コーパス検索結果 (1語後でソート)
通し番号をクリックするとPubMedの該当ページを表示します
1 treatment trials the anti-(IL-5) therapeutic Mepolizumab).
2 ly to achieve important asthma outcomes with mepolizumab.
3 d by 61% in the group receiving subcutaneous mepolizumab.
4 racteristics associated with the response to mepolizumab.
5 152 to 250 mg mepolizumab, and 156 to 750 mg mepolizumab.
6 rences among groups given different doses of mepolizumab.
7 al of 3 infusions) of 0.55, 2.5, or 10 mg/kg mepolizumab.
8 ied; they mostly focused on benralizumab and mepolizumab.
9 AERD patients before and after dupilumab and mepolizumab.
10 rbation and FEV(1) value than omalizumab and mepolizumab.
11 as broad anti-inflammatory effects on top of mepolizumab.
12 ect, improved when treatment was switched to mepolizumab.
13 nts with benralizumab and EGPA patients with mepolizumab.
14 d benralizumab and 26% of those who received mepolizumab.
15 k persisted in certain patients treated with mepolizumab.
16 The patient was treated successfully with mepolizumab.
17 and epithelial alarmins even when stable on mepolizumab.
18 rates and lung function than benralizumab or mepolizumab.
19 -19.71, -8.75) following the treatment with mepolizumab.
20 patients with EGPA experienced benefit with mepolizumab.
21 No deaths were attributed to mepolizumab.
22 associated with a poor clinical response to mepolizumab.
23 s, none of which were assessed as related to mepolizumab.
24 n the bronchial mucosa, was maintained after mepolizumab.
25 th after a single intravenous 750-mg dose of mepolizumab.
26 adjusted incidence rate ratios: dupilumab vs mepolizumab, 0.28 [95% CI = 0.09-0.84]; dupilumab vs oma
30 o receive a subcutaneous injection of either mepolizumab 100 mg or placebo, plus standard of care, ev
32 ouble-blind, parallel-group trials comparing mepolizumab (100 mg in METREX, 100 or 300 mg in METREO)
33 II trial, MEA115575) where subjects received mepolizumab (100 mg, n = 9) or placebo (n = 8), as six m
34 events occurred in seven patients receiving mepolizumab (14 events, including one death; mean [+/-SD
35 : 159 were assigned to placebo, 154 to 75 mg mepolizumab, 152 to 250 mg mepolizumab, and 156 to 750 m
37 tients were randomized (1:1) to subcutaneous mepolizumab (300 mg) or placebo every 4 weeks for 32 wee
38 1:1 ratio to receive benralizumab (30 mg) or mepolizumab (300 mg) subcutaneously every 4 weeks for 52
39 reduced from 1.91 with placebo to 1.01 with mepolizumab (47% reduction; rate ratio [RR] 0.53, 95% CI
40 cells per muL were randomly assigned 1:1 to mepolizumab (6-11 years: 40 mg; 12-17 years: 100 mg) or
43 to receive one of three doses of intravenous mepolizumab (75 mg, 250 mg, or 750 mg) or matched placeb
46 ed in BAL post SBP-Ag (299), decreased after mepolizumab (99), and increased in sputum after WLAC (36
52 ic phenotype may benefit from treatment with mepolizumab, a monoclonal antibody directed against inte
54 ion of eosinophilic airway inflammation with mepolizumab-a monoclonal antibody against interleukin 5-
56 t report of a case of severe asthma in which mepolizumab administration reversed the clinical deterio
62 ovided evidence for the clinical benefits of mepolizumab, an anti-IL-5 biologic, in severe asthma.
