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1 (53.4%) patients (all p<0.0001 vs placebo or etanercept).
2 s compared with TNF receptor fusion protein (etanercept).
3  mg vs etanercept and p=0.0010 for 100 mg vs etanercept).
4 olizumab), and an IgG1-TNFR2 fusion protein (etanercept).
5  mg vs etanercept and p=0.0663 for 100 mg vs etanercept).
6 (41.6%) patients (all p<0.0001 vs placebo or etanercept).
7 ive cohort (160 treated with adalimumab, 171 etanercept).
8 ial samples were tested (414 adalimumab, 421 etanercept).
9  and function of infliximab, adalimumab, and etanercept.
10 reased risk was observed with ustekinumab or etanercept.
11  both studies and were similar to those with etanercept.
12 ed by treatment with the TNF-alpha inhibitor etanercept.
13  was comparable to the results obtained with etanercept.
14 esence of TNFRI-AlbudAb, control-AlbudAb, or etanercept.
15 before and during therapy with infliximab or etanercept.
16  pruritic cutaneous eruption while receiving etanercept.
17 vitro by the competitive TNFalpha antagonist etanercept.
18 apy and those randomized to receive MTX plus etanercept.
19  size, and a possibly subtherapeutic dose of etanercept.
20 Fifty percent of these patients had received etanercept.
21 cted by conventional anti-TNF treatment with etanercept.
22 authorization requirements for adalimumab or etanercept.
23 locked by addition of the TNF decoy receptor etanercept.
24 ated with juvenile idiopathic arthritis than etanercept.
25 rakizumab 100 mg, 156 to placebo, and 313 to etanercept.
26 par with the effect of blocking TNF-alpha by etanercept.
27 collagen-induced arthritis were treated with etanercept.
28 er 12 weeks were similar for tofacitinib and etanercept.
29 5 mg/kg/week (maximum 40 mg) subcutaneously, etanercept 0.8 mg/kg/week (maximum 50 mg), and prednisol
30  mg of ustekinumab and in 70.0% who received etanercept; 1.9%, 1.2%, and 1.2%, respectively, had seri
31  as follows: non-biologic, 14.2 (11.5-17.4); etanercept, 15.3 (11.6-20.1); adalimumab, 13.9 (11.4-16.
32 , sphingosine kinase 1 deletion prevents and etanercept (2-week treatment initiated 6 weeks after myo
33          Day 28 complete response rates were etanercept 26%, MMF 60%, denileukin 53%, and pentostatin
34 onth than those who received saline (50%) or etanercept (42%) (P = 0.09).
35 dences of severe infections were as follows: etanercept 48%, MMF 44%, denileukin 62%, and pentostatin
36 mong patients who did not have a response to etanercept, 48.9% had at least 75% improvement in the PA
37 ab 200 mg, tildrakizumab 100 mg, placebo, or etanercept 50 mg (2:2:1:2).
38                                              Etanercept 50 mg once weekly is an optimal dosage in mos
39 ept 50 mg twice weekly (n = 160) or MTX plus etanercept 50 mg once weekly plus a placebo (n = 40) for
40 ptimal responders to treatment with MTX plus etanercept 50 mg once weekly were given MTX plus etanerc
41 r 10 mg twice daily at about 12 h intervals, etanercept 50 mg subcutaneously twice weekly at about 3-
42 ercept 50 mg once weekly were given MTX plus etanercept 50 mg twice weekly (n = 160) or MTX plus etan
43 aily dose of tofacitinib was non-inferior to etanercept 50 mg twice weekly and was superior to placeb
44 332 to tofacitinib 10 mg twice daily, 336 to etanercept 50 mg twice weekly, and 108 to placebo).
45 e daily dose did not show non-inferiority to etanercept 50 mg twice weekly.
46 ween tofacitinib (10 mg two times a day) and etanercept (50 mg biweekly), and by response status at w
47 b (40 mg subcutaneously every other week) or etanercept (50 mg per week subcutaneously) according to
48  ustekinumab (at weeks 0 and 4) or high-dose etanercept (50 mg twice weekly for 12 weeks).
49 onse system to receive subcutaneous placebo, etanercept (50 mg twice weekly), or one injection of 80
50 healthy levels upon effective treatment with etanercept, a biological drug targeting the TNF pathway
51  combined GEE model including adalimumab and etanercept, a body-mass index of 30 kg/m(2) or more was
52       However, treatment of CD patients with etanercept, a decoy receptor that binds soluble TNF, fai
53  in RA patients responding to treatment with etanercept, a modified TNF receptor-Fc fusion protein.
