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 ctivity may impact the anticancer effects of nelfinavir.

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

10 ased radiosensitivity to a similar extent as nelfinavir.

11 regrowth was detected between radiation and nelfinavir.

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

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

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

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

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

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

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

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

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

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

22 We find that the eEF2K agonist nelfinavir abolishes p-bodies in sensory neurons and imp

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

24 Nelfinavir affected the fluidity and composition of lipi

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

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

27 Nelfinavir also decreased the hypoxic induction of HIF-1

28 Nelfinavir also increased the sensitivity of U251MG cell

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

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

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

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

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

34 The combination of nelfinavir and chemoradiotherapy showed acceptable toxic

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

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

37 We validate top-ranked compounds, nelfinavir and honokiol, and identify that low expressio

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

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

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

41 Nelfinavir and its analogs are more potent inhibitors of

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

43 Nelfinavir and its analogs inhibit human homolog M. jann

44 Nelfinavir and its analogs inhibit proliferation and ind

45 The present study addresses the effects of nelfinavir and its major and pharmacologically active me

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

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

48 g cellular transactivation assays identified nelfinavir and M8 as partial agonists with EC(50) values

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

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

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

52 irs, such as Remdesivir and Thioguanosine or Nelfinavir and Raloxifene, on SARS-CoV-2 infection.

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

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

55 Among these promising hits, the antivirals nelfinavir and the parent of prodrug MK-4482 possess des

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

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

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

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

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

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

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

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

64 d in vivo, and it was found that mefloquine, nelfinavir, and extracts of Ganoderma lucidum (RF3), Per

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

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

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

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

69 200 copies/mL in the saquinavir, indinavir, nelfinavir, and placebo arms were 34% (40/116), 36% (25/

70 eatments of these foam cells with ritonavir, nelfinavir, and saquinavir at least doubled cholestryl e

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

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

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

74 framework, 3 commonly used ARTs (ritonavir, nelfinavir, and saquinavir) were found altering the acti

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

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

77 Nelfinavir anticancer activity may involve modulation of

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

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

80 the modification of lipid-rich membranes by nelfinavir as a novel mechanism of action to achieve bro

81 Impaired coactivator recruitment by nelfinavir as compared with the full agonist rifampin pr

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

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

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

85 Nelfinavir attenuated apoptosis as well as mitochondrial

86 inhibitor (PI)-refractory multiple myeloma, nelfinavir-based therapy resulted in 65% partial respons

87 Nelfinavir belongs to the protease inhibitor class of dr

88 4 pharmacophore model, which showed that the nelfinavir binding site is shared with chemotherapeutic

89 Nelfinavir blocked Mrp4-mediated export, which is consis

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

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

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

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

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

95 ide candidate genetic contributors affecting nelfinavir cytotoxicity.

96 consequently conferred survival advantage to nelfinavir cytotoxicity.

97 Nelfinavir decreased Akt phosphorylation and enhanced ra

98 Nelfinavir decreased Sp1 phosphorylation and decreased S

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

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

101 Nelfinavir decreases VEGF expression under normoxia via

102 Physiologic relevance of nelfinavir-dependent modulation of PXR activity was inve

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

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

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

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

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

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

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

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

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

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

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

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

115 Nelfinavir had multiple activity-specific binding partne

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

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

118 The HIV-protease inhibitor nelfinavir has shown broad anticancer activity in variou

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

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

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

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

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

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

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

126 sis, was previously shown to be activated by nelfinavir; however, the exact molecular mechanism is st

127 ajor and pharmacologically active metabolite nelfinavir hydroxy-tert-butylamide (M8) on PXR to elucid

128 Its major metabolite nelfinavir hydroxy-tert-butylamide exerts the same effec

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

130 The broad anticancer mechanism of action of nelfinavir implies that it interferes with fundamental a

131 identify protein partners that interact with nelfinavir in an activity-dependent manner alongside can

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

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

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

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

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

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

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

139 howed a synergistic anticancer activity with nelfinavir in vitro.

140 netically or with the HIV protease inhibitor nelfinavir increased its binding to Ub conjugates but de

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

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

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

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

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

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

147 pplementation with fatty acids prevented the nelfinavir-induced effect on mitochondrial metabolism, d

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

149 Nelfinavir induces lipid bilayer stress in cellular orga

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

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

152 Nelfinavir inhibits the growth of melanoma cell lines at

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

154 bined proteome-wide affinity-purification of nelfinavir-interacting proteins with genome-wide CRISPR/

155 we elucidate here the molecular mechanism of nelfinavir interaction with PXR.

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

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

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

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

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

161 The HIV protease inhibitor nelfinavir is currently being analyzed for repurposing a

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

163 Nelfinavir/ISRIB combination is highly effective to inhi

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

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

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

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

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

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

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

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

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

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

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

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

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

177 However, nelfinavir neither decreased Akt phosphorylation in immo

178 Nelfinavir (NFV) is a clinically important antiviral dru

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

208 Nelfinavir profoundly sensitizes BRAF and NRAS mutant me

209 Nelfinavir promotes apoptosis and arrests cell cycle at

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

211 Among nelfinavir recipients, a trend toward decreased virologi

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

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

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

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

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

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

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

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

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

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

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

223 other anti-infective drugs, and we identify nelfinavir, rupintrivir, and cobicistat as the most sele

224 oplasmic reticulum stress, which may explain nelfinavir's ability to enhance cell killing by proteaso

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

226 11 lowers the binding affinity of indinavir, nelfinavir, saquinavir, and ritonavir by factors of 4000

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

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

229 A nelfinavir-selected protease D30N substitution substanti

230 resistance mutations developed upon parallel nelfinavir selection.

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

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

233 Nelfinavir stabilizes vacant 80S ribosomes.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

248 Finally, nelfinavir treatment required Ddi2 to induce the unfolde

249 iability of preadipocytes were unaffected by nelfinavir treatment.

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

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

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

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

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

255 Sensitivity to nelfinavir was dependent on ADIPOR2, which maintains mem

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

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

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

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

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

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

262 Nelfinavir, which is being investigated for repurposing

263 ated by combining the HIV-protease inhibitor nelfinavir with ISRIB, an experimental drug that inhibit

264 Combining Nelfinavir with TRAIL led to a significantly enhanced le