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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
27 0.36 [95% CI = 0.12-1.09]; and omalizumab vs mepolizumab, 0.78 [95% CI = 0.32-1.91]).
28                       Biologics use included mepolizumab 1,115 (44.8%), benralizumab 925 (37.1%), oma
29 opulation comprised 274 patients assigned to mepolizumab 100 mg and 277 assigned to placebo.
30 o receive a subcutaneous injection of either mepolizumab 100 mg or placebo, plus standard of care, ev
31 ntinued omalizumab and immediately commenced mepolizumab 100 mg subcutaneously every 4 weeks.
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
36                          Among 407 patients (mepolizumab: 206; placebo: 201), mepolizumab versus plac
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
41 up, results were not significant but favored mepolizumab (60% vs 36%, P = .395).
42                 An open-label pilot study of mepolizumab (700 mg intravenously monthly for 3 months f
43 to receive one of three doses of intravenous mepolizumab (75 mg, 250 mg, or 750 mg) or matched placeb
44 e evaluated long-term safety and efficacy of mepolizumab (750 mg) in HES.
45              Eighty-eight patients initiated mepolizumab, 76 omalizumab, and 65 dupilumab.
46 ed in BAL post SBP-Ag (299), decreased after mepolizumab (99), and increased in sputum after WLAC (36
47                                              Mepolizumab, a humanised monoclonal antibody that target
48                                              Mepolizumab, a humanized monoclonal anti-IL-5 antibody,
49            Patients were assigned to receive mepolizumab, a humanized monoclonal antibody against int
50                                              Mepolizumab, a humanized monoclonal antibody that binds
51                                              Mepolizumab, a humanized monoclonal antibody that neutra
52 ic phenotype may benefit from treatment with mepolizumab, a monoclonal antibody directed against inte
53                                              Mepolizumab, a monoclonal antibody drug targeting IL-5,
54 ion of eosinophilic airway inflammation with mepolizumab-a monoclonal antibody against interleukin 5-
55                                              Mepolizumab administered either intravenously or subcuta
56 t report of a case of severe asthma in which mepolizumab administration reversed the clinical deterio
57                                     Finally, mepolizumab affected particularly RV16-induced macrophag
58                                              Mepolizumab also enhanced secretory IgA and reduced tryp
59            Despite reducing chronic OCS use, mepolizumab also resulted in similar reductions in exace
60          Our study shows that treatment with mepolizumab, an agent designed to target eosinophils, ca
61                                              Mepolizumab, an anti-IL-5 antibody, has recently been ap
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
64                                              Mepolizumab, an anti-IL-5 monoclonal antibody, has been
65                                              Mepolizumab, an anti-interleukin-5 monoclonal antibody a
66                                              Mepolizumab, an anti-interleukin-5 monoclonal antibody,
67                                              Mepolizumab, an antibody against IL-5, reduces esophagea
68 n children with EoE and whether therapy with mepolizumab, an antibody against IL-5, reduces the numbe
69                                   RATIONALE: Mepolizumab, an IL-5-blocking antibody, reduces exacerba
70       192 (70%) of 273 patients who received mepolizumab and 207 (74%) of 278 who received placebo re
71               Of 1192 patients, 846 received mepolizumab and 346 received placebo.
72  randomization, 403 were assigned to receive mepolizumab and 401 to receive placebo.
73 on, with 68 participants assigned to receive mepolizumab and 68 to receive placebo.
74                                              Mepolizumab and benralizumab depleted iEOs to a similar
75 nal sample size for MAIC of benralizumab vs. mepolizumab and benralizumab vs. dupilumab, respectively
76  transcriptomic data from clinical trials of mepolizumab and benralizumab.
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
80                Although the type 2 biologics mepolizumab and dupilumab show clinical efficacy in seve
81 es for patient populations between ZONDA and mepolizumab and dupilumab trials.
