivudine (3TC), nevirapine (Nvp), nelfinavir (Nfv), and ritonavir (Rtv).

152 calvaria assay, increased in the presence of nelfinavir (NFV; 47.2%, p = 0.001), indinavir (34.6%, p

153 C]/zidovudine [ZDV]/efavirenz [EFV], 3TC/ZDV/nelfinavir [NFV], or other regimens) and studied the rel

154 Nelfinavir (NLF), an antiretroviral agent, preserves mit

155 The inhibitory effect of nelfinavir occurred subsequent to critical early events

156 owed calculation of IC(50) values; e.g., for nelfinavir, of 3.4 muM (human Ddi1) and 0.44 muM (Leishm

157 The effect of nelfinavir on VEGF expression had the functional consequ

158 an do regimens with nucleoside analogues and nelfinavir or efavirenz alone.

159 ine and stavudine in combination with either nelfinavir or efavirenz.

160 on continued saquinavir or after a switch to nelfinavir or indinavir.

161 A clinical trial of nelfinavir or its analogs should be developed for castra

162 tiretrovirals were zidovudine/lamivudine and nelfinavir or lopinavir/ritonavir.

163 seen with saquinavir, ritonavir, indinavir, nelfinavir, or amprenavir at concentrations >200-fold th

164 ifferent nucleoside regimens with efavirenz, nelfinavir, or both.

165 ng-term suppression than triple therapy with nelfinavir (P=0.004).

166 In contrast, indinavir and nelfinavir, PIs that may promote or stabilize bone forma

167 essed plasma concentrations of efavirenz and nelfinavir, plasma HIV-1 RNA levels, and lymphocyte subp

168 l-naive subjects to receive efavirenz and/or nelfinavir plus 2 nucleoside analogues, with follow-up l

169 ed with nucleoside analogues, treatment with nelfinavir plus efavirenz and at least one new nucleosid

170 leoside analogues, nelfinavir, efavirenz, or nelfinavir plus efavirenz.

171 indinavir (efavirenz + indinavir group), or nelfinavir plus indinavir (nelfinavir + indinavir group)

172 r virologic response, whereas one containing nelfinavir plus indinavir resulted in an inferior respon

173 Nelfinavir plus two NRTIs (new or continued) resulted in

174 ive patients received lopinavir/ritonavir or nelfinavir, plus stavudine and lamivudine, for up to 96

175 spectively, 81 percent and 74 percent in the nelfinavir-plus-efavirenz group, 69 percent and 60 perce

176 Nelfinavir profoundly sensitizes BRAF and NRAS mutant me

177 Nelfinavir promotes apoptosis and arrests cell cycle at

178 dy included 340 efavirenz recipients and 348 nelfinavir recipients (184 of the 504 participants recei

179 Among nelfinavir recipients, a trend toward decreased virologi

180 Primary mutations related to nelfinavir resistance (D30N and/or L90M) were observed i

181 he initial active site mutation allowing for nelfinavir resistance is mediated by a unique amino acid

182 lationship between adherence and the risk of nelfinavir resistance was observed, with a maximum proba

183 resistance); 3 isolates also contained D30N (nelfinavir resistance).

184 the patient, reinstitution of treatment with nelfinavir resulted in a >95% reduction in tacrolimus do

185 We show that pretreatment of HUVEC with nelfinavir results in enhanced cytotoxicity, including i

186 Among the PIs evaluated (nelfinavir, ritonavir, amprenavir, saquinavir, and indin

187 loss of activity for indinavir, saquinavir, nelfinavir, ritonavir, and amprenavir, respectively.

188 sium channels, and we showed that lopinavir, nelfinavir, ritonavir, and saquinavir caused dose-depend

189 etermined the K(i) values for the inhibitors nelfinavir, ritonavir, indinavir, KNI272, and AG1776 as

190 nt increase (>10-fold) in K(i) for inhibitor nelfinavir, ritonavir, or AG-1776 displaying 22-, 19-, o

191 Subjects received nelfinavir, saquinavir, abacavir, and either another nuc

192 11 lowers the binding affinity of indinavir, nelfinavir, saquinavir, and ritonavir by factors of 4000

193 f the HIV-1 protease that affects indinavir, nelfinavir, saquinavir, ritonavir, amprenavir, and lopin

194 sed on the greater fitness impairment of the nelfinavir-selected D30N mutant are suggested to explain

195 A nelfinavir-selected protease D30N substitution substanti

196 ease in K(i) for all inhibitors tested, with nelfinavir showing the greatest increase.

197 Our study shows that HPIs, particularly nelfinavir, significantly enhance radiations effect on h

198 Cancer Cell, Smith et al. (2016) report that nelfinavir suppresses MITF expression induced by MAPK pa

199 f which was new, with the protease inhibitor nelfinavir, the nonnucleoside reverse-transcriptase inhi

200 bitors indinavir, ritonavir, saquinavir, and nelfinavir to the wild-type HIV-1 protease and to the V8

201 tients received saquinavir with ritonavir or nelfinavir together with delavirdine and/or adefovir and

202 study of saquinavir with either ritonavir or nelfinavir, together with delavirdine, adefovir, or both

203 ene expression, also was reduced markedly in nelfinavir-treated cells, whereas the level of the 125-k

204 ologic response was significantly higher for nelfinavir-treated patients than for lopinavir/ritonavir

205 udine resistance was significantly higher in nelfinavir-treated patients than in lopinavir/ritonavir-

206 Among all nelfinavir-treated patients, a bell-shaped relationship

207 For nelfinavir-treated patients, but not for lopinavir/riton

208 and/or L90M) were observed in 43 (45%) of 96 nelfinavir-treated subjects.

209 d stavudine was also significantly higher in nelfinavir-treated versus lopinavir/ritonavir-treated su

210 We found that Nelfinavir treatment led to ER stress-induced up-regulat

211 In addition, nelfinavir treatment of fully differentiated 3T3-L1 adip

212 iability of preadipocytes were unaffected by nelfinavir treatment.

213 ase, because these events were unaffected by nelfinavir treatment.

214 st, DR4 receptor expression was unchanged by Nelfinavir treatment.

215 t an inhibitor of the HIV aspartyl protease, Nelfinavir, triggers inflammasome formation and elicits

216 Ritonavir, but not the HIV PIs indinavir or nelfinavir, up-regulated the production of transcripts f

217 dence interval {CI}, 1.05-1.10]; P<.001) and nelfinavir use (OR, 2.4 vs. lopinavir/ritonavir [95% CI,

218 Reduced susceptibility to nelfinavir was found in 14 isolates, but only 1 possesse

219 Phospho-Akt downregulation by nelfinavir was monitored by immunoblotting in patient le

220 with stavudine, lamivudine, nevirapine, and nelfinavir were associated with improved long-term viral

221 inding strength to ritonavir, indinavir, and nelfinavir when compared to LAI and V6.

222 We found that both metformin and nelfinavir, when used alone, were moderately effective i

223 stance mutations despite the frequent use of nelfinavir, which has a low mutational barrier to resist

224 Combining Nelfinavir with TRAIL led to a significantly enhanced le