ライフサイエンスコーパス: NVP

1 NVP arm participants had significantly higher risk of VF

2 NVP loaded with BG505.SOSIP.664 (SOSIP) or SARS-CoV-2 re

3 NVP mutants decayed to <2% in 24/35 (68.6%) at a median

4 NVP resistance was detected in 9 of 24 infants (37.5%; 9

5 NVP resistance was identified by consensus sequencing an

6 NVP-AAM077 did not affect the VMR in either group.

7 NVP-AUY922 also significantly inhibited tumor cell chemo

8 NVP-BEZ235 abrogated the radiation-induced phosphorylati

9 NVP-BEZ235 also increased in vivo radiation response in

10 NVP-BEZ235 also induced significant cytotoxicity in WM c

11 NVP-BEZ235 interfered with DNA damage repair after radia

12 NVP-BEZ235 radiosensitized a variety of cancer cell line

13 NVP-BEZ235 suppressed the growth of Met-1 and MCNeuA tum

14 NVP-BEZ235 was effective at low nanomolar concentrations

15 NVP-BGJ398 inhibited FGFR3 downstream signaling pathways

16 NVP-BKM120 treatment decreased phosphorylation of Akt an

17 NVP-QAB-205 reduced AHR and the enhanced response to PM(

18 NVP-TNKS656 (43) was identified as an orally active anta

19 From 2010-2013, 298 NVP-exposed HIV-infected children >/=3 years of age were

20 )NVP, cell death was reduced 30% with 12-D(3)NVP vs NVP, while glucuronidated and glutathione-conjuga

21 otein 1 (IGFBP-1), were observed with 12-D(3)NVP vs NVP.

22 conjugated metabolites increased with 12-D(3)NVP vs NVP.

23 ld) hepatocytes incubated with 10 muM 12-D(3)NVP vs NVP.

24 t of twelfth-position trideuteration (12-D(3)NVP) on the hepatic metabolism of and response to NVP.

25 ocyte treatment (400 muM) with NVP or 12-D(3)NVP, cell death was reduced 30% with 12-D(3)NVP vs NVP,

26 associated with higher risk for SGA; ZDV-3TC-NVP was associated with higher risk of stillbirth, very

27 2); zidovudine, lamivudine, and NPV (ZDV-3TC-NVP) (647 of 1365 [47.4%]; ARR, 1.30; 95% CI, 1.20-1.41)

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

29 cantly more virological failure than AZT/3TC/NVP; a third study was terminated prematurely because of

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

31 Further study of TDF/3TC/NVP is required before it is widely deployed for initial

32 In 2 comparative studies, TDF/3TC/NVP was associated with significantly more virological f

33 TDF/3TC/NVP was the least well-studied and appeared the least ef

34 ty, including NR2A-preferring (PEAQX, n = 5; NVP-AAM077, n = 18), NR2B-selective (ifenprodil, n = 6;

35 of startle was tested after MK-801 (n = 6), NVP-AAM077, and Ro-6891 (n = 5) injection.

36 y of 98.2% based on DESI MSI data (PPV 0.96, NVP 1, specificity 0.96, sensitivity 1).

37 roquinoxalin- 5-yl)-methyl]-phosphonic acid (NVP-AAM077) and the NR2B-receptor-antagonist Ro25-6981 w

38 droquinoxalin-5 -yl)-methyl-phosphonic acid (NVP-AAM077), contains a unique combination of a dioxoqui

39 In addition, NVP-BEZ235 inhibited both rictor and raptor, thus abroga

40 In addition, NVP-BEZ235 targeted WM cells in the context of bone marr

41 In addition, NVP-HSP990 disrupted cell-cycle control mechanism by dec

42 Additionally, NVP-AAM077 at 0.3 nmol perfused into the contralateral v

43 ttenuated Hsp70 induction but did not affect NVP-AUY922-mediated mHtt clearance.

44 hat either drug increased cell killing after NVP-BEZ235 treatment and radiation.

45 etic means increases radiation killing after NVP-BEZ235 treatment; hence, autophagy seems to be cytop

46 PI3K/Akt/mTOR signaling with the oral agents NVP-BKM120 and NVP-BEZ235 decreased mammary tumor growth

47 resistance was generated with VER-50589 and NVP-AUY922.