82             At 12 years old, she switched to mepolizumab and has since maintained good control of ast
83                                              Mepolizumab and omalizumab are treatments for distinct b
84 ive insight into the differential effects of mepolizumab and omalizumab on the immunometabolic kineti
85                                              Mepolizumab and omalizumab were both effective (improved
86 be better predictors of clinical response to mepolizumab and omalizumab, than IL-5 or IgE, the target
87 omalizumab, than IL-5 or IgE, the targets of mepolizumab and omalizumab.
88 dge from this journey extended to the use of mepolizumab and other biologics across a broad spectrum
89       Similar proportions of patients in the mepolizumab and placebo groups experienced on-treatment
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
92 nistration, but nasal symptoms improved with mepolizumab and remained well controlled.
93 odies have been designed to neutralize IL-5 (mepolizumab and reslizumab).
94                  New anti-IL-5 therapeutics, mepolizumab and reslizumab, were US Food and Drug Admini
95 ood, BAL fluid, and sputum, before and after mepolizumab and RV16, were assessed.
96                  In MAIC of benralizumab vs. mepolizumab and vs. dupilumab, patient-level data from t
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.
99 ebo, 154 to 75 mg mepolizumab, 152 to 250 mg mepolizumab, and 156 to 750 mg mepolizumab.
100 d sputum proteins pre-mepolizumab, stable on mepolizumab, and at exacerbation.
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
106                                              Mepolizumab (anti-IL5 therapy) reduces asthma exacerbati
107                                              Mepolizumab approximately halved exacerbations requiring
108                               Omalizumab and Mepolizumab are biologic drugs with proven efficacy in c
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.
111                                              Mepolizumab arrests eosinophil maturation; however, the
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
114                          A greater effect of mepolizumab, as compared with placebo, on the annual rat
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
117                                              Mepolizumab at a dose of 100 mg was associated with a lo
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
120                                              Mepolizumab attenuated baseline blood eosinophils and th
121                            Studies show that mepolizumab can reduce the frequency of clinically signi
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
124 e Test patient-reported outcome score in the mepolizumab compared with placebo groups.
125                                              Mepolizumab depletes iEOs and reduces circulating eosino
126                                              Mepolizumab did not affect FEV(1), FVC, and fractional e
127                            In those studied, mepolizumab did not alter airway bacterial load or lead
128                            On RV16 challenge mepolizumab did not prevent eosinophil activation but di
129                                          All mepolizumab doses were combined and individual patient-l
130 lations of the two original studies, and all mepolizumab doses were combined for analysis.
131                            In these studies, mepolizumab ( DREAM: 75 mg, 250 mg, or 750 mg intravenou
132                                  Compared to mepolizumab, dupilumab had >90% chance for improving FEV
133       In 59 patients with asthma who started mepolizumab during observation, serum EPX levels normali
134     Patients received 100 mg of subcutaneous mepolizumab every 4 weeks plus standard of care until a
135                                              Mepolizumab failed to prevent activation of remaining eo
136 depleted in asthma patients using anti-IL-5 (mepolizumab), followed by a challenge with rhinovirus-16
137  for 7 of 7 outcomes, omalizumab for 2 of 7, mepolizumab for 1 of 7, and ASA-D for 1 of 7.
138 nt, mean difference between benralizumab and mepolizumab for OCS reduction was 6.08% (95% CI -22.22-3
139              Benralizumab was noninferior to mepolizumab for the induction of remission in patients w
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
147          Both FEV(1) and FVC improved in the mepolizumab group (FEV(1) + 20 mL/year; FVC +43 mL/year)
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
153                         Fifty percent of the mepolizumab group, 58% omalizumab, and 72% of dupilumab
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
165 oximately half the participants treated with mepolizumab had protocol-defined remission.
166 ildren with eosinophilic asthma treated with mepolizumab had significantly lower sputum eosinophils.
167                                              Mepolizumab has a favorable effect on disease flares in
168         Additionally, the efficacy of add-on mepolizumab has been observed in patients with severe ch
169                                              Mepolizumab has demonstrated favorable safety and effica
170 lustering of sputum proteins while stable on mepolizumab identified 2 clusters.
