ライフサイエンスコーパス: protease inhibitor

1 Trypsin was strongly inhibited by serine protease inhibitor.

2 and the inhibitory activity of a multidomain protease inhibitor.

3 ation on the third drug, which was usually a protease inhibitor.

4 e activity by preincubating the samples with protease inhibitor.

5 ir, atazanavir/ritonavir, or another boosted protease inhibitor.

6 adhesion molecule, and HAI-2, a cell surface protease inhibitor.

7 e peptide from the alpha1-antitrypsin serine protease inhibitor.

8 cies had prenatal TDF exposure and 6% used a protease inhibitor.

9 hism that impacts simeprevir, another NS3/4A protease inhibitor.

10 proving the resistance profile of HCV NS3/4A protease inhibitors.

11 d autoproteolytic activity and inhibition by protease inhibitors.

12 ingly need second-line regimens with boosted protease inhibitors.

13 ropensity to mutate in the presence of HIV-1 protease inhibitors.

14 eight proteins classically defined as serine protease inhibitors.

15 from this SAR exercise were theorized to be protease inhibitors.

16 ge and functionally diverse family of serine protease inhibitors.

17 triazoles as potential nonpeptidic cysteine protease inhibitors.

18 nd in releasing bioactive sequences from the protease inhibitors.

19 he design of more potent and effective HIV-1 protease inhibitors.

20 ly unless rescued by concomitant transfer of protease inhibitors.

21 templates for engineering reversible serine protease inhibitors.

22 characterizing the next generation of HIV-1 protease inhibitors.

23 ore complete Gag cleavage in the presence of protease inhibitors.

24 assessed in the presence/absence of specific protease inhibitors.

25 avenues for a systematic discovery of serine protease inhibitors.

26 activity relationship studies for optimizing protease inhibitors.

27 Deletion of the gene that encodes serine protease inhibitor 1 (SPI-1) of rabbitpox virus and vacc

28 reverse transcriptase inhibitors (3.0%) and protease inhibitors (1.9%).

29 gimen of grazoprevir (MK-5172; an HCV NS3/4A protease inhibitor; 100 mg/day) plus ruzasvir (MK-8408;

30 of patients harbor a mutation in the serine protease inhibitor 1A (SERPINA1) gene leading to a singl

31 eived 150 mg of maraviroc twice daily with a protease inhibitor, 2 (11%) received 300 mg twice daily

32 The function of serine protease inhibitor 2A (Spi2A) was studied in mouse TH2 c

33 Of patients previously treated with protease inhibitors, 53.7% had RASs in NS3 and 96.5% ach

34 ied (31% vs 22%; P = .04) and to use boosted protease inhibitors (84% vs 62%; P = .004).

35 Selective pressure exerted by HIV-1 protease inhibitors, a mainstay of current anti-HIV-1 th

36 A mixture of bacterial protease inhibitors abrogated the effect of MET-1 effect

37 in the asthma groups were defence response, protease inhibitor activity, inflammatory and calcium si

38 phosphatidylinositol 3-kinase, but not TIMP1 protease inhibitor activity.

39 r Microcystis abundances but did up-regulate protease inhibitors (aer and mcn gene sets) and microcys

40 IgE-tp interact with polymers of the serine protease inhibitor alpha-1-antitrypsin (A1AT).

41 tor), paritaprevir, and ritonavir (an NS3/4A protease inhibitor)-an interferon- and ribavirin-free re

42 hat peptidomimetic FISLE-412,1 a reduced HIV protease inhibitor analogue, was well-tolerated, altered

43 weeks of response-guided therapy with an NS3 protease inhibitor and dual NS5A inhibitor-NS5B nucleoti

44 n stored baseline samples in patients in the protease inhibitor and NRTI group and calculated the pre

45 vailable in 391 (92%) of 426 patients in the protease inhibitor and NRTI group.

