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 although with a slightly lower affinity than anakinra.

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

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

7 evation of markers of inflammation should be anakinra.

8 ing treatment with the interleukin-1 blocker anakinra.

9 atory disease but that also responds well to anakinra.

10 gnificantly extended half-life compared with anakinra.

11 32.8%) of subjects, prompting utilization of anakinra.

12 rapidly and completely during treatment with anakinra.

13 e recombinant human IL-1 receptor antagonist anakinra.

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

15 the IL-1 receptor-targeting biological agent anakinra.

16 erleukin-1 (IL1) receptor antagonist (IL1RA) anakinra.

17 the effect of the IL-1beta receptor blocker anakinra.

18 e disease with the IL-1 receptor antagonist, anakinra.

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

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

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

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

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

24 th the interleukin-1 receptor blocking agent anakinra.

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

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

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

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

29 suPAR 6 ng/ml were assigned to subcutaneous anakinra 100 mg once daily for 10 days.

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

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

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

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

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

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

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

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

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

39 e (10 patients) or combined with intravenous anakinra (12 patients).

40 lin (IVIG) (71%), corticosteroids (61%), and anakinra (18%).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

56 Anakinra, a recombinant form of IL-1Ra, is used to treat

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

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

59 ant recipients at 1-hour posttransplant with Anakinra, a US Food and Drug Administration (FDA)-approv

60 Anakinra abolished an increase in AHR.

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

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

63 n MSU-induced peritonitis, whereas equimolar anakinra administered 24 h before MSU challenge was inef

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

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

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

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

68 63 patients received early AIT (30 received anakinra alone and 33 received anakinra plus a glucocort

69 Anakinra also improved outcomes in patients with pericar

70 Anakinra also increased Aspergillus-induced LC3 recruitm

71 Anakinra also significantly reduced brain TTP-induced da

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

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

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

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

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

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

78 malized by administration of anti-IL-beta or anakinra, an inhibitor of IL-1beta signaling.

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

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

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

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

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

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

85 Of these, 65 were treated with anakinra and methylprednisolone and 55 were untreated hi

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

87 Both Anakinra and parthenolide significantly reduced graft in

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

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

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

91 % CI -0.11 to 0.14; p=0.86), and between the anakinra and the placebo groups at 9 months was 0.02 nmo

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

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

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

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

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

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

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

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

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

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

102 Anakinra attenuated browning of white adipose tissue in

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

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

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

106 eptor type 1 (IL-1R1) blockade with the drug anakinra, but not treatment with the glucocorticoid pred

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

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

109 Biologics included adalimumab, anakinra, certolizumab pegol, etanercept, golimumab, inf

110 After 72 h from treatment, anakinra compared to placebo led to a statistically sign

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

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

113 Treatment with anakinra completely resolved the symptoms and lesions.

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

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

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

117 Anakinra decreased serum and muscle expression of IL-6,

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

119 Anakinra delivery additionally attenuated the inflammato

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

121 Anakinra did not result in any difference in time to mec

122 Anakinra effectively reduced airway neutrophilic inflamm

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

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

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

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

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

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

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

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

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

132 [11.5] years) were randomly assigned to the anakinra group (92 patients) or to the SoC group (87 pat

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

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

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

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

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

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

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

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

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

142 creased incidence of anemia was noted in the anakinra group; and hemorrhage in the recombinant human

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

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

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

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

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

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

149 Anakinra, IL-1 receptor antagonist, limited metastasis,

150 All of the patients treated with anakinra improved clinically (P < 0.01), with no deaths,

151 he mitochondrial redox balance to autophagy, anakinra improved the dysregulated proteostasis network

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

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

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

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

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

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

158 00 PAS residues, respectively), with that of anakinra in mice.