171                                              Mepolizumab improved the Asthma Control Questionnaire sc
172 orted by the investigator as possibly due to mepolizumab in 3 subjects.
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
176 support the long-term safety and efficacy of mepolizumab in patients with SEA.
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
180                   We aimed to further assess mepolizumab in patients with severe eosinophilic asthma
181 biomarker for the efficacy of treatment with mepolizumab in patients with severe eosinophilic asthma.
182 DREAM (Dose Ranging Efficacy And Safety With Mepolizumab in Severe Asthma, NCT01000506).
183 f an anti-interleukin-5 monoclonal antibody, mepolizumab, in patients with the hypereosinophilic synd
184                                              Mepolizumab increases the frequencies of circulating ILC
185                  Segmental challenge without mepolizumab induced a rise in circulating eosinophils, b
186                                     Notably, mepolizumab induced significant gain in correlation of g
187                                            A mepolizumab-induced increase in serum IL-5 was observed
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
191                                              Mepolizumab is a humanized monoclonal antibody that bind
192                                              Mepolizumab is a humanized monoclonal antibody that targ
193                                              Mepolizumab is an anti-IL-5 mAb treatment for severe eos
194                              INTERPRETATION: Mepolizumab is an effective and well tolerated treatment
195                                              Mepolizumab is approved for the treatment of severe eosi
196 lizumab (MD -16.09 [95% CI -19.88, -12.30]), mepolizumab (MD -12.89 [95% CI -16.58, -9.19], ASA-D (MD
197 ent from that of tezepelumab (tezepelumab vs mepolizumab; MD: 0.14; 95% CI: -0.10 to 0.38).
198       Active treatment was 75 mg intravenous mepolizumab (MENSA) or 100 mg subcutaneous mepolizumab (
199 s mepolizumab (MENSA) or 100 mg subcutaneous mepolizumab (MENSA, SIRIUS).
200 b, 68 receiving omalizumab, and 65 receiving mepolizumab met the inclusion criteria.
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.
204           One hundred five patients received mepolizumab (n = 54) or placebo (n = 51).
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
207                     In this clinical cohort, mepolizumab, omalizumab, and dupilumab had beneficial ef
208 , limited data exist regarding the impact of mepolizumab on airway remodeling.
209 d exacerbations with dupilumab versus either mepolizumab or benralizumab and also with tezepelumab ve
210                      Biologic treatment with mepolizumab or omalizumab for severe asthma-induced asth
211  failing to demonstrate clinical response to mepolizumab or omalizumab respectively.
212  ratios with subsequent clinical response to mepolizumab or omalizumab.
213     Patients received 300 mg of subcutaneous mepolizumab or placebo every 4 weeks for 52 weeks.
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
216         Patients received either intravenous mepolizumab or placebo while the prednisone dose was tap
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.
219 ificantly greater number of hEOs remained in mepolizumab participants at follow-up.
220                 Conversely, compared to SNB, Mepolizumab patients were predominantly older males, dia
221  After directly switching from omalizumab to mepolizumab, patients with uncontrolled severe eosinophi
222                        In patients receiving mepolizumab, prednisolone significantly downregulated sp
223                                              Mepolizumab reduced airway eosinophil numbers but had a
224                                              Mepolizumab reduced eosinophils in sinonasal tissue, dem
225                                              Mepolizumab reduced the need for sinus surgery in the SY
226                                    In MENSA, mepolizumab reduced the rate of exacerbations by 57% (pr
227                                              Mepolizumab reduced the risk of further sinus surgery in
228               Anti-IL-5 monoclonal antibody (mepolizumab) reduces baseline bronchial mucosal eosinoph
229 re eosinophilic asthma respond positively to mepolizumab regardless of prior use of omalizumab.
230  the pathogenesis of asthma (eg, omalizumab, mepolizumab, reslizumab).
231 flammatory pathways (IL-5R and IL-5), namely mepolizumab, reslizumab, and benralizumab, are effective
232 eline ACQ6 was independently associated with Mepolizumab response (p = .007).