48 le amide compounds VER-49009, VER-50589, and NVP-AUY922.

49 ignaling with the oral agents NVP-BKM120 and NVP-BEZ235 decreased mammary tumor growth in the hyperin

50 nd the effects of the competitive antagonist NVP-AAM077.

51 N1 agonist glycine and the GluN2A antagonist NVP-AAM077.

52 corticostriatal slices with NR2A antagonist NVP-AAM077 or with NR2A blocking peptide induces a signi

53 Next, the GluN2A-selective antagonist NVP or GluN2B-selective antagonist Ro25 was infused into

54 corticostriatal slices with NR2A antagonist (NVP-AAM077) and D1 receptor agonist augmented the increa

55 t, Ro25,6981, the NR2A-prefering antagonist, NVP-AAM077, or the non-subunit-selective NMDAR antagonis

56 proliferation and response to NVP-HSP990, as NVP-HSP990 attenuated cell proliferation in Olig2-high G

57 treatment with p53-HDM2 inhibitors, such as NVP-CGM097.

58 Inactivation of FoxO attenuated NVP-BEZ235-induced AKT Ser473 phosphorylation and render

59 CRF02_AG, 8 treatment-naive and 4 on 3TC-AZT-NVP] showed 3 to 4 mutations in the Gag P2/NC CS: S373Q/

60 Associations between NVP-resistant mutants and VF or death were determined an

61 ) blocker RAD001 and PI3-kinase/mTOR blocker NVP-BEZ235.

62 Studies of RT in the presence of both NVP and MgATP indicate a strong negative cooperativity.

63 in the OVA/OVA mice, which was abrogated by NVP-QAB-205.

64 -Glu781 reduced the potency of inhibition by NVP-AAM077, thus confirming the involvement of the GluN1

65 In HN10 cells, Hsp90 inhibition by NVP-AUY922 enhanced mHtt clearance in the absence of any

66 ons relative to the clinical trial candidate NVP-AUY922, and consequently may be less susceptible to

67 Pre-cART NVP-resistant variants were detected in 18% (39/219) of

68 e H activity, whereas mutation in p51 caused NVP resistance and impaired RNase H, demonstrating that

69 Mutation in either subunit caused NVP resistance during RNA-dependent and DNA-dependent DN

70 ion in p66 alone (p66(N348I)/p51(WT)) caused NVP resistance without significantly affecting RNase H a

71 Chronic NVP-AAM077 or D-APV treatment had little effect on these

72 Poly(HEMA-co-AA-co-AM-co-NVP-co-PEG200DMA) soft contact lenses were prepared (100

73 We show that when using P(IA-co-NVP) hydrogel microparticles with 3 mol% tetra(ethylene

74 ct on the delivery capability of the P(IA-co-NVP) hydrogel.

75 onic acid-co-N-vinyl-2-pyrrolidone) (P(IA-co-NVP)) hydrogel microparticles were tested in vitro with

76 zymatically-degradable hydrogels of P(MAA-co-NVP) crosslinked with the peptide sequence MMRRRKK were

77 Our data offer a rationale for combining NVP-BEZ235 along with an autophagy inhibitor (i.e., chlo

78 Compound NVP-BEZ235 (1) is a potent inhibitor of human phospoinos

79 proliferation, the use of a novel compound, NVP-BEZ235, that dually inhibits both PI3K and mTOR kina

80 ipants receiving failing regimens containing NVP or EFV, respectively.

81 In contrast, NVP HSR protection is afforded by a cluster of HLA-B all

82 In GIC cultures, NVP-HSP990 elicited a dose-dependent growth inhibition w

83 ate that primary predisposition to cutaneous NVP HSR, seen across ancestral groups, can be attributed

84 for multiple HLA associations with cutaneous NVP HSR and advance insight into its pathogenic mechanis

85 t decrease inhibitor binding (increase K(d)(-NVP)) by primarily decreasing the association rate of th

86 However, 35 (14%) women discontinued NVP because of adverse events, most in the first 8 weeks

87 Low-dose NVP-BGJ398 treatment reduced intervertebral disc defects

88 in women with prior exposure to single-dose NVP (sdNVP).