54                                              Etanercept, a soluble tumor necrosis factor receptor, ha
55 e blockade of tumor necrosis factor (TNF) by etanercept, a soluble version of the human TNF receptor
56        At week 12, 57% of patients receiving etanercept achieved PASI 75, as compared with 11% of tho
57 eumatoid arthritis, coverage was extended to etanercept, adalimumab, and anakinra in addition to the
58 49 per 100 patient-years in the ustekinumab, etanercept, adalimumab, and infliximab cohorts, respecti
59                                              Etanercept, adalimumab, and infliximab were similar in t
60 ing between non-biologic systemic therapies, etanercept, adalimumab, and ustekinumab for the treatmen
61 1; and 994 participants were included in the etanercept, adalimumab, ustekinumab cohorts, respectivel
62 increase in serious infections compared with etanercept (aHR, 1.26 [95% CI, 1.07-1.47]) and adalimuma
63 ee patients during treatment with open-label etanercept; all resolved without sequelae.
64 3 mg/kg/week], maximum dosage 1 mg/kg/week), etanercept alone (0.8 mg/kg/week, maximum dose 50 mg), o
65 te the long-term safety and effectiveness of etanercept alone or in combination with methotrexate (MT
66                                              Etanercept also reduced levels of acute-phase reactants,
67 terleukin-12 and interleukin-23 blocker) and etanercept (an inhibitor of tumor necrosis factor alpha)
68         Renal interstitial administration of Etanercept, an inhibitor of TNFalpha, significantly atte
69 n with lifelong TRAPS in whom treatment with etanercept and anakinra had failed, was administered toc
70 tly various types of TNF antagonists such as etanercept and infliximab have been used successfully.
71                             Small studies of etanercept and infliximab have showed these TNF-alpha bl
72 ary metabolite changes distinguished between etanercept and infliximab treatment.
73 or necrosis factor alpha antagonists such as etanercept and infliximab, as well as with interleukin r
74                                              Etanercept and methotrexate combination is more effectiv
75 oups (-2.1 with triple therapy and -2.3 with etanercept and methotrexate, P=0.26); triple therapy was
76 , P=0.26); triple therapy was noninferior to etanercept and methotrexate, since the 95% upper confide
77 ab groups vs placebo; p<0.0001 for 200 mg vs etanercept and p=0.0010 for 100 mg vs etanercept).
78 ab groups vs placebo; p=0.0031 for 200 mg vs etanercept and p=0.0663 for 100 mg vs etanercept).
79 s in demographic characteristics between the etanercept and placebo groups.
80 % and 65% for patients initially assigned to etanercept and placebo, respectively.
81 ches effective for human psoriasis, that is, Etanercept and Rosiglitazone, are effective in alleviati
82 aseline between the group receiving MTX plus etanercept and the group receiving oral triple therapy (
83 ween subjects randomized to receive MTX plus etanercept and those randomized to triple therapy, regar
84  syndrome was severe; cytokine blockade with etanercept and tocilizumab was effective in reversing th
85 g were efficacious compared with placebo and etanercept and were well tolerated in the treatment of p
86 models, as well as selective TNF blockade by etanercept and XPro1595 in wild-type mice, demonstrate t
87 51.1% with 150 mg of secukinumab, 27.2% with etanercept, and 2.8% with placebo (P<0.001 for each secu
88 67.0% with 150 mg of secukinumab, 44.0% with etanercept, and 4.9% with placebo (P<0.001 for each secu
89 ncies associated with the use of infliximab, etanercept, and adalimumab in children in whom therapy w
90 ed with successful narrow band UVB (NB-UVB), etanercept, and anti-IL-17 treatments.
91 , and 21.6 per 100 patient-years in the MTX, etanercept, and etanercept plus MTX groups, respectively
92 , and 294 patients were enrolled in the MTX, etanercept, and etanercept plus MTX groups, respectively
93 nally associated with the use of infliximab, etanercept, and in a lesser extent adalimumab.
