ライフサイエンスコーパス: zanamivir

1 rget for the influenza drugs oseltamivir and zanamivir.

2 omized to receive placebo and 553 to receive zanamivir.

3 -fold reduction in the enzyme sensitivity to zanamivir.

4 uperior to oseltamivir or 300 mg intravenous zanamivir.

5 1.5 days or greater with 600 mg intravenous zanamivir.

6 nfluenza virus neuraminidase (NA) inhibitor, zanamivir.

7 oseltamivir, later combined with intravenous zanamivir.

8 support further investigation of intravenous zanamivir.

9 vir and peramivir and partially resistant to zanamivir.

10 degree of resistance to oseltamivir but not zanamivir.

11 ains are sensitive to oseltamivir and all to zanamivir.

12 idase inhibitors oseltamivir carboxylate and zanamivir.

13 an be inhibited by the small receptor analog zanamivir.

14 person, and have retained susceptibility to zanamivir.

15 eased susceptibility to both oseltamivir and zanamivir.

16 ess was treated with either 10 mg of inhaled zanamivir (163 subjects) or placebo (158) twice a day fo

17 x-membered ring inhibitors such as DANA (2), zanamivir (3), and oseltamivir (4).

18 on [IC(50)]) and reduction in sensitivity to zanamivir (3-7-fold increase in IC(50) or 50% effective

19 Zanamivir (4-guanidino-Neu5Ac2en [4-GU-DANA]) inhibits n

20 ther family members received either 10 mg of zanamivir (414 subjects) or placebo (423) once a day as

21 Patients were treated with intravenous zanamivir 600 mg twice daily, adjusted for renal impairm

22 rmine the prophylactic effect of intravenous zanamivir (600 mg 2x/day for 5 days), a highly selective

23 st common adverse events (300 mg intravenous zanamivir, 600 mg intravenous zanamivir, oseltamivir) we

24 rophylactic efficacy against illness of both zanamivir (75%, 95% confidence interval (CI): 54, 86) an

25 -dehydro-N-acetylneuraminic acid (4-GU-DANA; zanamivir), a sialic acid transition-state analog design

26 During prolonged treatment with zanamivir, a mutant virus was isolated from an immunocom

27 Zanamivir, a neuraminidase inhibitor, has shown promise

28 Zanamivir, a novel neuraminidase inhibitor, is effective

29 The neuraminidase inhibitor zanamivir, a sialic acid analog administered directly to

30 Zanamivir administered once daily is efficacious and wel

31 The efficacy and safety of zanamivir, administered 2x or 4x daily over 5 days, was

32 r (P=0.02) and the 85 patients given inhaled zanamivir alone (P=0.05) than in the 89 patients given p

33 nfectiousness was 19% (95% CI: -160, 75) for zanamivir and 80% (95% CI: 43, 93) for oseltamivir.

34 with the strongest interactions with site I-zanamivir and BCX 2798-lead to the activation of site II

35 , rimantadine, and the newly available drugs zanamivir and oseltamivir are effective for influenza pr

36 several times in a blinded fashion with both zanamivir and oseltamivir carboxylate (GS4071) to determ

37 Extended-duration zanamivir and oseltamivir chemoprophylaxis seems to be h

38 of this enzyme have been developed, and two (zanamivir and oseltamivir) have been approved for human

39 lues are comparable or superior to those for zanamivir and oseltamivir, agents recently approved by t

40 These drugs, zanamivir and oseltamivir, prevent the release of newly

41 rated drug susceptibility of two antivirals, Zanamivir and Oseltamivir, using the assay.

42 sed, randomized clinical trials, two each of zanamivir and oseltamivir, were designed primarily to es

43 replicates the chemotherapeutic mechanism of zanamivir and oseltamivir, while rhamnose and DNP recrui

44 R371K mutations conferred resistance to both zanamivir and oseltamivir, while the D151E mutation redu

45 nfer drug resistance to two antiviral drugs, zanamivir and oseltamivir.

