ライフサイエンスコーパス: anakinra

1 systemic administration of IL-1R antagonist (anakinra).

2 IL-1beta signaling (canakinumab, rilonacept, anakinra).

3 nse to recombinant IL-1 receptor antagonist (anakinra).

4 re colitis with IL-1 receptor blockade using anakinra.

5 evation of markers of inflammation should be anakinra.

6 lasts (CAFs), and this effect was blocked by anakinra.

7 ing treatment with the interleukin-1 blocker anakinra.

8 atory disease but that also responds well to anakinra.

9 rapidly and completely during treatment with anakinra.

10 ells, which was abrogated by the addition of anakinra.

11 e recombinant human IL-1 receptor antagonist anakinra.

12 ebo and then were randomized to all doses of anakinra.

13 ng Abs to IL-1beta and the rIL-1R antagonist anakinra.

14 eukin-1beta are rilonacept, canakinumab, and anakinra.

15 by administration of the recombinant IL-1Ra, anakinra.

16 th the interleukin-1 receptor blocking agent anakinra.

17 lacement therapy with the recombinant IL-1Ra anakinra.

18 sham operation) and were treated with either anakinra 1 mg/kg or NaCl 0.9% (saline).

19 The ACR20 response rate in the anakinra 1.0-mg/kg (46%; P = 0.001) and 2.0-mg/kg (38%;

20 and 22 mice treated with increasing doses of anakinra (1 mg/kg [n=6], 10 mg/kg [n=6], and 100 mg/kg [

21 harge, to daily subcutaneous injections with anakinra 100 mg for 2 weeks, 12 weeks, or placebo.

22 th the interleukin-1 receptor blocking agent anakinra 100 mg/d was started.

23 RA were randomly assigned to receive either anakinra (100 mg) or placebo treatment (4:1 anakinra-to-

24 riod of 1 wk, the protocol was repeated with anakinra (100 mg/d) subcutaneously.

25 These patients were then treated with anakinra (100 mg/day subcutaneously) for 12 weeks, and t

26 f-dosage etanercept (25 mg once weekly) plus anakinra (100 mg/day) for 6 months in a double-blind stu

27 -dosage etanercept (25 mg twice weekly) plus anakinra (100 mg/day), or half-dosage etanercept (25 mg

28 mice pretreated with either IL-1R antagonist anakinra (100 mg/kg per day) or vehicle alone (control)

29 were randomly assigned to daily subcutaneous anakinra, 100 mg (n = 25), or placebo (n = 25) for 4 wee

30 HF at 24 weeks was 6%, 31%, and 30%, in the anakinra 12-week, anakinra 2-week, and placebo groups, r

31 s no significant changes occurred within the anakinra 2-week or placebo groups.

32 s 6%, 31%, and 30%, in the anakinra 12-week, anakinra 2-week, and placebo groups, respectively (log-r

33 randomized to receive treatment with topical anakinra, 2.5% (n = 30), anakinra, 5% (n = 15), or vehic

34 weeks of therapy, participants treated with anakinra, 2.5%, achieved a 46% reduction in their mean C

35 By week 12, treatment with anakinra, 2.5%, and treatment with anakinra, 5%, led to

36 Treatment with topical anakinra, 2.5%, for 12 weeks was safe and significantly

37 noted in 8 of 28 patients (29%) treated with anakinra, 2.5%, vs in 2 of 29 patients (7%) treated with

38 ent of small TAAs, WT mice were treated with anakinra 3 days after TAA induction.

39 Patients received subcutaneous injections of anakinra (30, 75, or 150 mg) once daily.

40 atment with topical anakinra, 2.5% (n = 30), anakinra, 5% (n = 15), or vehicle (1% carboxymethylcellu

41 ed with baseline); participants treated with anakinra, 5%, achieved a 17% reduction in their mean CFS

42 ment with anakinra, 2.5%, and treatment with anakinra, 5%, led to significant reductions in symptoms

43 TAA formation (control: 99.2+/-15.5% versus anakinra: 68.3+/-19.2%; P<0.005).

44 n monoclonal anti-interleukin-1 antibody, or anakinra, a human interleukin-1 receptor antagonist, imp