89 feeding infants after receipt of single-dose NVP to prevent mother-to-child transmission is not well

90 ombined use of the clinically relevant drugs NVP-BEZ235, which targets the cell cycle, and Obatoclax,

91 properties, and high lipophilic efficiency, NVP-TNKS656 is a novel tankyrase inhibitor that is well

92 DF)/emtricitabine (FTC) once/day plus either NVP (n = 249) or LPV/r (n = 251) twice/day, and followed

93 In contrast, infants in the extended NVP arm who were HIV infected after birth were more like

94 dissociate reconsolidation from extinction, NVP was infused into IL-mPFC after four 10-min reactivat

95 receptor antagonists, including fevipiprant (NVP-QAW039 or QAW039), which is currently in development

96 We also report a novel mechanism for NVP-BEZ235 involving the suppression of multiple autocri

97 ciency virus (HIV) infection but selects for NVP-resistant virus, which compromises subsequent NVP-ba

98 Low-frequency NVP- or 3TC/FTC-resistant mutants at codons 103, 181, an

99 with prior exposure to sdNVP, low-frequency NVP-resistant mutants were associated with increased ris

100 We hypothesized that low-frequency NVP-resistant mutants, missed by population genotype, ex

101 The risk of VF on NVP-based cART from NVP-resistant variants differs between sdNVP-exposed and

102 pine (NVP) (n = 3), TDF/ emtricitabine (FTC)/NVP (n = 9), TDF/3TC/efavirenz (EFV) (n = 6), and TDF/FT

103 TDF/FTC/NVP was either equivalent or inferior to its comparator

104 Furthermore, NVP-BEZ235 radiosensitized autophagy-deficient ATG5(-/-)

105 istance by population genotype, 70 (35%) had NVP-resistant mutants detected by allele-specific PCR.

106 ho were HIV infected at birth frequently had NVP resistance detected.

107 However, NVP-based ART had a marginal benefit in CD4 percentage (

108 PDAC cells to a clinical inhibitor of HSP90, NVP-AUY922, both in vitro and in vivo.

109 anti-HIV drug nevirapine (NVP) to 12-hydroxy-NVP (12-OHNVP) has been implicated in NVP toxicities.

110 nd acutely inhibited by the imidazoquinoline NVP-BHS345.

111 ictor is a key downstream target of FoxOs in NVP-BEZ235-mediated feedback regulation.

112 ydroxy-NVP (12-OHNVP) has been implicated in NVP toxicities.

113 t least a partially activated p53 pathway in NVP-CGM097-sensitive tumors.

114 phagy related 5 (ATG5) and beclin1 increased NVP-BEZ235-mediated radiosensitization.

115 IV transmission does not appear to influence NVP resistance.

116 hway, including the PI3K/mTOR dual inhibitor NVP-BEZ235, are currently being tested in various precli

117 election strategy for the p53-HDM2 inhibitor NVP-CGM097, currently under evaluation in clinical trial

118 evaluate two inhibitors, the HSP90 inhibitor NVP-AUY922, and the mTOR inhibitor everolimus, both of w

119 sed the potent and selective Hsp90 inhibitor NVP-AUY922.

120 lts comparable to the potent Hsp90 inhibitor NVP-AUY922.

121 oth, treatment with the FAK kinase inhibitor NVP-TAE226 and FAK down-regulation by siRNA reduced RET

122 cer, the potent and selective MDM2 inhibitor NVP-CGM097 (1) with an excellent in vivo profile was sel

123 xamined whether the oral PI3K/mTOR inhibitor NVP-BEZ235 augmented the tumor suppressing effects of PI

124 I3K activity by the dual PI3K/mTOR inhibitor NVP-BEZ235 led to growth inhibition of PCaPs.

125 Similar to AZD8055, the PI3K/mTOR inhibitor NVP-BEZ235, the PI3K inhibitor NVP-BKM120 and Akt inhibi

126 tidylinositol 3-kinase (PI3K)/mTOR inhibitor NVP-BEZ235.