94 cluding ustekinumab, infliximab, adalimumab, etanercept, and nonbiologics (with or without methotrexa
95 gnificant skin and nail disease, adalimumab, etanercept, and ustekinumab are strongly recommended, an
96 (64.6-76.5) vs placebo; 36.9% (29.1-44.7) vs etanercept]) and 291 (75.4%; [68.7% (62.3-75.0) vs place
97  75.6-86.0) vs placebo; 47.2% (39.9-54.4) vs etanercept]) and 310 (80.5%; [73.8% (67.7-79.9) vs place
98 (69.5-80.8) vs placebo; 35.9% (28.2-43.6) vs etanercept]) and 325 (84.2%; [76.9% (71.0-82.8) vs place
99  82.9-91.8) vs placebo; 48.1% (41.2-55.0) vs etanercept]) and 336 (87.3%; [80.0% (74.4-85.7) vs place
100                        Abatacept (CTLA4-Ig), etanercept (anti-TNF), or phosphate-buffered saline were
101                        Anti-TNF therapy with etanercept appears to further increase the risk of malig
102                            Biologics such as etanercept are the most successful drugs used in anti-cy
103 2 weeks; UNCOVER-2 and UNCOVER-3 also had an etanercept arm (50 mg twice weekly).
104 ks), placebo, or (in the FIXTURE study only) etanercept at a dose of 50 mg (administered twice weekly
105                         It can be induced by etanercept, but has also been described during adalimuma
106 patients (69.2%), biologic agents (primarily etanercept) by 106 (27.2%), acitretin by 57 (14.6%), cyc
107  concomitant use of acitretin, the dosing of etanercept can be reduced to maintain similar levels of
108 d the tumor necrosis factor-alpha inhibitor, etanercept, combined with corticosteroids in treating 15
109                              Tofacitinib and etanercept commonly reduced IL-6, CCL20, and CXCL10, but
110                                         High etanercept concentrations were associated with better tr
111 ted that the TNF-alpha-neutralizing molecule etanercept could be an effective treatment for patients
112       Here, we hypothesized that response to etanercept could be monitored by radionuclide imaging in
113 of both forms of tumour necrosis factor with etanercept does not result in protection.
114                 Protocols with daclizumab or etanercept during induction had higher rates of II and l
115 study was to generate a panel of mAbs toward etanercept (ETN) and to determine ETN and anti-ETN conce
116 lammation, we used the TNF-alpha antagonist, etanercept (ETN), for studies in syngeneic rat hepatocyt
117 ever, this could not be attributed solely to etanercept exposure during the trial.
118 the OLE, for a total of 318 patient-years of etanercept exposure.
119 s reported in patients with > or =5 years of etanercept exposure.
120            The removal of the N-glycans from etanercept facilitated the selective characterization of
121 ctively inhibited vascular permeability, and etanercept failed to affect either outcome.
122 were noted for functional capacity, in which etanercept fared worse than the other treatments: steroi
123 llowup period, patients continued to receive etanercept for a median of 3.3 years, with a number of p
124 in atopic dermatitis, safety and efficacy of etanercept for the treatment of psoriasis in children, n
125 re observed at years 1, 2, and 3 in both the etanercept group (7.4, 10.0, and 13.0 percentile points)
126  placebo group and 151 patients (48%) in the etanercept group (p<0.0001 for comparisons of both tildr
127  placebo group and 149 patients (48%) in the etanercept group (p<0.0001 for comparisons of both tildr
128 an BMI percentiles were observed in both the etanercept group (range 9.6-13.8 percentile points) and
129 w solid malignancies were detected, 8 in the etanercept group and 5 in the placebo group.
130 ur (2.4%) and 13 (6.7%) patients; and in the etanercept group by 129 (36.0%) and 159 (41.6%) patients
131 ur (2.4%) and 14 (7.3%) patients; and in the etanercept group by 149 (41.6%) and 204 (53.4%) patients
132 rtality rate was significantly higher in the etanercept group compared with the placebo group (57.7%
133 ation, the risk of solid malignancies in the etanercept group was increased (SIR 3.92 [95% confidence
134 0 in the tofacitinib 10 mg group, 335 in the etanercept group, and 107 in the placebo group).