45 The effects of arterially perfused anakinra, a human recombinant IL-1beta receptor antagoni

46 -associated MAS dramatically benefiting from anakinra, a recombinant IL-1 receptor antagonist, but th

47 Antagonizing IL-1beta with Anakinra, a rheumatoid arthritis therapeutic, prevented

48 trate here that the IL-1 receptor antagonist anakinra abrogates IL-22 production and reduces tumor gr

49 nts treated with full-dosage etanercept plus anakinra achieved an ACR 50% response, compared with 41%

50 cebo or 0.04, 0.1, 0.4, 1.0, or 2.0 mg/kg of anakinra administered in a single, daily, subcutaneous i

51 ing ischemia in the mouse and one of delayed anakinra administration 24 hours after ischemia in the r

52 mal studies were conducted: one of immediate anakinra administration during ischemia in the mouse and

53 patients, respectively, who continued taking anakinra (all dose groups) and in 20% and 1% of patients

54 Anakinra also increased Aspergillus-induced LC3 recruitm

55 Here we show that mice treated with anakinra, an antagonist of the interleukin (IL)-1beta re

56 Anakinra, an IL-1 receptor antagonist protein, inhibited

57 A 100% clinical resolution was achieved with anakinra, an IL-1 receptor antagonist.

58 leukin-1 (IL-1), we treated the patient with anakinra, an IL-1 receptor antagonist.

59 Anakinra, an IL-1R antagonist, blocked the IL-31 effects

60 monstrated that intra-articular injection of Anakinra, an IL-1R antagonist, improved range of movemen

61 Importance: Anakinra, an interleukin 1beta recombinant receptor anta

62 We investigated the effects of anakinra, an interleukin-1 receptor antagonist, on coron

63 latelet-derived growth factor receptors, and anakinra, an interleukin-1 receptor antagonist, respecti

64 were partially attenuated by treatment with anakinra, an interleukin-1 receptor antagonist.

65 ith identifiable CIAS1 mutations) to receive anakinra, an interleukin-1-receptor antagonist (1 to 2 m

66 nd IL-18, using the IL-1 receptor antagonist anakinra and anti-IL-18 antibodies, conferred complete p

67 h persistently active RA, the combination of anakinra and MTX was safe and well tolerated and provide

68 were 42.8 (13.8) and 36 (11.3) years in the anakinra and placebo groups, respectively.

69 The 28-day survival was similar in both anakinra and placebo-treated non-hepatobiliary dysfuncti

70 production with the IL-1 receptor antagonist anakinra and the IL-6 receptor blocker tocilizumab.

71 % CI -0.11 to 0.14; p=0.86), and between the anakinra and the placebo groups at 9 months was 0.02 nmo

72 ultimately treated with recombinant IL-1Ra, anakinra, and experienced significant clinical improveme

73 umab), the interleukin-1 receptor antagonist anakinra, and to a much lesser extent the CD20 inhibitor

74 children for interleukin-1 receptor agonist (Anakinra), antiinterleukin-6 receptor antibody (MRA), an

75 lacebo arm compared with 67% (6 of 9) of the anakinra arm (P = .04).

76 f the placebo arm and in 78% (7 of 9) of the anakinra arm (P = .04).

77 o a new HS exacerbation was prolonged in the anakinra arm by log-rank test (log rank, 6.137; P = .01)

78 by peripheral blood mononuclear cells in the anakinra arm was decreased, and the production of interl

79 Anakinra as first-line therapy for systemic JIA was asso

80 Patients with systemic JIA receiving anakinra as part of initial disease-modifying antirheuma

81 ypertrophy could be reversed with the use of Anakinra as well as an IGF1 neutralizing antibody.

82 Pretreatment of WT mice with anakinra attenuated TAA formation (control: 99.2+/-15.5%

83 hat of the classic IL-1 receptor antagonist (anakinra), because low concentrations were optimal for i

84 be specifically attributable to IL-1 because anakinra blocked the upregulation of different endotheli

85 Subjects received 100 mg anakinra by subcutaneous injection for 84 days, followed

86 ane and infra-patellar fat pad and therefore Anakinra can likely have an inhibitory effect on fibrobl

87 The effect of anakinra compared with placebo on airway neutrophil coun

88 ce and corticosteroid dependence, the use of anakinra compared with placebo reduced the risk of recur