46 t statistically significantly differ between zanamivir and oseltamivir.

47 issue culture and mice by the NA inhibitors, zanamivir and oseltamivir.

48 e drug susceptibility of current antivirals, Zanamivir and Ostelamivir using this microarray and coul

49 lecular dynamics simulations of oseltamivir, zanamivir and peramivir bound to H7N9, H7N9-R292K, and a

50 uencies (104/2698, 3.85%) and caused reduced zanamivir and peramivir inhibition.

51 nM) but were sensitive to the NA inhibitors zanamivir and peramivir.

52 examined were susceptible to oseltamivir and zanamivir and resistant to adamantane antiviral medicati

53 NHBE cells in the presence of oseltamivir or zanamivir and that virus with the H274Y NA substitution

54 NHBE cells in the presence of oseltamivir or zanamivir and the fitness advantage of rg-H274Y over rg-

55 rmediates, two potent anti-influenza agents, zanamivir and zanaphosphor, were synthesized in 50% and

56 e literature on the efficacy of oseltamivir, zanamivir, and baloxavir prophylaxis for influenza in lo

57 ate receptor binding even in the presence of zanamivir, and it differs from the second receptor bindi

58 to the currently approved NAIs oseltamivir, zanamivir, and peramivir by assessing recombinant viruse

59 ith reduced inhibition by NAIs (oseltamivir, zanamivir, and peramivir): (i) novel subtype-specific su

60 We produced a MEDI8852-zanamivir antibody-drug conjugate (ADC) that engages Fc-

61 such as anti-influenza drugs oseltamivir and zanamivir, are major sialidase inhibitors.

62 enza before and after the rollout of inhaled zanamivir as the first-line antiviral in Taiwan.

63 4-GU-DANA (zanamivir) (as well as DANA and 4-AM-DANA) was found to

64 nges, the sensitivity of the mutant virus to zanamivir assessed by a standard test in MDCK cells was

65 It closes upon zanamivir binding.

66 The receptor analog, zanamivir, blocks receptor binding and cleavage activiti

67 -2009 NA reduced efficacy of oseltamivir and zanamivir by 45 and 10 times, (1) respectively.

68 sal spray plus 10 mg by inhalation, 10 mg of zanamivir by inhalation plus placebo spray, or placebo b

69 signed to one of three treatments: 6.4 mg of zanamivir by intranasal spray plus 10 mg by inhalation,

70 ance of influenza virus to amantadine and to zanamivir, by use of the ferret model of influenza virus

71 These results suggest that zanamivir can significantly reduce the duration and over

72 The MEDI8852-zanamivir conjugate extends the circulatory half-life of

73 The MEDI8852-zanamivir conjugate protected mice from a lethal (10 x L

74 CD388 is a novel multivalent zanamivir conjugate that is stably linked to a proprieta

75 Oseltamivir or zanamivir could provide some benefit but low statistical

76 CD388 improves the antiviral activity of zanamivir, demonstrating potent, universal activity acro

77 ral prophylaxis, particularly oseltamivir or zanamivir, despite acknowledging the inadequate supporti

78 ON: Time to clinical response to intravenous zanamivir dosed at 600 mg was not superior to oseltamivi

79 e (NA) inhibitors (BCX-1812, oseltamivir, or zanamivir), drug-resistant variants of influenza A virus

80 rus, the HN receptor avidity is increased by zanamivir, due to activation of a second site that has h

81 Individuals given oseltamivir or zanamivir experienced the fewest symptomatic, test-confi

82 stments for renal impairment yielded similar zanamivir exposures.