46 mpared with 312 (81%) of 383 patients in the protease inhibitor and raltegravir group at week 144 (p=

47 of pH and temperature, as well as effect of protease inhibitors and chosen metal ions on the aminope

48 resistance to inhibition by canonical serine protease inhibitors and in cleaving these inhibitors as

49 e specificity may aid the development of new protease inhibitors and provide insight into associated

50 lso resolved binding of zinc, lipids and HIV protease inhibitors and showed that drug binding blocked

51 en these proteases may affect sensitivity to protease inhibitors and the suitability of MNV as a mode

52 igned to receive grazoprevir (100 mg, NS3/4A protease inhibitor) and elbasvir (50 mg, NS5A inhibitor;

53 d safety of grazoprevir (MK-5172; HCV NS3/4A protease inhibitor) and two doses of elbasvir (MK-8742;

54 (11%) received 300 mg twice daily without a protease inhibitor, and 4 (22%) had an alternative regim

55 ng minimally discussed, including vicilin, a protease inhibitor, and a flavonol synthase/flavanone 3-

56 Era of listing was divided into interferon, protease inhibitor, and direct-acting antiviral.

57 ses in serum IL-8, IL-6, secretory leukocyte protease inhibitor, and regenerating islet-derived prote

58 n of proteins and inactivation of endogenous protease inhibitors, and facilitates removal of matrix c

59 (BPTI) and amyloid precursor protein Kunitz protease inhibitor (APPI), and for the ability to hydrol

60 HIV-1 protease inhibitors are crucial for treatment of HIV-1/A

61 Kunitz-type (KT) protease inhibitors are low molecular weight proteins cl

62 Protease inhibitors are potent, with a high genetic barr

63 n NS5A inhibitor) and grazoprevir (an NS3/4A protease inhibitor) are direct-acting antiviral agents r

64 n NS5A inhibitor) and grazoprevir (an NS3/4A protease inhibitor) are direct-acting antiviral agents r

65 treatment of adults and children requiring a protease inhibitor as part of antiretroviral treatment r

66 These results suggest the use of select protease inhibitors as a strategy for treating MD.

67 yl triazole TCMDC-134379 (1), a known serine protease inhibitor, as an excellent starting point for S

68 ry of a back-up to the hepatitis C virus NS3 protease inhibitor asunaprevir (2) is described.

69 which produced a clinical candidate: the NS3 protease inhibitor asunaprevir (64), marketed as Sunvepr

70 nanoparticles containing the antiretroviral protease inhibitor atazanavir.

71 O DESSICATION-21 and its cognate cytoplasmic protease inhibitor ATSERPIN1.

72 omplexes led us to the identification of the protease inhibitor AtSerpin1.

73 s studied in mouse TH2 cells, and the serine protease inhibitor B3 (SERPINB3) and SERPINB4 genes were

74 icitabine and tenofovir disoproxil fumarate (protease inhibitor based regimen); regimens were masked

75 ase inhibitor regimen and 286 to receive the protease inhibitor based regimen.

76 y soluble human immunodeficiency virus (HIV) protease inhibitor based upon in vivo test results.

77 e receiving an integrase inhibitor- versus a protease inhibitor-based regimen (p = 0.022).

78 se inhibitor-based regimen and 30/86 (35%) a protease inhibitor-based regimen.

79 tion (1.75, 1.06-2.88; p=0.028), and boosted protease inhibitor-based regimens (1.55, 1.45-2.11; p=0.

80 as not significantly associated with boosted protease inhibitor-based regimens (vs non-nucleoside rev

81 Protease inhibitor-based regimens in children aged <3 ye

82 al studies to assess the efficacy of boosted protease inhibitor-based regimens in low-income and midd

83 to overcome barriers to scaling up pediatric protease inhibitor-based regimens in sub-Saharan Africa

84 with HIV-1C, especially in those on boosted protease inhibitor-based regimens.

85 ight not accurately predict NRTI activity in protease inhibitor-based second-line ART.

86 t advanced HCV and at greatest need of cure, protease inhibitor-based triple therapy achieved approxi

87 patients with HCV genotype 1 who had failed protease inhibitor-based triple therapy, and in 4 of 4 (

88 was similar across ARV regimens (P = .774): protease inhibitor-based, 97% (95% confidence interval [

89 itonavir, lopinavir/ritonavir, other boosted protease inhibitors before baseline were excluded.