89 Treatment with anakinra completely resolved the symptoms and lesions.

90 acological inhibition of IL-1R activation by Anakinra corrects transcriptional changes, restores MeCP

91 Furthermore, IL1Ra/anakinra cotreatment inhibited ricin-mediated inflammato

92 of IL-1 (interleukin-1) receptor antagonist (anakinra) could inhibit the inflammatory response and im

93 Blocking IL-1 with the receptor antagonist (anakinra) decreases neutrophil recruitment and T helper

94 Treatment with anakinra did not affect peak Vo2 or VE/Vco2 slope at 2 w

95 Anakinra effectively reduced airway neutrophilic inflamm

96 Further studies are required to assess anakinra efficacy and dosing, and to further delineate d

97 tration of the IL-1beta receptor antagonist, anakinra, efficiently decreased nitric oxide production

98 randomized withdrawal trial (open label with anakinra followed by a double-blind withdrawal step with

99 Peripheral IL-1 inhibition using anakinra for 4 weeks does not result in a clinically sig

100 Objective: To determine the efficacy of anakinra for colchicine-resistant and corticosteroid-dep

101 se observations support the long-term use of anakinra for the treatment of patients with RA.

102 This is the first report of anakinra for treatment of a child with super-refractory

103 ate, 0.11% of patients per year) assigned to anakinra, for an incidence rate difference of -1.95% (95

104 pisodes were observed more frequently in the anakinra group (2.1% versus 0.4% in the placebo group).

105 the placebo group and was not reached in the anakinra group (P <.001).

106 as evaluated in 1,399 patients (1,116 in the anakinra group and 283 in the placebo group; 15 patients

107 rawal due to adverse events was 13.4% in the anakinra group and 9.2% in the placebo group.

108 rse events occurred at a similar rate in the anakinra group and the placebo group (7.7% and 7.8%, res

109 One patient in the anakinra group discontinued treatment because of an adve

110 Patients in the anakinra group had more injection site reactions (68% [1

111 In the anakinra trial, patients in the anakinra group had significantly higher grades of advers

112 serious infection was slightly higher in the anakinra group, no infection was attributed to opportuni

113 er number of injection site reactions in the anakinra group.

114 ts: Eleven patients (7 female) randomized to anakinra had a mean age of 46.5 (SD, 16.3) years; 10 pat

115 TRAPS in whom treatment with etanercept and anakinra had failed, was administered tocilizumab for 6

116 ult Scnn1b-Tg mice with the IL-1R antagonist anakinra had protective effects on neutrophilic inflamma

117 Anakinra has the potential to be an effective and well-t

118 f anti-interleukin therapies, daclizumab and anakinra, have supported a role for these therapies in s

119 atory drugs etanercept (TNFalpha inhibitor), anakinra (IL-1 receptor antagonist), prednisone (NFkappa

120 self-administered subcutaneous injections of anakinra in a cohort of patients with active RA were mai

121 anti-IL-1beta in a prophylactic setting and anakinra in a quasi-therapeutic setting (i.e., when skin

122 was extended to etanercept, adalimumab, and anakinra in addition to the previously covered inflixima

123 ntifying a potential mechanism of action for Anakinra in arthrofibrosis following TKA.

124 s the safety of the IL-1 receptor antagonist anakinra in conjunction with inhaled LPS and (2) to test

125 inical trial of the IL-1 receptor antagonist anakinra in corticosteroid-resistant AIED patients.

126 ta secretion by the IL-1 receptor antagonist anakinra in phagocytes of patients with CGD.

127 ecombinant interleukin-1-receptor antagonist anakinra in the first patient prompted us to test for th

128 The use of anakinra in these patients seemed to be effective, witho

129 ant human interleukin-1 receptor antagonist (anakinra) in experimental acute myocardial infarction.