63 the hypereosinophilic syndrome have received mepolizumab, an anti-IL-5 monoclonal antibody, for as lo
68 n children with EoE and whether therapy with mepolizumab, an antibody against IL-5, reduces the numbe
75 nal sample size for MAIC of benralizumab vs. mepolizumab and benralizumab vs. dupilumab, respectively
77 to 61) among patients receiving intravenous mepolizumab and by 53% (95% CI, 37 to 65) among those re
78 ed by 32% in the group receiving intravenous mepolizumab and by 61% in the group receiving subcutaneo
79 alizumab demonstrated efficacy comparable to mepolizumab and dupilumab for OCS dosage reduction, OCS
84 ive insight into the differential effects of mepolizumab and omalizumab on the immunometabolic kineti
86 be better predictors of clinical response to mepolizumab and omalizumab, than IL-5 or IgE, the target
88 dge from this journey extended to the use of mepolizumab and other biologics across a broad spectrum
90 an on-treatment serious adverse event in the mepolizumab and placebo groups, respectively; the most c
91 vated in responders versus non-responders to mepolizumab and plasma CXCL10 levels were differentially
97 the therapeutic niche of anti-interleukin-5 (mepolizumab) and anti-CD52 (alemtuzumab) antibody therap
98 in severe asthma that are suppressed by IL5 (mepolizumab) and IL5 receptor (benralizumab) blockade.
101 frequency, corticosteroid-sparing effect of mepolizumab, and development of antimepolizumab antibodi
102 linically important thresholds, tezepelumab, mepolizumab, and dupilumab achieved a >99% probability o
103 to compare the effectiveness of omalizumab, mepolizumab, and dupilumab in individuals with moderate-
104 ore and after administering a single dose of mepolizumab (anti-IL-5 monoclonal antibody) to reduce ai
105 -controlled clinical trial that demonstrated mepolizumab (anti-IL-5) reduced exacerbations and blood
109 i-IgE (omalizumab) and anti-IL-5 antibodies (mepolizumab), are used in the treatment of severe pediat
110 d severe asthma, biologic therapies, such as mepolizumab, are increasingly used to control disease.
112 These results add to and support the use of mepolizumab as a favourable add-on treatment option to s
113 ks was achieved in 95% of patients receiving mepolizumab, as compared with 45% of patients receiving
115 37 to 65) among those receiving subcutaneous mepolizumab, as compared with those receiving placebo (P
116 mboxane levels were lower in subjects taking mepolizumab, as were urinary levels of tetranor-prostagl
118 py were assigned, in a 1:1 ratio, to receive mepolizumab (at a dose of 100 mg) or placebo subcutaneou
119 ompared the glucocorticoid-sparing effect of mepolizumab (at a dose of 100 mg) with that of placebo a
122 will examine how evidence generated from the mepolizumab clinical development program showed that blo
123 cantly lower among participants treated with mepolizumab compared with placebo (58% lower, 0.35% diff
134 Patients received 100 mg of subcutaneous mepolizumab every 4 weeks plus standard of care until a
136 depleted in asthma patients using anti-IL-5 (mepolizumab), followed by a challenge with rhinovirus-16
138 nt, mean difference between benralizumab and mepolizumab for OCS reduction was 6.08% (95% CI -22.22-3
140 t, approval, and real-world effectiveness of mepolizumab for the treatment of patients with severe eo
141 y miss airway eosinophilic inflammation, and mepolizumab frequently fails to normalize airway eosinop
142 95% CI 31-61%; p<0.0001), 1.46 in the 250 mg mepolizumab group (39% reduction, 19-54%; p=0.0005), and
143 Baseline eosinophil count was highest in the mepolizumab group (405 cells/mcL) and lowest for omalizu
144 year in the placebo group, 1.24 in the 75 mg mepolizumab group (48% reduction, 95% CI 31-61%; p<0.000
145 n, 19-54%; p=0.0005), and 1.15 in the 750 mg mepolizumab group (52% reduction, 36-64%; p<0.0001).