83 y or FA-2 and the highest IC(50) values with zanamivir; FA-2 showed the highest values with oseltamiv

84 immunocompromised child with oseltamivir and zanamivir for A(H1N1)pdm09 virus infection led to the em

85 A double-blind, randomized study of inhaled zanamivir for the prevention of influenza in families wa

86 e-blind, placebo-controlled study of inhaled zanamivir for the treatment and prevention of influenza

87 B/Yamagata/88 virus and given the antiviral zanamivir (GG167) intranasally as prophylaxis or early t

88 The sialic acid analogue zanamivir (GG167) is a selective inhibitor of influenza

89 to 1.06) did not differ between the inhaled zanamivir group (n = 595 897, 68.9%, the reference) and

90 9 to 0.75; p=0.25) in the 300 mg intravenous zanamivir group and 5.63 days (difference of -0.48 days,

91 ature and incidence of adverse events in the zanamivir group did not differ from placebo.

92 whom influenza developed was smaller in the zanamivir group than in the placebo group (4 percent vs.

93 tion of symptoms was 2.5 days shorter in the zanamivir group than in the placebo group (5.0 vs. 7.5 d

94 ponse of 5.14 days in the 600 mg intravenous zanamivir group, the median time to clinical response wa

95 tion of major symptoms was four days in both zanamivir groups and seven days in the placebo group (P<

96 However, because of its small size, zanamivir has a short half-life and requires repeated do

97 imentally directly to the respiratory tract, zanamivir has potent antiviral effects.

98 Inhaled zanamivir has shown benefit in treating acute influenza

99 ith neuraminidase inhibitors (oseltamivir or zanamivir); however, the efficacy of these agents for in

100 the N294S mutation reduced susceptibility to zanamivir (IC(50) increase, >3.0-fold).

101 tion (IC50), and E119D conferred the highest zanamivir IC50.

102 g and neuraminidase, and the receptor mimic, zanamivir, impairs viral entry by blocking receptor bind

103 We assessed the therapeutic activity of zanamivir in adults with acute influenza.

104 ence of the NAIs oseltamivir carboxylate and zanamivir in MDCK cells.

105 er, none exhibited reduced susceptibility to zanamivir in neuraminidase (NA) inhibition assays.

106 owever, data on the effectiveness of inhaled zanamivir in preventing hospitalization and death are la

107 binding of the NA inhibitors oseltamivir and zanamivir in the wild-type and the IR and IRHY mutant st

108 irus clones grew in plaque assays containing zanamivir, indicating possible reduced susceptibility; h

109 Intravenous zanamivir is a neuraminidase inhibitor suitable for trea

110 Zanamivir is approved for children >7 years of age, and

111 Zanamivir is delivered by inhalation because of its low

112 Inhaled zanamivir is not inferior to oral oseltamivir as outpati

113 h-risk subgroups further showed that inhaled zanamivir is not inferior to oral oseltamivir in either

114 nt of family members with once-daily inhaled zanamivir is well tolerated and prevents the development

115 the influenza virus neuraminidase inhibitor zanamivir, linked to a CH1-Fc hybrid domain of human IgG

116 Inhaled zanamivir may lead to shorter symptom duration (23 hours

117 Therapy with oral oseltamivir and inhaled zanamivir may provide a net benefit over no treatment of

118 hundred thirty patients received intravenous zanamivir (median, 5 days; range, 1-11) a median of 4.5

119 V than VHH(kappa)-Zan carrying only a single zanamivir molecule.

120 ation of a VHH(kappa) adduct modified with 4 zanamivir molecules (VHH(kappa)-Zan(4)) was ~10-fold mor

121 produced VHH(kappa) adducts with 1, 2, or 4 zanamivir molecules attached in a site-specific manner,

122 domly assigned to receive 300 mg intravenous zanamivir (n=201), 600 mg intravenous zanamivir (n=209),

123 venous zanamivir (n=201), 600 mg intravenous zanamivir (n=209), or 75 mg oral oseltamivir (n=205) twi

124 an identical single course of treatment with zanamivir, no evidence of reduced susceptibility was dem

125 A comparison of sensitivity to zanamivir of a panel of influenza A and B viruses using

126 The effects of oseltamivir, peramivir, or zanamivir on mortality compared with placebo or standard

127 Zanamivir, on the other hand, binds to the active site o

128 iviral therapy (rimantadine, oseltamivir, or zanamivir or no treatment) should infection develop.