233 sinophilic granulomatosis with polyangiitis, mepolizumab resulted in significantly more weeks in remi
234                                              Mepolizumab's safety profile was comparable with that of
235          Treatment of severe asthmatics with mepolizumab significantly attenuated blood eosinophils a
236           Treatment with 100 mg subcutaneous mepolizumab significantly attenuated systemic differenti
237                       Compared with placebo, mepolizumab significantly reduced the occurrence of flar
238                                              Mepolizumab significantly reduced the rate of exacerbati
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
249 ent with an anti-IL-5 neutralizing antibody (mepolizumab) to reduce airway eosinophilia.
250 ion correlated with poorer asthma control in mepolizumab-treated individuals.
251                                           In mepolizumab-treated participants, CD62L(int) and CD62L(h
252  recent phase III trial (NCT02020889) 53% of mepolizumab-treated versus 19% of placebo-treated patien
253                                              Mepolizumab treatment increased circulating type 2 innat
254 opical corticosteroids who required surgery, mepolizumab treatment led to a greater reduction in the
255                                              Mepolizumab treatment led to significantly more accrued
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
258                                              Mepolizumab treatment reduced the expression of tissue h
259                                              Mepolizumab treatment resulted in a reduction of airway
260                                              Mepolizumab treatment resulted in loss of correlation am
261  responsiveness of airway inflammation after mepolizumab treatment to find potentially treatable infl
262                             After 12 months, mepolizumab treatment was associated with significant im
263  In Case 1, nasal symptoms persisted despite mepolizumab treatment, and CRS recurred early after endo
264                            Over 24 months of mepolizumab treatment, Arg/Arg patients had an increased
265                                       Before mepolizumab treatment, bronchoalveolar lavage eosinophil
266 a similar pattern following benralizumab and mepolizumab treatment, the lack of correlation between A
267 ional and functional changes associated with mepolizumab treatment.
268 reductions in the rate of exacerbations with mepolizumab treatment.
269           We investigated whether anti-IL-5 (mepolizumab) treatment reduced esophageal mast cell accu
270 ated with poorer clinical outcomes following mepolizumab-treatment.
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
275 estigate the clinical efficacy and safety of mepolizumab versus placebo in patients with HES.
276 patients experienced clinical benefit 1 with mepolizumab versus placebo in the blood eosinophil count
277         The exacerbation rate reduction with mepolizumab versus placebo increased progressively from
278 7 patients (mepolizumab: 206; placebo: 201), mepolizumab versus placebo reduced the risk of being inc
279                                              Mepolizumab versus placebo reduced the risk of sinus sur
280                                              Mepolizumab versus placebo showed significant improvemen
281                                         With mepolizumab versus placebo, 78% versus 32% of patients e
282 cebo) and nasopharyngitis (in 31 [11%] given mepolizumab vs 46 [17%] given placebo).
283 on of which were headache (in 45 [16%] given mepolizumab vs 59 [21%] given placebo) and nasopharyngit
284 s asthma in both groups (in three [1%] given mepolizumab vs nine [3%] given placebo).
285 ma control and quality of life improved with mepolizumab vs placebo in both studies independent of pr
286                At 12-months post-initiation, mepolizumab was also associated with a reduction in oral
287                                              Mepolizumab was associated with a reduction from baselin
288 n vivo, reduction of EOS in the airway using mepolizumab was associated with diminished IL-17 express
289                              INTERPRETATION: Mepolizumab was associated with significant improvements
290 n rate reduction favouring benralizumab over mepolizumab was observed, although it was not statistica
291 han 150 cells per muL, predicted efficacy of mepolizumab was reduced.
292                        The safety profile of mepolizumab was similar to that observed in previous stu
293                        The safety profile of mepolizumab was similar to that of placebo.
294  In a small cohort of participants with EAE, mepolizumab was unsuccessful in substantially reducing c
295                                              Mepolizumab was well tolerated and effective as a long-t
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

 
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