146 5 person years (1.32 per person year) in the mepolizumab group (adjusted incidence rate ratios: dupil
148 cantly greater proportion of patients in the mepolizumab group compared with the placebo group no lon
149 d-dose stratum was 2.39 times greater in the mepolizumab group than in the placebo group (95% confide
150 type (462 patients) was 1.40 per year in the mepolizumab group versus 1.71 per year in the placebo gr
151 not occur in 47% of the participants in the mepolizumab group versus 81% of those in the placebo gro
152 xacerbations was 1.19 per year in the 100-mg mepolizumab group, 1.27 per year in the 300-mg mepolizum
154 polizumab group, 1.27 per year in the 300-mg mepolizumab group, and 1.49 per year in the placebo grou
155 The annualized relapse rate was 1.14 in the mepolizumab group, as compared with 2.27 in the placebo
156 point was reached in 84% of patients in the mepolizumab group, as compared with 43% of patients in t
157 A total of 44% of the participants in the mepolizumab group, as compared with 7% of those in the p
158 ne in the glucocorticoid dose was 50% in the mepolizumab group, as compared with no reduction in the
159 reduced glucocorticoid dose, patients in the mepolizumab group, as compared with those in the placebo
160 e benralizumab group and 96% of those in the mepolizumab group; serious adverse events were reported
161 s for exacerbations in the 100-mg and 300-mg mepolizumab groups versus the placebo group were 0.80 (9
162 greater in the intravenous and subcutaneous mepolizumab groups, respectively, than in the placebo gr
163 42 points and 0.44 points greater in the two mepolizumab groups, respectively, than in the placebo gr
164 orticoid therapy to maintain asthma control, mepolizumab had a significant glucocorticoid-sparing eff
166 ildren with eosinophilic asthma treated with mepolizumab had significantly lower sputum eosinophils.
173 en-label Long Term Extension Safety Study of Mepolizumab in Asthmatic Subjects, NCT01691859) was an o
174 onducted during 2 clinical trials evaluating mepolizumab in HES, a 32-week randomized placebo-control
175 investigate post hoc the clinical benefit of mepolizumab in patients with EGPA using a comprehensive
177 od eosinophil count and clinical efficacy of mepolizumab in patients with severe eosinophilic asthma
178 the effect of humanized monoclonal antibody mepolizumab in patients with severe eosinophilic asthma
179 valuate the long-term safety and efficacy of mepolizumab in patients with severe eosinophilic asthma
181 biomarker for the efficacy of treatment with mepolizumab in patients with severe eosinophilic asthma.
183 f an anti-interleukin-5 monoclonal antibody, mepolizumab, in patients with the hypereosinophilic synd
188 Seventy-eight subjects received 1 to 66 mepolizumab infusions each (including mepolizumab infusi
189 to 66 mepolizumab infusions each (including mepolizumab infusions received in the placebo-controlled
190 ized for eosinophil numbers, received 750 mg mepolizumab intravenously in a placebo-controlled double
196 lizumab (MD -16.09 [95% CI -19.88, -12.30]), mepolizumab (MD -12.89 [95% CI -16.58, -9.19], ASA-D (MD
201 n-gamma, intravenous immunoglobulins (IVIG), mepolizumab, methotrexate (MTX), omalizumab, upadacitini
202 children treated with 0.55, 2.5, or 10 mg/kg mepolizumab monthly for 12 weeks followed by no treatmen
203 were followed for 18 months after initiating mepolizumab (n = 36) or Omalizumab (n = 20) treatment.
205 misation criteria, were randomly assigned to mepolizumab (n=146) or placebo (n=144), and were include
206 us adverse events in the overall population, mepolizumab (odds ratio, 0.67; 95% CI, 0.48 to 0.92) and
209 d exacerbations with dupilumab versus either mepolizumab or benralizumab and also with tezepelumab ve
214 Patients received 750 mg of intravenous mepolizumab or placebo every 4 weeks for a total of 6 do
215 with severe eosinophilic asthma treated with mepolizumab or placebo in addition to standard of care f
217 lone or prednisone dose to receive 300 mg of mepolizumab or placebo, administered subcutaneously ever
218 th severe asthma before and after anti-IL-5 (mepolizumab) or anti-IL-5Ralpha (benralizumab) therapy.