127 the PI3K/mTOR pathway by the novel inhibitor NVP-BEZ235 showed higher cytotoxicity on WM cells compar

128 TOR inhibitor NVP-BEZ235, the PI3K inhibitor NVP-BKM120 and Akt inhibitor synergize with ABT-737 to t

129 Importantly, the FGFR selective inhibitor NVP-BGJ-398 significantly inhibited the growth of FU-DDL

130 The Syk inhibitor NVP-QAB-205 was nebulized intratracheally by using a tre

131 Treatment with an IGF1R inhibitor (NVP-AEW541) showed no discernable antitumor activity and

132 ated the effects of a novel HSP90 inhibitor, NVP-HSP990, in glioma tumor-initiating cell (GIC) popula

133 tively reverted by the RET kinase inhibitor, NVP-BBT594.

134 reverted using the dual PI3K/mTOR inhibitor, NVP-BEZ235, both in vitro and in vivo.

135 Using a dual PI3K-mTOR inhibitor, NVP-BEZ235, we evaluated whether PI3K-mTOR inhibition al

136 3K with the oral pan-class I PI3K inhibitor, NVP-BKM120 reduced the growth of Met-1 and MCNeuA mammar

137 We showed that the selective PI3K inhibitor, NVP-BKM120, both decreased NRF2 protein levels and sensi

138 in MM using a novel synthetic Smo inhibitor, NVP-LDE225 (Novartis), which decreased MM cell viability

139 t two structurally different ALK inhibitors, NVP-TAE684 and AP26113, were highly active against the r

140 iated with virologic failure (VF) of initial NVP-based combination antiretroviral therapy (cART) in w

141 08 trial 1 who had taken sdNVP and initiated NVP-based cART.

142 out prior sdNVP who were starting first-line NVP-based cART in the OCTANE/A5208 trial 2.

143 egimens at preventing the emergence of minor NVP resistance variants.

144 h of dual therapy after SD-NVP prevents most NVP resistance to minimal toxicity.

145 A dual inhibitor of PI3K and mTOR, NVP-BEZ235, was also effective.

146 m (ES) cells and in ES cell-derived neurons, NVP-AUY922 treatment substantially reduced soluble full-

147 Nevirapine (NVP) is widely used in antiretroviral treatment (ART) of

148 Nevirapine (NVP) resistance emerges in up to 70% of women exposed to

149 Nevirapine (NVP), is an HIV-1 antiretroviral with treatment-limiting

150 g regimens: TDF/lamivudine (3TC)/nevirapine (NVP) (n = 3), TDF/ emtricitabine (FTC)/NVP (n = 9), TDF/

151 6.4%]) compared with TDF-FTC and nevirapine (NVP) (317 of 760 [41.7%]; ARR, 1.15; 95% CI, 1.04-1.27);

152 tors (NNRTI) efavirenz (EFV) and nevirapine (NVP) in first-line antiretroviral therapy (ART).

153 f RT-RNA/DNA-dATP and RT-RNA/DNA-nevirapine (NVP) ternary complexes at 2.5 and 2.9 A resolution, resp

154 metabolism of the anti-HIV drug nevirapine (NVP) to 12-hydroxy-NVP (12-OHNVP) has been implicated in

155 Low-frequency nevirapine (NVP)-resistant variants have been associated with virolo

156 The interaction of the NNRTI nevirapine (NVP) with HIV-1 reverse transcriptase (RT) is characteri

157 anism of resistance to the NNRTI nevirapine (NVP).

158 y, we showed that another NNRTI, nevirapine (NVP), stimulated K101E+G190S virus replication during th

159 Acquisition of nevirapine (NVP)-resistant human immunodeficiency virus type 1 (HIV-

160 lopinavir/ritonavir (LPV/r) over nevirapine (NVP) in antiretroviral therapy (ART), regardless of prio

161 Intrapartum single-dose (SD) nevirapine (NVP) reduces perinatal transmission of human immunodefic

162 cleavage, enhance resistance to nevirapine (NVP) and delavirdine (DLV), but not to efavirenz (EFV) a

163 d lopinavir/ritonavir (LPV/r) to nevirapine (NVP) for antiretroviral therapy and showed a lower risk

164 iency virus (HIV) and exposed to nevirapine (NVP) for prevention of mother-to-child transmission.