90 Protease nexin-1 (PN-1) is a serine protease inhibitor belonging to the serpin superfamily.

91 ts toward the development of next-generation protease inhibitors beyond the currently approved drugs.

92 human and murine cell lines and that serine protease inhibitors block Xps-mediated rounding and deta

93 A serine protease inhibitor blocked peptide and oligosaccharide h

94 ral therapy (ART) based on ritonavir-boosted protease inhibitors (bPIs) represents the only available

95 g cART, every additional 10% time on boosted protease inhibitors (BPIs) was associated with reduced K

96 A serine protease inhibitor but not inhibitors of cysteine protea

97 esents a novel evolutionary adaptation of KT protease inhibitors by F. hepatica, with its prime purpo

98 athways and allows the identification of new protease inhibitors by genome mining.

99 f Kunitz-bovine pancreatic trypsin inhibitor protease inhibitors by mesotrypsin, finding that the var

100 bition, which is in contrast to other serine protease inhibitors (camostat mesylate and aprotinin), a

101 de the intriguing discovery that several HIV-protease inhibitors can function as decoy antigens to sp

102 xperimental results suggesting that NS5A- or protease-inhibitors can generate non-infectious virus, w

103 The enriched protease inhibitors CER-based protein extract resulted i

104 ir (NS5A inhibitor) and paritaprevir (NS3/4A protease inhibitor; co-dosed with ritonavir) plus ribavi

105 tment duration of grazoprevir (an HCV NS3/4A protease inhibitor) combined with elbasvir (an HCV NS5A

106 AgNP15-induced ATF-6 degradation with Site-2 protease inhibitors completely blocked the effect of AgN

107 Computational modeling revealed that HIV-protease inhibitors comprised structural features presen

108 protein fraction, which we termed as Lunasin Protease Inhibitor Concentrate (LPIC), contains three ab

109 irst-line therapy and which should receive a protease-inhibitor-containing regimen.

110 HIV-1 protease inhibitors continue to play an important role i

111 The cysteine protease inhibitor cystatin C is internalized by some ca

112 In contrast, the cysteine protease inhibitor cystatin C was expressed only in tubu

113 se transcriptase (RT) inhibitors (NRTIs) and protease inhibitors designed for HIV-1.

114 Viruses resistant to NS3-4A protease inhibitors disappear from peripheral blood in a

115 lupus medications, thrombin inhibitors, HIV protease inhibitors, DNA gyrase inhibitors and many othe

116 -binding proteins that possess a Kunitz-type protease inhibitor domain.

117 bitor, and paritaprevir (ABT-450), an NS3/4A protease inhibitor dosed with ritonavir (ombitasvir plus

118 NS5A inhibitor, and paritaprevir, an NS3/4A protease inhibitor dosed with ritonavir, plus ribavirin

119 he progeria-like side effects of certain HIV protease inhibitor drugs, but also highlight new approac

120 alities similar to that seen with a cysteine protease inhibitor, E-64 (I-1).

121 Importantly, the cysteine protease inhibitor E64 prevented mucous degradation, muc

122 The serine protease inhibitor, elafin, is a critical component of t

123 amide versus continuing a regimen of boosted protease inhibitor, emtricitabine, and tenofovir disopro

124 servational Study of the Consequences of the Protease Inhibitor Era) cohort, a clinic-based cohort of

125 way and alpha1-antitrypsin protein (a serine protease inhibitor) expression and downregulation of neu

126 Virions treated with protease inhibitors failed to release Vpx, indicating th

127 sitism genes, including certain protease and protease inhibitor families, as well as fatty acid- and

128 at the protein may belong to the Kunitz-type protease inhibitor family and therefore may potentially

129 biquitously-expressed member of the cysteine protease inhibitor family that is present at notably hig

130 tors (BBIs) are a well-known family of plant protease inhibitors first described 70 years ago.

131 gylated interferon and ribavirin (PR), and a protease inhibitor for HCV genotype (G) 1 and PR alone f

132 ve research has led to a variety of approved protease inhibitors for the treatment of HIV/AIDS.