129 ncluded all outpatients treated with inhaled zanamivir or oral oseltamivir within 48 hours after a cl

130 Contacts received either 10 mg zanamivir or placebo inhaled once daily for 10 days.

131 randomly assigned to receive either inhaled zanamivir or placebo.

132 dase inhibitors (ie, oseltamivir, peramivir, zanamivir, or laninamivir) or an endonuclease inhibitor

133 resistance to NAIs (oseltamivir carboxylate, zanamivir, or peramivir) as determined using a fluoresce

134 (NHBE) cells in the presence of oseltamivir, zanamivir, or peramivir.

135 was determined in complex with oseltamivir, zanamivir, or sialic acid, and structural analysis was p

136 ays) to receive 300 mg or 600 mg intravenous zanamivir, or standard-of-care (75 mg oral oseltamivir)

137 mg intravenous zanamivir, 600 mg intravenous zanamivir, oseltamivir) were diarrhoea (10 [5%], 15 [7%]

138 Zanamivir, oseltamivir, laninamivir, and baloxavir might

139 Zanamivir, oseltamivir, laninamivir, and baloxavir proba

140 Zanamivir, oseltamivir, laninamivir, and baloxavir proba

141 by our search, 33 trials of six antivirals (zanamivir, oseltamivir, laninamivir, baloxavir, amantadi

142 Post-exposure prophylaxis with zanamivir, oseltamivir, laninamivir, or baloxavir might

143 Post-exposure prophylaxis with zanamivir, oseltamivir, laninamivir, or baloxavir probab

144 sted NAIs (827-, 25-, 286-, and 702-fold for zanamivir, oseltamivir, peramivir, and laninamivir, resp

145 oseltamivir but still strongly inhibited by zanamivir owing to an altered hydrophobic pocket in the

146 the 88 patients given inhaled and intranasal zanamivir (P=0.02) and the 85 patients given inhaled zan

147 inhibition by 4 NA inhibitors: oseltamivir, zanamivir, peramivir, and laninamivir.

148 d NA inhibition (NI) assay with oseltamivir, zanamivir, peramivir, and laninamivir.

149 ions (oseltamivir PP: 0.7%, 95%CI: 0.1-4.7%, zanamivir PP: 3.0%, 95%CI: 0.9-9.4%) and ILIs (oseltamiv

150 ILIs (oseltamivir PP: 2.8%, 95%CI: 1.8-4.3%, zanamivir PP: 3.4%, 95%CI: 1.3-7.2%).

151 Treatment with zanamivir prevented the infection and abrogated the loca

152 Zanamivir provided protection against both influenza A a

153 e influenza A prophylaxis studies, 15% of 61 zanamivir recipients versus 61% of 33 placebo recipients

154 A early treatment trial, 32% of 31 infected zanamivir recipients versus 73% of 26 infected placebo r

155 Zanamivir reduced nights of disturbed sleep, time to res

156 ulation with or without influenza infection, zanamivir reduced the median number of days to reach thi

157 In a model of lethal challenge in mice, zanamivir reduces lung titers of the virus and decreases

158 idase (NA) inhibitors, either oseltamivir or zanamivir, reduces the duration of symptoms, the duratio

159 No fatalities were considered zanamivir related.

160 Zanamivir (Relenza) and oseltamivir (Tamiflu), the two c

161 Oseltamivir (Tamiflu) and zanamivir (Relenza) are two currently used neuraminidase

162 sion/1/18 H1N1) and that of its complex with zanamivir (Relenza) at 1.65-A and 1.45-A resolutions, re

163 ected patients are oseltamivir (Tamiflu) and zanamivir (Relenza), both of which target the neuraminid

164 (NA) inhibitors, oseltamivir (Tamiflu), and zanamivir (Relenza).

165 ntiviral agents are amantadine, rimantadine, zanamivir [Relenza, Glaxo Wellcome, Inc., Research Trian

166 minidase and hemagglutinin genes revealed no zanamivir-resistant variants.