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

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

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

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

163 Anakinra increased IFN signaling and survival of CLL cel

164 Anakinra induced no significant change in PTF or TBF.

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

166 with icatibant (bradykinin-B2-antagonist) or anakinra (interleukin-1-antagonist) reduces disease acti

167 Anakinra is a potential therapeutic candidate for treatm

168 Anakinra is a recombinant version of the human interleuk

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

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

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

172 However, anakinra is rapidly cleared from the body and requires d

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

174 Anakinra is substantially less costly but is also less e

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

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

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

178 Anakinra lowered blood lymphocytes and lymph node sizes

179 Daily injections of anakinra markedly improved clinical and laboratory manif

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

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

182 Anakinra, monoclonal antibody to interleukin-6 receptor,

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

184 60% of patients, including 8 of 10 receiving anakinra monotherapy, attained a complete response witho

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

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

187 Anakinra normalized food intake and weight gain, fat and

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

189 An effect of anakinra on patient-reported outcomes was not evident.

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

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

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

193 IRI by blocking IL-1Rsignaling pathways with Anakinra or inflammasome activity with parthenolide prov

194 The 6-h pretreatment with equimolar anakinra or PAS800-IL-1Ra before MSU challenge similarly

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

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

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

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

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

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

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

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

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

204 In cultured A549 lung carcinoma cells, anakinra, PAS600-IL-1Ra, and PAS800-IL-Ra reduced IL-1al

205 A combination of anakinra, pentoxifylline plus zinc provides similar surv

206 (30 received anakinra alone and 33 received anakinra plus a glucocorticoid) at admission, and 65 pat

207 Anakinra plus methotrexate showed lower odds compared wi

208 the association of IL-1 receptor antagonist anakinra plus methylprednisolone in severe COVID-19 pneu

209 Treatment with anakinra plus methylprednisolone may be a valid therapeu

210 uated to investigate the effect of high-dose anakinra plus methylprednisolone on survival.

211 Anakinra pretreatment significantly diminished airway ne

212 Anakinra promoted H2O2-driven autophagy through a xenobi

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

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

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

216 Anakinra rapidly terminated seizures, prevented their re

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

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

219 II clinical trials show promising data with anakinra, recombinant IL-1 receptor antagonist, in patie

220 Blocking the IL-1 receptor with anakinra reduced inflammation and NET release, restored

221 Patients treated with anakinra responded rapidly.

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

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

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

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

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

227 Anakinra significantly decreased TTP-induced cardiac dam

228 In vitro, anakinra significantly prevented apoptosis induced by si

229 Anakinra significantly reduced mortality of mice (P < .0

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

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

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

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

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

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

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

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

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

239 nical complications associated with extended anakinra therapy.

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

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

242 ing IL1RN, revealing the promise of the drug anakinra to treat acute gout flares.

243 vo, the addition of IL-1 receptor antagonist anakinra to whole blood reduced staphylococcal killing,

244 vo, addition of the IL-1 receptor antagonist anakinra to whole blood reduced staphylococcal killing,

245 for clinically licensed antagonists, such as anakinra, to prevent or treat CRPS via blocking IL-1 act

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

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

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

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

250 levels was seen, with a -76% (-87%, -36%) in anakinra-treated patients and -48% (-77%, +14%) in the p

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

252 Anakinra treatment administered at 1-hour posttransplant

253 Anakinra treatment also reversed the established sensiti

254 22.3% with anakinra treatment and 59.2% comparators (hazard ratio,

255 Anakinra treatment in WT mice with small TAAs reduced ao

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

257 Anakinra treatment resulted in a rapid and sustained imp

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

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

260 ased frequency of infections attributable to anakinra treatment.

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

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

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

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

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

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

267 12 months (canakinumab trial) and 9 months (anakinra trial).

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

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

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

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

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

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

274 Treatment with anakinra was associated with a significant reduction in

275 Anakinra was associated with decrease in circulating int

276 Treatment with anakinra was associated with significant improvement in

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

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

279 Anakinra was given at a dose of 100 mg 4 times a day int

280 Anakinra was initiated; the patient achieved 100% contro

281 The effect of anakinra was rapid, as judged by significant decrease of

282 Anakinra was safe and well tolerated.

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

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

285 Anakinra was then administered with minimal toxicity to

286 a levels 3 days post-administration, whereas anakinra was undetectable after 24 h.

287 Anakinra was well tolerated and effective.

288 Topical anakinra was well tolerated compared with vehicle, with

289 Anakinra was well tolerated for 76 weeks.

290 Anakinra was well tolerated over 76 weeks.

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

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

293 7 days, 15 of the 16 mice (94%) treated with anakinra were alive versus 11 of the 20 mice (55%) treat

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

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

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

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

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

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

300 Administration of anakinra within 24 hours of acute myocardial infarction