133 vely, these results indicate that a cysteine protease inhibitor from bacterial origin could be a suit

134 he selectivity of ShPI-1, a versatile serine protease inhibitor from the sea anemone Stichodactyla he

135 ed for the efficient recovery of patatin and protease inhibitors from potato pulp.

136 treatment with the combination of the NS3/4A protease inhibitor glecaprevir and the NS5A inhibitor pi

137 se at 12 weeks (SVR12) rate using the NS3/4A protease inhibitor grazoprevir and the NS5A inhibitor el

138 week 48 compared with 231 (81%) women in the protease inhibitor group (adjusted difference 6.5%; 95%

139 19 women in the protease inhibitor group discontinued because of adverse

140 articipants ([1%]; all Met184Val/Ile) in the protease inhibitor group.

141 tients treated with LDV, SOF, and the NS3/4A protease inhibitor GS-9451 for 6 weeks, 76% (38 of 50; 9

142 e NS5A inhibitor velpatasvir, and the NS3/4A protease inhibitor GS-9857 in patients with hepatitis C

143 e NS5A inhibitor velpatasvir, and the NS3/4A protease inhibitor GS-9857 in these patients.

144 he NS5A inhibitor velpatasvir and the NS3/4A protease inhibitor GS-9857, in patients with hepatitis C

145 cleoside polymerase-inhibitor (GS-9669) or a protease-inhibitor (GS-9451) and after 12 weeks with sof

146 h HIV-1C who were given therapy with boosted protease inhibitors had earlier time-to-secondary virolo

147 The design of protease inhibitors has been informed by insights into t

148 e of their S proteins for entry, a number of protease inhibitors have been proposed as antiviral agen

149 he absence of the cognate Kunitz-type serine protease inhibitors, hepatocyte growth factor activator

150 Inhibitors of the HIV aspartyl protease [HIV protease inhibitors (HIV-PIs)] are the cornerstone of tr

151 tage antiplasmodial activity of the aspartic protease inhibitor hydroxyl-ethyl-amine-based scaffold c

152 monary disease, the physiologic role of this protease inhibitor in lung development and homeostasis i

153 f the Toll and JAK/STAT pathways, and serine protease inhibitors in both social and solitary bees.

154 emical and viral mechanisms of resistance to protease inhibitors in patients with non-B subtypes of H

155 evolution of three types of multifunctional protease inhibitors in plants.

156 ck for several clinical and experimental HIV protease inhibitors including the highly important drug

157 nown family of aldehyde-containing, peptidic protease inhibitors, including antipain, chymostatin, le

158 minth immunomodulator AvCystatin, a cysteine protease inhibitor, induces a novel regulatory macrophag

159 The combined change in the two kinds of protease-inhibitor interactions is correlated with the o

160 e follicle wall was prevented by infusion of protease inhibitors into the ovarian bursa.

161 mbalance between NSP activity and endogenous protease inhibitors is associated with chronic inflammat

162 wman-Birk inhibitor (BBI), a soybean-derived protease inhibitor, is known to have anti-inflammatory e

163 tigma protein with homology with Kunitz-type protease inhibitors, is essential to SI in Nicotiana spp

164 ome marker EEA1 and that, in the presence of protease inhibitors, it can be detected in lysosomes.

165 Multifunctional protease inhibitors juggle jobs by targeting different e

166 The loss-of-function mutations of serine protease inhibitor, Kazal type 1 (SPINK1) gene are assoc

167 -amylase inhibitor CM2 (Tri a 29.02), serine protease inhibitor-like allergen (Tri a 39), and 1-cys-p

168 omly assigned to receive a ritonavir-boosted protease inhibitor (lopinavir 400 mg with ritonavir 100

169 riant is located in the gene encoding serine protease inhibitor, low levels of which are associated w

170 ng EETs and the expression of filaggrin, the protease inhibitor lympho-epithelial Kazal-type-related

171 Notably, Indinavir; an HIV protease inhibitor, may be effective in reducing the vir

172 Because many protease inhibitors mimic protease substrates, differenc

173 e testing); or with raltegravir; or alone as protease inhibitor monotherapy (discontinued after week

174 tegy of physician-selected ritonavir-boosted protease inhibitor monotherapy (PI-mono); we recommended

175 otease inhibitor plus raltegravir group), or protease inhibitor monotherapy (plus raltegravir inducti

176 p=0.02) and 233 (61%) of 280 patients in the protease inhibitor monotherapy group at week 96 (p<0.000

177 sified to combination therapy after week 96; protease inhibitor monotherapy group).