167 wer affinity for oseltamivir carboxylate and zanamivir, respectively, compared with wild-type NA.

168 4Y, rg-N294S, and rg-R371K, N2 numbering) or zanamivir (rg-E119A and rg-R371K) failed to be inhibited

169 individuals at high risk of severe disease (zanamivir: risk ratio 0.35, 95% CI 0.25-0.50; oseltamivi

170 Zanamivir should be considered as first-line therapy for

171 A combination of favipiravir and zanamivir successfully cleared influenza B infection in

172 t comparison of oral oseltamivir and inhaled zanamivir suggests no important differences in key outco

173 njugate extends the circulatory half-life of zanamivir, targets both influenza HA and NA, and shows e

174 315675 and >175-fold-lower susceptibility to zanamivir than did wild-type virus, but it retained a hi

175 ylate and a 175-fold-lower susceptibility to zanamivir than did wild-type virus.

176 nfluenza virus B, and was more variable with zanamivir than was the CL assay.

177 d an E119D NA mutation was identified during zanamivir therapy.

178 ite-specific conjugation of the NA inhibitor zanamivir to MEDI8852, an HA-specific fully human monocl

179 pressing cells in the presence of 4-GU-DANA (zanamivir) to release target cells bound only by HN-rece

180 tion of a selective neuraminidase inhibitor, zanamivir, to the respiratory tract is safe and reduces

181 t had a growth preference over the parent in zanamivir-treated animals.

182 Pooled virus shed by zanamivir-treated ferrets was used to infect another gro

183 s rapidly produces antiviral resistance, but zanamivir use does not, although nucleotide changes were

184 IC(50) values for zanamivir using the NA-STAR were in the range 1.0-7.5 nM

185 Four percent of zanamivir versus 19% of placebo households (P<.001) had

186 the influenza B prophylaxis trial, 16% of 25 zanamivir versus 44% of 9 placebo recipients showed abno

187 erse events with oseltamivir, peramivir, and zanamivir (very low certainty evidence).

188 Efficacy in reducing pathogenicity for zanamivir was 52% (95% CI: 19, 72) and 56% (95% CI: 14,

189 Zanamivir was 67% efficacious (95% confidence interval [

190 We studied whether intravenous zanamivir was a suitable treatment in this setting.

191 tcomes, high-quality evidence indicated that zanamivir was associated with the shortest TTAS (hazard

192 sessed were associated with shortening TTAS; zanamivir was associated with the shortest TTAS, and bal

193 IAP or the antiviral neuraminidase inhibitor zanamivir was therapeutic by maintaining IAP abundance a

194 Zanamivir was well tolerated and was effective in preven

195 Zanamivir was well tolerated.

196 The topically administered zanamivir was well tolerated.

197 gs in the group given inhaled and intranasal zanamivir were significantly lower than those in the pla

198 n total, 487 households (242 placebo and 245 zanamivir) were enrolled, with 1291 contacts randomly as

199 gs indicate that the neuraminidase inhibitor zanamivir, which is effective in reducing experimental i

200 able neuraminidase inhibitors are limited to zanamivir, which is topically administered.

201 d treatment with the neuraminidase inhibitor zanamivir, which suggests that such models may prove use

202 of isolates from phase 2 clinical studies of zanamivir, which were undetectable in the fluorogenic as

203 uch compounds achieve half-life extension of zanamivir, while recruiting polyclonal immunoglobulins o

204 by conjugating the neuraminidase inhibitor, zanamivir, with the highly immunogenic hapten, dinitroph

205 In particular, the caffeic acid (CA)-bearing zanamivir (ZA) conjugates ZA-7-CA (1) and ZA-7-CA-amide

206 ntly conjugating multiple copies of the drug zanamivir (ZA; the active ingredient in Relenza) via a f

207 te as those of other NAIs, oseltamivir (OS), zanamivir (ZAN), and peramivir, and may share common res

208 aminidase that bind the antiviral inhibitors zanamivir (ZANA) and 2-deoxy-2,3-didehydro-N-acetylneura