165 esults available; of these, 5 (1.2%) had new NVP resistance detected by population genotype: 4 of 215

166 he primary endpoint was the emergence of new NVP resistance mutations as detected by standard populat

167 sdNVP, resulted in a low rate (1.2%) of new NVP-resistance mutations when assessed at 2 and 6 weeks

168 Among women with ASP results, new NVP resistance mutations emerged significantly more ofte

169 ment discontinuation occurred in 80 (32%) of NVP and 54 (22%) of LPV/r arms (HR = 1.7, 95% CI 1.2-2.4

170 Here, we tested the anti-MM activity of NVP-BEZ235 (BEZ235), which inhibits PI3K/Akt/mTOR signal

171 reatest shift sensitivity to the addition of NVP.

172 FLT-uptake on day 2 after administration of NVP-AUY299, but a significant reduction in FLT-uptake up

173 was attenuated by a single administration of NVP-QAB-205 (0.3 and 3 mg/kg).

174 of magnitude between the binding affinity of NVP for RT in the presence or absence of primer/template

175 Binding of NVP slides the RNA/DNA non-uniformly over RT, and the RN

176 olvement of the GluN1 subunit for binding of NVP-AAM077.

177 Finally, the combination of NVP-AST487 with standard chemotherapeutic agents leads t

178 erapeutic gain observed after combination of NVP-BEZ235 with irradiation has conceptual implications

179 Detection of NVP resistance in plasma virus at study entry by standar

180 potential influence of different dosages of NVP and different viral load thresholds.

181 Moreover, we demonstrated that a low dose of NVP-BGJ398, injected subcutaneously, was able to penetra

182 sent study was to investigate the effects of NVP-BEZ235 (BEZ; dactolisib), a dual PI3K/mTOR inhibitor

183 /OCTANE trial was to compare the efficacy of NVP-based versus lopinavir/ritonavir (LPV/r)-based initi

184 in vivo studies showed antitumor efficacy of NVP-LDE225 in combination with bortezomib.

185 ssociated with increased risk for failure of NVP-containing ART.

186 it is typically viewed as the severe form of NVP and has been reported to occur in 0.3-10.8% of pregn

187 quinoxalinyl ring and the phosphono group of NVP-AAM077 in the glutamate-binding pocket in GluN2A and

188 The incidence of NVP resistance mutations at day 10 or week 6 post partum

189 Reverse microdialysis of NVP-AAM077 had no effect on basal and CRD-induced ACC ne

190 imescale, but become slow in the presence of NVP due to the slow binding of RT with the inhibitor.

191 We describe the biological properties of NVP-AUY922, a novel resorcinylic isoxazole amide heat sh

192 ine (ZDV) was hypothesized to lower rates of NVP-resistance.

193 xpected plasma concentration-time results of NVP-1, an investigational drug candidate, observed in th

194 ation of this series led to the selection of NVP-HSP990 as a development candidate.

195 Recent advances in the genetic study of NVP and HG suggest a placental component to the aetiolog

196 ional display of antigens on the surfaces of NVP.

197 ated the rate of breast milk transmission of NVP-resistant HIV and the concentrations of mutants over

198 to explain most of the affinity variation of NVP for RT.

199 rquartile range [IQR], 4.3-6.4), with 52% on NVP and 88% on LPV/r as originally randomized.

200 nts were offered a switch in regimens (if on NVP) and continued observational follow-up.

201 The risk of VF on NVP-based cART from NVP-resistant variants differs betwe

202 the association rate of the inhibitor (k(on-NVP)).

203 and were unaffected by PM(2.5) plus O(3) or NVP-QAB-205.

204 e highly specific drugs 17-AAG, SNX-5422, or NVP-AUY922 reduced TSSK protein levels in cells.

205 w lipid-based nanoparticle vaccine platform (NVP) that presents viral proteins (HIV-1 and SARS-CoV-2

206 ingle-dose nevirapine (SD NVP) at birth plus NVP prophylaxis for the infant up to 6 weeks of age is s

207 Postpartum NVP-resistance was lower among 31 taking ZDV+sdNVP compa

208 Nausea and vomiting of pregnancy (NVP) is a common condition that affects as many as 70% o

209 etroviral therapy (ART), regardless of prior NVP exposure.

210 were enrolled into 2 cohorts based on prior NVP exposure and randomized to NVP- or LPV/r-based ART.