178 In the protease inhibitor monotherapy group, 292 (78%) of 375 h

179 Protease inhibitor monotherapy is an acceptable alternat

180 ptase inhibitor (NNRTI) mutations (2.9%) and protease inhibitor mutations (2.0%).

181 ible inhibition of RD21 activity by a Kunitz protease inhibitor named water-soluble chlorophyll-bindi

182 rug-repositioning screen identified the HIV1-protease inhibitor nelfinavir as potent suppressor of PA

183 The HIV1 protease inhibitor nelfinavir is being investigated as a

184 n 1997 and 2011 and carrying the most common protease inhibitors, nonnucleoside and nucleotide revers

185 High abundance proteins like protease inhibitors of plasma display a multitude of int

186 Some of the cyanobacteria produce protease inhibitor oligopeptides such as cyanopeptolins

187 e results indicate a conserved function of a protease inhibitor on cell death regulators from differe

188 we have investigated the effects of aspartic protease inhibitors on both enzymes and comparatively st

189 ass spectrometry to study the effects of HIV protease inhibitors on the human zinc metalloprotease ZM

190 leukocyte protease inhibitor [SLPI]; Elafin) protease inhibitors on the resolution of LPS-induced inf

191 s of C57/BL6J-betaENaC-Tg mice with a serine protease inhibitor ONO-3403, a derivative of camostat me

192 , p<0.0001), but not other ritonavir-boosted protease inhibitors or abacavir.

193 r-boosted lopinavir, other ritonavir-boosted protease inhibitors, or abacavir.

194 Serine protease inhibitors, or serpins, are paradigms for this

195 this study, the roles of rice bran cysteine protease inhibitors, oryzacystatins, were considered for

196 Extensive studies on resistance to viral protease inhibitors, particularly those of HIV-1 and hep

197 tional processing is inhibited by the serine protease inhibitor, phenylmethylsulfonyl fluoride.

198 enofovir disoproxil fumarate (TDF) without a protease inhibitor (PI) (0.18 [interquartile range {IQR}

199 in vitro and in vivo models to show that HIV protease inhibitor (PI) class ARVs induced neuronal dama

200 We report that GRL-09510, a novel HIV-1 protease inhibitor (PI) containing a newly-generated P2-

201 ine whether treatment with ritonavir-boosted protease inhibitor (PI) monotherapy is associated with d

202 ith viral load (VL) suppression on a boosted protease inhibitor (PI) regimen, a switch to raltegravir

203 ta on second-line failure and development of protease inhibitor (PI) resistance in sub-Saharan Africa

204 e inhibitor (NNRTI) resistance, and 4.2% had protease inhibitor (PI) resistance.

205 the gp41 cytoplasmic domain (gp41-CD) reduce protease inhibitor (PI) susceptibility without PI-resist

206 I]) among HIV-HCV-coinfected users of modern protease inhibitor (PI)- and nonnucleoside reverse trans

207 been reported that pregnant women receiving protease inhibitor (PI)-based combination antiretroviral

208 Protease inhibitor (PI)-based combination antiretroviral

209 stance in patients who are not responding to protease inhibitor (PI)-based regimens in resource-limit

210 Protease inhibitor (PI)-based response-guided triple the

211 HIV-infected children initiating protease inhibitor (PI)-containing second-line ART withi

212 as divided into interferon (IFN; 2003-2010), protease inhibitor (PI; 2011-2013), and direct-acting an

213 wever, only three of nine FDA-approved HIV-1 protease inhibitors (PI) are active against HIV-2.

