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

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

4 NVP resistance was detected in a similar proportion of i

5 NVP resistance was identified by consensus sequencing an

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

7 NVP-AST487, which selectively targets mutant FLT3 protei

8 NVP-AUY922 also significantly inhibited tumor cell chemo

9 NVP-AUY922 has entered phase I clinical trials.

10 NVP-AUY922 inhibited proliferation, chemomigration, and

11 NVP-AUY922 potently inhibits HSP90 (K(d) = 1.7 nmol/L) a

12 NVP-AUY922 was glucuronidated less than previously descr

13 NVP-BEZ235 abrogated the radiation-induced phosphorylati

14 NVP-BEZ235 also increased in vivo radiation response in

15 NVP-BEZ235 also induced significant cytotoxicity in WM c

16 NVP-BEZ235 interfered with DNA damage repair after radia

17 NVP-BEZ235 radiosensitized a variety of cancer cell line

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

19 NVP-BEZ235 was effective at low nanomolar concentrations

20 NVP-BGJ398 inhibited FGFR3 downstream signaling pathways

21 NVP-BKM120 treatment decreased phosphorylation of Akt an

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

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

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

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

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

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

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

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

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

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

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

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

34 /BIIB021, the isoxazole derivative VER-52296/NVP-AUY922, and the carbazol-4-one benzamide derivative

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 We analyzed NVP resistance after receipt of SD NVP in 57 previously

48 We analyzed NVP resistance in HIV-infected Ugandan infants who recei

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

88 n infants were 6 weeks old, ViroSeq detected NVP resistance in a higher proportion of infants in the

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

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

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

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

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

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

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

96 The use of extended NVP prophylaxis was also associated with detection of NV

97 fants who received either SD NVP or extended NVP prophylaxis.

98 onths (7 of 7 [100%] infants in the extended NVP arm had resistance detected, compared with 1 of 6 [1

99 higher proportion of infants in the extended NVP arm than in the SD NVP arm (21 of 25 [84%] vs. 12 of

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

115 nd acutely inhibited by the imidazoquinoline NVP-BHS345.

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

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

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

119 IV transmission does not appear to influence NVP resistance.

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

121 e effects of the novel mutant FLT3 inhibitor NVP-AST487 on primary patient cells and cell lines expre

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

137 n of VEGFR-2 by a specific kinase inhibitor (NVP-AAD777) enhanced the CS-induced oxidative stress, ca

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

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

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

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

142 3K with the oral pan-class I PI3K inhibitor, NVP-BKM120 reduced the growth of Met-1 and MCNeuA mammar

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

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

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

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

147 08 trial 1 who had taken sdNVP and initiated NVP-based cART.

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

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

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

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

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

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

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

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

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

157 6.4%]) compared with TDF-FTC and nevirapine (NVP) (317 of 760 [41.7%]; ARR, 1.15; 95% CI, 1.04-1.27);

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

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

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

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

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

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

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

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

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

167 Single-dose (SD) nevirapine (NVP) significantly reduces mother-to-child transmission

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

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

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

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

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

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

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

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

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

177 reatest shift sensitivity to the addition of NVP.

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

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

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

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

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

183 Combination of NVP-AEW541 and imatinib in GIST cell lines induced a str

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

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

186 ylaxis was also associated with detection of NVP resistance by ViroSeq at 6 months (7 of 7 [100%] inf

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

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

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

190 Daily dosing of NVP-AUY922 (50 mg/kg i.p. or i.v.) to athymic mice gener

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

215 4,5-c]quin olin-1-yl]phenyl} propanenitrile (NVP-BEZ235) (Novartis, Basel Switzerland), a dual phosph

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

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

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

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

220 n 57 previously SD NVP-naive women, in 34 SD NVP-experienced women, and in 17 HIV-infected infants.

221 ected Ugandan infants who received either SD NVP or extended NVP prophylaxis.

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

223 analyzed NVP resistance after receipt of SD NVP in 57 previously SD NVP-naive women, in 34 SD NVP-ex

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

225 after receipt of SD NVP in 57 previously SD NVP-naive women, in 34 SD NVP-experienced women, and in

226 fants in the extended NVP arm than in the SD NVP arm (21 of 25 [84%] vs. 12 of 24 [50%]; P = .01).

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

228 mpared with 1 of 6 [16.7%] infants in the SD NVP arm; P = .005).

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

230 n a similar proportion of infants born to SD NVP-naive versus SD NVP-experienced women.

231 on of infants born to SD NVP-naive versus SD NVP-experienced women.

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

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

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

235 roup who received prenatal zidovudine and SD-NVP.

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

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

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

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

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

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

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

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

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

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

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

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

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

249 Collectively, the data show that NVP-AUY922 is a potent, novel inhibitor of HSP90, acting

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

251 42 women (37 VFs, five deaths; 17%) in the NVP and 50 (43 VFs, seven deaths; 20%) in the LPV/r arm

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

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

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

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

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

257 due to more treatment discontinuation in the NVP arm.

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

259 13 (45%) of 29 women tested in the NVP versus six (15%) of 40 in the LPV/r arm had any drug

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

282 in GIST and viability were analyzed by using NVP-AEW541, an inhibitor of IGF1R, alone and in combinat

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

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

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

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

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

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

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

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

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

292 1/2A over GluN1/2B is improved compared with NVP-AAM077, a widely used GluN2A-selective antagonist, w

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

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

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

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

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

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

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

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

301 hirds of endpoints occurred in women without NVP resistance.

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