211 4,5-c]quin olin-1-yl]phenyl} propanenitrile (NVP-BEZ235) (Novartis, Basel Switzerland), a dual phosph

212 lele-specific PCR at study entry to quantify NVP-resistant mutants down to 0.1% for 103N and 190A and

213 ecific polymerase chain reaction to quantify NVP-resistant mutants in human immunodeficiency virus-in

214 Furthermore, mice immunized with RBD-NVP induced robust and long-lasting antibody responses a

215 ed treatment, 14% and 16% of women receiving NVP and LPV/r experienced grade 3/4 signs/symptoms and 2

216 Short-course ZDV was associated with reduced NVP-resistance mutations among women taking sdNVP.

217 Single-dose nevirapine (SD NVP) at birth plus NVP prophylaxis for the infant up to

218 Repeated use of SD NVP to prevent HIV transmission does not appear to influ

219 at 6 weeks, compared with infants in the SD NVP arm.

220 nfant up to 6 weeks of age is superior to SD NVP alone for prevention of vertical transmission of hum

221 to 70% of women exposed to single-dose (sd) NVP for prevention of mother-to-child transmission of hu

222 "tail" of lamivudine and zidovudine after SD-NVP decreases the risk of resistance.

223 therapy or 1 month of dual therapy after SD-NVP prevents most NVP resistance to minimal toxicity.

224 roup who received prenatal zidovudine and SD-NVP.

225 other-to-child-transmission of HIV-1 selects NVP-resistance.

226 Rabbits immunized with SOSIP-NVP elicited strong neutralizing antibody responses agai

227 Fourteen women started NVP-ART more than 6 months after sdNVP therapy; resistan

228 esistant virus, which compromises subsequent NVP-based therapy.

229 increases the risk of failure of subsequent NVP-containing antiretroviral therapy (ART), especially

230 nefits of switching virologically suppressed NVP-exposed HIV-infected children >/=3 years of age from

231 erinsulinemia developed with NVP-BEZ235 than NVP-BKM120.

232 EFV was significantly less likely than NVP to lead to virologic failure in both trials (RR 0.85

233 ore likely to achieve virologic success than NVP, though marginally significant, in both randomised c

234 We conclude that NVP-BEZ235 radiosensitizes cells and induces autophagy b

235 Together, our data demonstrate that NVP-BGJ398 corrects pathological hallmarks of ACH and su

236 We demonstrated that NVP-AAM077, a potent antagonist for NR2A-containing rece

237 nce and impaired RNase H, demonstrating that NVP resistance may occur independently from defects in R

238 ncer drug repurposing approaches reveal that NVP-AUY922 downregulates PAF and decreases breast cancer

239 We show that NVP was readily taken up by dendritic cells (DCs) and pr

240 Here, we show that NVP-BEZ235, a dual inhibitor of phosphoinositide-3-kinas

241 These results suggest that NVP is a promising platform technology for vaccination a

242 42 women (37 VFs, five deaths; 17%) in the NVP and 50 (43 VFs, seven deaths; 20%) in the LPV/r arm

243 Mean CD4% was significantly higher in the NVP arm up to 1 year after ART initiation, but not beyon

244 ints occurred in 12 (32%) of 38 women in the NVP arm vs. 3 (9%) of 32 in the lopinavir/ritonavir-cont

245 The occurrence of a primary endpoint in the NVP arm was significantly associated with the presence o

246 r-age z scores were marginally higher in the NVP arm, but height-for-age z scores did not differ.

247 associated with the primary endpoint in the NVP arm, but two-thirds of endpoints occurred in women w

248 due to more treatment discontinuation in the NVP arm.

249 on genotype, explained excess failure in the NVP treatment arm.

250 13 (45%) of 29 women tested in the NVP versus six (15%) of 40 in the LPV/r arm had any drug

251 eath) was significantly more frequent in the NVP-containing treatment arm than in the lopinavir/riton

252 hances the dissociation rate constant of the NVP, resulting in an increase of the open/closed interco

253 to NVP, as indicated by the intensity of the NVP-perturbed M230 resonance, and enhances the dissociat

254 ere, we have reported that the pan-FGFR TKI, NVP-BGJ398, reduces FGFR3 phosphorylation and corrects t

255 of MgATP reduces the fraction of RT bound to NVP, as indicated by the intensity of the NVP-perturbed

256 ely to lead to virologic failure compared to NVP-based ART.