135 tinib 10 mg group, 222 (66.3%) of 335 in the etanercept group, and 16 (15.0%) of 107 in the placebo g
136 facitinib 10 mg group, 11 (3%) of 335 in the etanercept group, and four (4%) of 107 patients in the p
137 tinib 10 mg group, 197 (58.8%) of 335 in the etanercept group, and six (5.6%) of 107 in the placebo g
138 itinib 10 mg group, seven (2%) of 335 in the etanercept group, and two (2%) of 107 in the placebo gro
139 baseline differences between the placebo and etanercept groups in demographics or disease severity pa
140      However, patients continuing to receive etanercept had reduced symptoms at followup.
141  risk of serious infection were observed for etanercept (hazard ratio [HR] = 1.10, 95% CI = 0.75-1.60
142     As compared with adalimumab, patients on etanercept (HR 1.63; 95% CI: 1.45-1.84) or infliximab (H
143 gic systemic therapies or methotrexate-only (etanercept: HR = 1.47, 95% CI = 0.95-2.28; adalimumab: H
144 of sulfasalazine plus hydroxychloroquine (or etanercept, if necessary, after 6 months) is a reasonabl
145 ment arms: immediate treatment with MTX plus etanercept, immediate oral triple therapy (MTX plus sulf
146 ults suggest that the combination of EXN and etanercept improve engraftment and long-term islet survi
147  a phase 3 clinical trial of tofacitinib and etanercept in adults with moderate-to-severe psoriasis.
148 rofiles during treatment with infliximab and etanercept in RA and PsA may reflect distinct mechanisms
149 her tildrakizumab is superior to placebo and etanercept in the treatment of chronic plaque psoriasis.
150 h each secukinumab dose than with placebo or etanercept: in the ERASURE study, the rates were 65.3% w
151 h each secukinumab dose than with placebo or etanercept: in the ERASURE study, the rates were 81.6% w
152 tment with the TNFalpha signaling inhibitor, etanercept, indicating the involvement of TNFalpha in th
153 07) protocol uses antithymocyte globulin and etanercept induction, islet culture, heparinization, and
154                                  Adalimumab, etanercept, infliximab and tocilizumab all showed statis
155       A total of 1,283 RA patients receiving etanercept, infliximab, or adalimumab therapy were studi
156 We identified new users of anti-TNF therapy (etanercept, infliximab, or adalimumab) or nonbiologic di
157 rexate, cyclosporine, acitretin, adalimumab, etanercept, infliximab, or ustekinumab or phototherapy f
158  therapy approved for psoriasis (adalimumab, etanercept, infliximab, ustekinumab) with the possibilit
159                   Systemic administration of Etanercept inhibited MHC-I(high) melanoma growth in immu
160 line nor the TNF-alpha-neutralizing compound etanercept inhibited the induction of hyperexcitability
161 te administration of the TNF-alpha inhibitor etanercept inhibits carbon tetrachloride (CCL4)-induced
162 erapy has failed, treatment with adalimumab, etanercept, intralesional corticosteroids, ustekinumab,
163                                              Etanercept is a highly glycosylated therapeutic Fc-fusio
164 rtality rate after 6 months, indicating that etanercept is not effective for the treatment of patient
165 gents such as infliximab and adalimumab, and etanercept is not effective for treatment of Crohn's dis
166              Although long-term adherence to etanercept is poor, continuing to receive etanercept may
167 with infliximab demonstrating no benefit and etanercept leading to encouraging results warranting fur
168        Moreover, treatment of psoriasis with etanercept led to significantly decreased IL-1F5, -1F6,
169 tioned as F(ab')2 fragments, whereas cleaved etanercept lost its ability to neutralize TNF.
170 to etanercept is poor, continuing to receive etanercept may provide continued symptomatic benefit.
