ライフサイエンスコーパス: zanamivir

1 omized to receive placebo and 553 to receive zanamivir.

2 -fold reduction in the enzyme sensitivity to zanamivir.

3 uperior to oseltamivir or 300 mg intravenous zanamivir.

4 1.5 days or greater with 600 mg intravenous zanamivir.

5 oseltamivir, later combined with intravenous zanamivir.

6 support further investigation of intravenous zanamivir.

7 vir and peramivir and partially resistant to zanamivir.

8 degree of resistance to oseltamivir but not zanamivir.

9 ains are sensitive to oseltamivir and all to zanamivir.

10 idase inhibitors oseltamivir carboxylate and zanamivir.

11 an be inhibited by the small receptor analog zanamivir.

12 person, and have retained susceptibility to zanamivir.

13 rget for the influenza drugs oseltamivir and zanamivir.

14 eased susceptibility to both oseltamivir and zanamivir.

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

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

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

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

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

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

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

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

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

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

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

26 Zanamivir, a neuraminidase inhibitor, has shown promise

27 Zanamivir, a novel neuraminidase inhibitor, is effective

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

29 Zanamivir administered once daily is efficacious and wel

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

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

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

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

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

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

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

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

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

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

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

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

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

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

44 t statistically significantly differ between zanamivir and oseltamivir.

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

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

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

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

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

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

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

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

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

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

55 4-GU-DANA (zanamivir) (as well as DANA and 4-AM-DANA) was found to

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

57 It closes upon zanamivir binding.

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

59 -2009 NA reduced efficacy of oseltamivir and zanamivir by 45 and 10 times, (1) respectively.

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

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

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

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

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

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

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

67 stments for renal impairment yielded similar zanamivir exposures.

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

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

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

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

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

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

74 9 to 0.75; p=0.25) in the 300 mg intravenous zanamivir group and 5.63 days (difference of -0.48 days,

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

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

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

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

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

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

81 Inhaled zanamivir has shown benefit in treating acute influenza

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

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

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

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

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

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

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

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

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

91 Intravenous zanamivir is a neuraminidase inhibitor suitable for trea

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

93 Zanamivir is delivered by inhalation because of its low

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

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

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

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

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

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

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

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

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

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

104 randomly assigned to receive either inhaled zanamivir or placebo.

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

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

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

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

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

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

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

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

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

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

115 Treatment with zanamivir prevented the infection and abrogated the loca

116 Zanamivir provided protection against both influenza A a

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

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

119 Zanamivir reduced nights of disturbed sleep, time to res

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

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

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

123 No fatalities were considered zanamivir related.

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

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

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

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

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

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

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

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

132 4Y, rg-N294S, and rg-R371K, N2 numbering) or zanamivir (rg-E119A and rg-R371K) failed to be inhibited

133 Zanamivir should be considered as first-line therapy for

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

135 315675 and >175-fold-lower susceptibility to zanamivir than did wild-type virus, but it retained a hi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

151 Zanamivir was well tolerated and was effective in preven

152 Zanamivir was well tolerated.

153 The topically administered zanamivir was well tolerated.

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

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

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

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

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

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

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

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

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