214 is essential for retroviral replication, and protease inhibitors (PI) are important for treating HIV

215 iptase Inhibitors (EFV) or ritonavir-boosted Protease Inhibitors (PI) with the same backbone of Nucle

216 ubtypes and contributes to susceptibility to protease inhibitors (PI), a critical class of antiretrov

217 5B inhibitor) combined with simeprevir (SIM; protease inhibitor [PI]); however, supporting evidence i

218 ting antivirals against HCV including NS3/4A protease inhibitors (PIs) has greatly improved treatment

219 erapy (ART) occurs, and its association with protease inhibitors (PIs) is unclear.

220 In this article, we show that HIV protease inhibitors (PIs) prescribed to HIV-infected per

221 Binding of protease inhibitors (PIs) to the protease active site bl

222 Very high affinity protease inhibitors (PIs) with an interesting activity o

223 HIV-1-specific nonnucleoside RTIs (NNRTIs), protease inhibitors (PIs), and integrase inhibitors (IIs

224 f Gag in establishing resistance of HIV-1 to protease inhibitors (PIs), very limited data are availab

225 erse transcriptase inhibitors (NNRTIs) and 2 protease inhibitors (PIs).

226 e 3D regimen) with commonly prescribed HIV-1 protease inhibitors (PIs).

227 e activation compared with ritonavir-boosted protease inhibitors (PIs).

228 have been treated with therapies containing protease inhibitors (PIs).

229 ity lipoprotein cholesterol with the boosted protease inhibitors (PIs); each PI had greater increases

230 s than 400 copies per mL; p=0.003 versus the protease inhibitor plus NRTI group at 144 weeks.

231 alysis at 144 weeks, 317 (86%) of 367 in the protease inhibitor plus NRTI group had viral loads of le

232 plus two or three clinician-selected NRTIs (protease inhibitor plus NRTI group), protease inhibitor

233 r plus raltegravir offered no advantage over protease inhibitor plus NRTI in virological efficacy or

234 retroviral therapy, WHO recommends a boosted protease inhibitor plus nucleoside or nucleotide reverse

235 T) of a pharmacologically enhanced (boosted) protease inhibitor plus nucleoside or nucleotide reverse

236 NRTIs (protease inhibitor plus NRTI group), protease inhibitor plus raltegravir (400 mg twice per da

237 Recent WHO guidelines recommend a boosted protease inhibitor plus raltegravir as an alternative se

238 In the primary analysis, protease inhibitor plus raltegravir did not meet non-inf

239 per mL compared with 312 (81%) of 383 in the protease inhibitor plus raltegravir group (p=0.07; lower

240 itor plus raltegravir (400 mg twice per day; protease inhibitor plus raltegravir group), or protease

241 INTERPRETATION: Protease inhibitor plus raltegravir offered no advantage

242 ption offers any advantage over the standard protease inhibitor plus two nucleoside reverse-transcrip

243 The combination of ABT-493 (NS3/4A protease inhibitor) plus ABT-530 (NS5A inhibitor) has sh

244 ven different hydrolases (e.g. alpha-amylase/protease inhibitors preventing both early germination an

245 alpha1-Antitrypsin is a serine protease inhibitor produced in the liver that is respons

246 The cyclic peptides reported here as DENV protease inhibitors provide novel scaffolds that enable

247 as the serum cytokines, secretory leukocyte protease inhibitor, regenerating islet-derived protein 3

248 disoproxil fumarate compared with a boosted protease inhibitor regimen of ritonavir-boosted atazanav

249 reduced use of expensive second-line boosted protease inhibitor regimens, this policy option is also

250 In vitro, cysteine protease inhibitors restored granularity, demonstrating

251 s of mutations associated with resistance to protease inhibitors, reverse transcriptase inhibitors (n

252 inhibition of glucose transport with the HIV protease inhibitor ritonavir elicited growth arrest and/

253 an important synthetic precursor to the HIV-protease inhibitor, saquinavir, by formation of an NHS e

254 The intracellular protease inhibitor Sb9 (SerpinB9) is a regulator of the

255 phil apoptosis and efferocytosis in a serine-protease inhibitor-sensitive manner.