257 ased on prior NVP exposure and randomized to NVP- or LPV/r-based ART.

258 efficiency and causes in vitro resistance to NVP by decreasing inhibitor binding.

259 HIV-1 resistance to NVP following sdNVP therapy persists longer in cellular

260 and G190A mutations conferring resistance to NVP, DLV, and EFV and several HIV-1 clades A in PBMC.

261 s299 xenotransplants, which are resistant to NVP-AUY922 and sensitive to everolimus treatment, showed

262 factor pathways and cell models responded to NVP-BEZ235 (a PI3K/mTOR inhibitor) and dasatinib (an abl

263 pas299 to assess early treatment response to NVP-AUY922 or everolimus in vivo.

264 component of MTOR complex 2, in response to NVP-BEZ235 treatment and revealed that Rictor is a key d

265 AKT phosphorylation at Ser473 in response to NVP-BEZ235 treatment in renal cancer cells.

266 ated with cell proliferation and response to NVP-HSP990, as NVP-HSP990 attenuated cell proliferation

267 on the hepatic metabolism of and response to NVP.

268 lated genes that predicts for sensitivity to NVP-CGM097 in both cell lines and in patient-derived tum

269 Olig2 GIC may exhibit greater sensitivity to NVP-HSP990 treatment, establishing a foundation for furt

270 reening assay, it was remarkably superior to NVP and EFV and comparable to ETV.

271 e domain mutations reduced susceptibility to NVP (8.9-13-fold), EFV (4-56-fold), etravirine (ETV; 1.9

272 IV-1 infection and reduces susceptibility to NVP, EFV, ETV, and AZT.

273 dered renal cancer cells more susceptible to NVP-BEZ235-mediated cell growth suppression in vitro and

274 teratogenic and may be effective in treating NVP.

275 phatidylinositol 3 kinase/AKT pathway, using NVP-BKM120, increased active caspase 3 and decreased vim

276 the greater antiviral activity of EFV versus NVP and longer intracellular half-life of FTC-triphospha

277 e patients on regimens containing EFV versus NVP from randomised trials and observational cohort stud

278 ell death was reduced 30% with 12-D(3)NVP vs NVP, while glucuronidated and glutathione-conjugated met

279 (IGFBP-1), were observed with 12-D(3)NVP vs NVP.

280 ted metabolites increased with 12-D(3)NVP vs NVP.

281 atocytes incubated with 10 muM 12-D(3)NVP vs NVP.

282 nt discontinuations associated with LPV/r vs NVP (hazard ratio, 0.56 [95% CI, .41-.75]) but no differ

283 out prior sdNVP exposure, 8 of 39 (21%) with NVP-resistant variants experienced VF or death vs 31 of

284 Initial ART with NVP+TDF/FTC demonstrated equivalent virologic efficacy b

285 tization, but not to the same degree as with NVP-BEZ235.

286 he risk for a study endpoint associated with NVP-resistant mutant levels did not decrease with time.

287 The treatment of cells with NVP-BEZ235 also promoted autophagy.

288 1/2A over GluN1/2B is improved compared with NVP-AAM077, a widely used GluN2A-selective antagonist, w

289 glycemia and hyperinsulinemia developed with NVP-BEZ235 than NVP-BKM120.

290 Infection of breast-feeding infants with NVP-resistant HIV resulted in mutants persisting as the

291 Combinations of HER-family inhibitors with NVP-AEW541, dasatinib or crizotinib (inhibitors of IGF-1

292 ng mouse hepatocyte treatment (400 muM) with NVP or 12-D(3)NVP, cell death was reduced 30% with 12-D(

293 nemia developed in the MKR mice treated with NVP-BKM120.

294 was significantly reduced on treatment with NVP-AEW541 in parallel with signaling pathway ablation.

295 h may indefinitely compromise treatment with NVP-based antiretroviral regimens.

296 Inhibition of IGF1R activity in vitro with NVP-AEW541 or down-regulation of expression with siIGF1R

297 The majority of women with NVP can be managed with dietary and lifestyle changes, b

298 Of 201 women without NVP resistance by population genotype, 70 (35%) had NVP-

299 hirds of endpoints occurred in women without NVP resistance.

300 sociated with the presence of K103N or Y181C NVP-resistant mutations at frequencies >1%.