130 Anakinra induced no significant change in PTF or TBF.

131 by treatment with IL-1R antagonist (IL-1Ra; Anakinra) inhibited colitis acceleration in TLR2/MDR1A d

132 Anakinra is a potential therapeutic candidate for treatm

133 Anakinra is a recombinant version of the human interleuk

134 Despite equivocal results in sepsis trials, anakinra is effective in treating macrophage activation

135 suggest that the favorable safety profile of anakinra is maintained in a high-risk patient population

136 In fact, the IL-1 blocker anakinra is now regarded as standard of care for SJIA pa

137 ebo-controlled safety study demonstrate that anakinra is safe and well tolerated in a diverse populat

138 Anakinra is substantially less costly but is also less e

139 eptor antagonists, the competitive inhibitor anakinra (Kineret) and a potent noncompetitive inhibitor

140 s report, the patients had been treated with anakinra (Kineret), a recombinant human IL-1 receptor an

141 Treatment with anakinra led to the disappearance of neutrophils, but CD

142 Daily injections of anakinra markedly improved clinical and laboratory manif

143 ceived 2 daily subcutaneous doses of 1 mg/kg anakinra (maximum dose, 100 mg) or saline (placebo).

144 ded, these encouraging results indicate that anakinra may be a suitable treatment for fulminant myoca

145 Anakinra, monoclonal antibody to interleukin-6 receptor,

146 mong 46 patients meeting inclusion criteria, anakinra monotherapy was used in 10 patients (22%), whil

147 60% of patients, including 8 of 10 receiving anakinra monotherapy, attained a complete response witho

148 of pericarditis were randomized to continue anakinra (n = 11) or switch to placebo (n = 10) for 6 mo

149 r 12 months and 69 were randomly assigned to anakinra (n=35) or placebo (n=34) daily for 9 months.

150 The primary end point was the effect of anakinra on HS disease severity.

151 needed to validate the effects of prolonged anakinra on peak Vo2 and rehospitalization for HF.

152 dy was to assess the effects of imatinib and anakinra on PTF and TBF in colorectal cancer metastases

153 -type mice treated with the IL-1R antagonist anakinra or anti-IL-1beta.

154 ut) were randomized to a single injection of anakinra or placebo and after 48 hours to the alternativ

155 b or placebo monthly for 12 months or 100 mg anakinra or placebo daily for 9 months.

156 lowed by a double-blind withdrawal step with anakinra or placebo until recurrent pericarditis occurre

157 Within each treatment group (anakinra or placebo), incidence rates were summarized fo

158 andomly assigned to treatment with 100 mg of anakinra or placebo, administered daily by subcutaneous

159 l study cohort, randomized to receive either anakinra or placebo.

160 each were randomized to the group to receive anakinra or the placebo group.

161 g nonfibrillar transthyretin deposition with anakinra or transthyretin siRNA, Pcdh10 protein levels w

162 n injections of an IL-1 receptor antagonist (anakinra) or antibodies to deplete IL-1alpha and IL-1bet

163 Anakinra plus methotrexate showed lower odds compared wi

164 Anakinra pretreatment significantly diminished airway ne

165 Last, the IL-1 receptor antagonist anakinra protected animals against anti-MPO antibody-ind

166 Combination therapy with etanercept plus anakinra provided no treatment benefit over etanercept a

167 Combination therapy with etanercept and anakinra provides no added benefit and an increased risk

168 Anakinra rapidly terminated seizures, prevented their re

169 At 4 weeks, 8% (2 of 25) of anakinra recipients and 20% (5 of 25) of placebo recipie

170 er treatment (post-NL) with the IL-1 blocker anakinra (recombinant IL-1 receptor antagonist, Kineret(

171 Patients treated with anakinra responded rapidly.

172 dition to decreased inflammasome activation, anakinra restored autophagy in CGD mice in vivo, with in

173 ministration of the IL-1 receptor antagonist anakinra restored locomotor function post-SCI.

174 m clinical corticosteroid nonresponders with anakinra resulted in repression of IL-1beta release, sug

175 inflammatory disease, and that blockade with anakinra should be further studied as a treatment for pa

176 At 12 weeks, patients continued on anakinra showed an improvement in peak Vo2 from 14.5 (10

177 In vitro, anakinra significantly prevented apoptosis induced by si

178 ly, we demonstrate that the IL-1R antagonist anakinra significantly reduces CHS responses, as measure

179 rom identical syringes containing placebo or anakinra subcutaneously once daily for 12 weeks.