256 Many members of the serine protease inhibitor (serpin) family are activated by glyc

257 eted proteins Fibronectin 1 (FN1) and serine protease inhibitor (serpin) family E member 2 (SERPINE2)

258 served a compensatory increase in the serine protease inhibitor Serpina3n in mouse models of MD and a

259 Elevated levels of the serine protease inhibitors SERPINB3 and SERPINB4 are seen in pa

260 ne peptide isostere developed as an aspartic protease inhibitor shows that it is a flexible architect

261 IV]; Eglin) and natural (secretory leukocyte protease inhibitor [SLPI]; Elafin) protease inhibitors o

262 study that evaluated simeprevir (HCV NS3/4A protease inhibitor) + sofosbuvir (HCV nucleotide analogu

263 interleukin-6 receptor (IL6R), cell surface protease inhibitor Spint-1, the collagen receptor tyrosi

264 Serine protease inhibitors (SPIs) regulate protease-mediated ac

265 rmation) were randomly assigned to a boosted protease inhibitor (standardised to ritonavir-boosted lo

266 es revealed that most commercially available protease inhibitors target unexpected proteases in plant

267 an C1-inhibitor (C1INH) is a multifunctional protease inhibitor that regulates coagulation, vascular

268 opeptides are homologous to the I9 family of protease inhibitors that have only been described in fun

269 mutation that commonly arises in response to protease inhibitor therapy creates a functional but inef

270 s led to several strategies to improve viral protease inhibitors to counter resistance, such as explo

271 the generation of the most potent human HTRA protease inhibitors to date.

272 cular modelling suggested lower affinity for protease inhibitors to HIV-1C protease than to HIV-1B.

273 (PF-MC) made up of N-terminal portion of the protease inhibitor Trappin-2 (which is a substrate of tr

274 Gag processing efficiency in the context of protease inhibitor treatment, thereby enhancing the drug

275 irrhosis, prior decompensation, and previous protease inhibitor treatments were less likely to achiev

276 thought of as a functionally self-contained protease inhibitor unit.

277 ract enriched with patatin (up to 60.0%) and protease inhibitors (up to 72.0%), respectively.

278 eb-response system and stratified by boosted protease inhibitor use at baseline.

279 a-1 antitrypsin (AAT; Prolastin-C), a serine protease inhibitor used for the treatment of AAT deficie

280 The serpin family of metastable protease inhibitors uses large conformational changes th

281 dentified KCs as a rich source of the serpin protease inhibitor vaspin (serpinA12), originally descri

282 vir, the NS5A inhibitor velpatasvir, and the protease inhibitor voxilaprevir (150 patients) or matchi

283 and velpatasvir plus the pangenotypic NS3/4A protease inhibitor voxilaprevir (sofosbuvir-velpatasvir-

284 th or without the nonstructural protein 3/4A protease inhibitor voxilaprevir.

285 d was stratified by the third agent (boosted protease inhibitor vs other agent).

286 TMPRSS2, but Zhou et al. found that a serine protease inhibitor was more protective than a cathepsin

287 erized apoplastic effector EPIC1, a cysteine protease inhibitor, was also secreted from haustoria.

288 SerpinA3N, a serine protease inhibitor, was upregulated in the dorsal root g

289 sequences derived from natural or synthetic protease inhibitors, we have generated antibodies that i

290 Compared with efavirenz, protease inhibitors were associated with higher and nevi

291 2 diabetes mellitus, and nelfinavir, an HIV protease inhibitor, when used alone or in combination.

292 upeptin, elastatinal, and microbial alkaline protease inhibitor, which have been widely used for over

293 SLPI is a secreted serine protease inhibitor, which is overexpressed in a number o

294 the use of virus entry antagonists, such as protease inhibitors, which might be most effective when

295 176 (89%) of 198 patients prescribed a protease inhibitor with no predicted-active NRTIs had vi

296 A regimen of protease inhibitor with NRTIs remains the best standardi

297 ction that was unsuccessfully treated with a protease inhibitor with peginterferon and ribavirin (50%

298 reverse transcriptase inhibitors or boosted protease inhibitors with 2 NRTIs.

299 Using protease inhibitors with increasing specificity, we iden

300 tor (NNRTI)-based regimen to one including a protease inhibitor, with adjustment of one or more nucle