221 After directly switching from omalizumab to mepolizumab, patients with uncontrolled severe eosinophi
231 flammatory pathways (IL-5R and IL-5), namely mepolizumab, reslizumab, and benralizumab, are effective
233 sinophilic granulomatosis with polyangiitis, mepolizumab resulted in significantly more weeks in remi
239 Findings from previous studies showed that mepolizumab significantly reduces the rate of exacerbati
240 differentially expressed sputum proteins pre-mepolizumab, stable on mepolizumab, and at exacerbation.
241 philic chronic rhinosinusitis received 100mg mepolizumab subcutaneously at four-weekly intervals for
242 rticipated in a randomized clinical trial of mepolizumab (substudy of a larger GSK sponsored global p
243 ml greater in patients receiving intravenous mepolizumab than in those receiving placebo (P=0.02) and
244 l greater in patients receiving subcutaneous mepolizumab than in those receiving placebo (P=0.03).
245 evere asthma who switched from omalizumab to mepolizumab therapy and achieved good control over her a
246 the underlying mechanisms of omalizumab and mepolizumab therapy are distinct, it is recommended to u
247 eosinophils per high-power field [hpf] after mepolizumab therapy), and 77% of all subjects had decrea
248 ction in the number of symptomatic flares on mepolizumab therapy, and 1 participant withdrew before s
252 recent phase III trial (NCT02020889) 53% of mepolizumab-treated versus 19% of placebo-treated patien
254 opical corticosteroids who required surgery, mepolizumab treatment led to a greater reduction in the
256 Exploratory end points included effects of mepolizumab treatment on other cell lineages (numbers an
257 ch can explain the differences observed with Mepolizumab treatment over 18 months and significantly c
261 responsiveness of airway inflammation after mepolizumab treatment to find potentially treatable infl
263 In Case 1, nasal symptoms persisted despite mepolizumab treatment, and CRS recurred early after endo
266 a similar pattern following benralizumab and mepolizumab treatment, the lack of correlation between A
271 humanized, monoclonal antibody against IL-5 (mepolizumab) using a randomized double-blind, placebo-co
272 es were lower for tezepelumab, dupilumab and mepolizumab versus benralizumab; and with eosinophils< 1
273 ithdrawing from the study was 50% lower with mepolizumab versus placebo (15 of 54 [28%] vs 30 of 54 [
274 sought to assess the efficacy and safety of mepolizumab versus placebo for severe bilateral nasal po
276 patients experienced clinical benefit 1 with mepolizumab versus placebo in the blood eosinophil count
278 7 patients (mepolizumab: 206; placebo: 201), mepolizumab versus placebo reduced the risk of being inc
283 on of which were headache (in 45 [16%] given mepolizumab vs 59 [21%] given placebo) and nasopharyngit
285 ma control and quality of life improved with mepolizumab vs placebo in both studies independent of pr
288 n vivo, reduction of EOS in the airway using mepolizumab was associated with diminished IL-17 express
290 n rate reduction favouring benralizumab over mepolizumab was observed, although it was not statistica
294 In a small cohort of participants with EAE, mepolizumab was unsuccessful in substantially reducing c
296 line blood eosinophil counts and efficacy of mepolizumab we did a secondary analysis of data from two
297 ts with severe eosinophilic asthma receiving mepolizumab were compared with those from 31 individuals
298 In a difficult asthma cohort, Omalizumab and Mepolizumab were used in distinct clinical phenotypes bu
299 s were significantly elevated in children on mepolizumab who had exacerbations, suggesting that eosin
300 peutic options include the anti-IL5 antibody mepolizumab, whose efficacy has been described in small