180 L-18 in patients' serum, and the response to anakinra, suggest that Schnitzler syndrome is associated

181 ytokines before treatment that normalized on anakinra, suggesting a potential pathogenic role for neu

182 The remarkable response of MWS to anakinra suggests that IL-1beta has a fundamental role i

183 Moreover, the IL-1 receptor antagonist anakinra suppressed acute-phase proteins in a patient wi

184 e show that blocking IL-1beta receptors with anakinra, the human recombinant form of the endogenous I

185 After 3 months of anakinra therapy, only 2 of 26 patients (8%) achieved an

186 and an acceptable (>/=30%) response rate to anakinra therapy.

187 nical complications associated with extended anakinra therapy.

188 After anakinra, there was a greater improvement of flow-mediat

189 This may open the door for using anakinra to prevent postischemic cardiac remodeling and

190 anakinra (100 mg) or placebo treatment (4:1 anakinra-to-placebo allocation ratio), with study drug a

191 ted patients in the canakinumab trial and 25 anakinra-treated and 26 placebo-treated patients in the

192 Compared with saline-treated animals, anakinra-treated mice and rats showed signs of more favo

193 ICAM-1 was decreased in IL-1R-deficient and anakinra-treated mice injected with anti-COL7.

194 Similar improvements in anakinra-treated subjects were noted in individual ACR c

195 Anakinra treatment in WT mice with small TAAs reduced ao

196 levels were significantly reduced during the anakinra treatment period compared with those seen after

197 Anakinra treatment resulted in a rapid and sustained imp

198 Subjects tolerated the anakinra treatment well without an increased frequency o

199 During anakinra treatment, 20 of 21 patients (95.2%) experience

200 ased frequency of infections attributable to anakinra treatment.

201 y 14 (control treatment: 89.1+/-18.6% versus anakinra treatment: 59.7+/-25.7%; P=0.01).

202 Design, Setting, and Participants: The Anakinra-Treatment of Recurrent Idiopathic Pericarditis

203 Nov 12, 2010, and April 11, 2011, and in the anakinra trial between Jan 26, 2009, and May 25, 2011.

204 trial were aged 6-45 years and those in the anakinra trial were aged 18-35 years.

205 sites in the USA and Canada and those in the anakinra trial were enrolled at 14 sites across Europe.

206 eated and 26 placebo-treated patients in the anakinra trial were included in the primary analyses.

207 12 months (canakinumab trial) and 9 months (anakinra trial).

208 In the anakinra trial, patients in the anakinra group had signi

209 Withdrawal of anakinra uniformly resulted in relapse within days; retr

210 incidence of serious infectious events with anakinra use was similar between high-risk patients (2.5

211 To evaluate the effect of subcutaneous anakinra versus placebo on fatigue severity in female pa

212 ed intravascular coagulation patients (65.4% anakinra vs 35.3% placebo), with hazard ratio for death

213 Interventions: Anakinra was administered at 2 mg/kg per day, up to 100

214 Treatment with anakinra was associated with a significant reduction in

215 Treatment with anakinra was associated with significant improvement in

216 provement was seen in those patients in whom anakinra was continued for 12 weeks.

217 The durability of the response to anakinra was further demonstrated in an evaluation of th

218 Anakinra was initiated; the patient achieved 100% contro

219 Anakinra was safe and well tolerated.

220 The antiapoptotic effect of anakinra was tested in a primary rat cardiomyocyte cultu

221 In the base case analysis, anakinra was the least effective and least costly strate

222 Anakinra was well tolerated and effective.

223 Topical anakinra was well tolerated compared with vehicle, with

224 Anakinra was well tolerated for 76 weeks.

225 Anakinra was well tolerated over 76 weeks.

226 In 11 patients, anakinra was withdrawn at three months until a flare occ

227 recombinant human IL-1 receptor antagonist (anakinra) was ineffective treatment.

228 7 days, 15 of the 16 mice (94%) treated with anakinra were alive versus 11 of the 20 mice (55%) treat

229 The efficacy and safety of anakinra were previously demonstrated in a double-blind,

230 Canakinumab and anakinra were safe but were not effective as single immu

231 ently decompensated systolic HF treated with anakinra, whereas an improvement was seen in those patie

232 Among patients receiving anakinra who entered the extension phase, the level of i

233 All 18 patients had a rapid response to anakinra, with disappearance of rash.

234 The patient responded to treatment with anakinra within 2 weeks, with resolution of the signs an

235 Administration of anakinra within 24 hours of acute myocardial infarction