171 ce, -0.52 [CI, -1.85 to 0.81]; P = 0.44) and etanercept (mean difference, -0.92 [CI,-2.28 to 0.44]; P
172  -1.26 [95% CI, -2.79 to 0.27]; P = 0.11) or etanercept (mean difference, -1.01 [CI, -2.60 to 0.58];
173 orse than the other treatments: steroids vs. etanercept (mean difference, -16.16 [CI, -26.05 to -6.27
174 ong-term perspective, an initial strategy of etanercept-methotrexate and biologics with similar cost
175                     The ICERs for first-line etanercept-methotrexate and triple therapy were $2.7 mil
176 alysis: The within-trial analysis found that etanercept-methotrexate as first-line therapy provided m
177                                              Etanercept-methotrexate first versus triple therapy firs
178 al found triple therapy to be noninferior to etanercept-methotrexate in patients with active rheumato
179       To determine the cost-effectiveness of etanercept-methotrexate versus triple therapy as a first
180  lifetime analysis suggested that first-line etanercept-methotrexate would result in 0.15 additional
181 a moderate quality of evidence compared with etanercept monotherapy (Psoriasis Area and Severity Inde
182 erapy (the EM/EM group; n = 111) or received etanercept monotherapy (the EM/E group; n = 111) in year
183                  Early sustained combination etanercept-MTX therapy was consistently superior to MTX
184 eive methylprednisolone 2 mg/kg per day plus etanercept, mycophenolate mofetil (MMF), denileukin dift
185 d with anti-TNF medications (total n = 1050, etanercept n = 455, infliximab n = 450), we investigated
186   Data for patients on adalimumab (n=1,879), etanercept (n=1,098), infliximab (n=96), and ustekinumab
187 ned to receive subcutaneous placebo (n=168), etanercept (n=358), or ixekizumab every 2 weeks (n=351)
188 andomly assigned to receive placebo (n=193), etanercept (n=382), ixekizumab every 2 weeks (n=385), or
189 ce registry (n = 1,239; adalimumab, n = 538; etanercept, n = 104; ustekinumab, n = 597).
190 0), anti-tumor necrosis factor-a (TNF-alpha; etanercept, n=50), or cyclosporine treatment (n=50).
191 60 given placebo, and 14 (1.9%) of 739 given etanercept; no deaths were noted.
192 h polyarticular or systemic JIA treated with etanercept only, etanercept plus methotrexate, or methot
193  in those injected with conventional MSCs or etanercept only.
194 y to be non-adherent compared to those using etanercept or adalimumab (29.2% vs. 16.4%; P </= 0.001).
195 term cyclosporine use has been combined with etanercept or adalimumab to control psoriasis flares.
196 5 mg/week) and stable dose of TNF inhibitor (etanercept or adalimumab) for >/= 12 weeks were randomiz
197                 Combining biologics, such as etanercept or adalimumab, with phototherapy likely resul
198  of other long-term studies and suggest that etanercept or etanercept plus MTX has an acceptable safe
199  of subjects who initiated biologic therapy (etanercept or infliximab) and reported consistent use at
200 monotherapy or combination therapy (MTX plus etanercept or MTX plus sulfasalazine plus hydroxychloroq
201 o one of the combination therapies (MTX plus etanercept or MTX plus sulfasalazine plus hydroxychloroq
202 en up to 6 subcutaneous injections of either etanercept or placebo for 3 weeks.
203 compare two tofacitinib doses with high-dose etanercept or placebo in this patient population.
204 odds ratio (OR) = 1.50, P(corr) = 0.050) and etanercept (OR = 1.64, P(corr) = 0.016).
205            Therapeutically antagonizing TNF (etanercept) or S1P (JTE013) signaling corrects this defe
206           2 epidural injections of steroids, etanercept, or saline, mixed with bupivacaine and separa
207 gimens had greater efficacy than placebo and etanercept over 12 weeks in two independent studies.
208 5 or 90 mg was superior to that of high-dose etanercept over a 12-week period in patients with psoria
209 y poorer response compared with TNF-308GG in etanercept (P = 0.001, n = 7) but not infliximab (P = 0.
210 as compared with 49.0% of those who received etanercept (P<0.001 for both comparisons).
211 as compared with 56.8% of those who received etanercept (P=0.01 and P<0.001, respectively).
212 adalimumab, but not the soluble TNF receptor etanercept, paradoxically promoted the interaction betwe
213  wild-type mice, and TNF-alpha blockade with etanercept partially prevented renal atrophy in IRAK-M(-
214 atment of mice with the TNFalpha antagonist, etanercept, partially blunted BCG-induced IDO activation
215 completed 12 month follow-up and none of the etanercept patients.
216 (74.4-85.7) vs placebo; 33.9% (27.0-40.7) vs etanercept]) patients; in the ixekizumab every 4 weeks g
217 (67.7-79.9) vs placebo; 38.9% (31.7-46.1) vs etanercept]) patients; in the ixekizumab every 4 weeks g
218 (62.3-75.0) vs placebo; 33.8% (26.3-41.3) vs etanercept]) patients; in the placebo group by four (2.4
219 (71.0-82.8) vs placebo; 30.8% (23.7-37.9) vs etanercept]) patients; in the placebo group, by four (2.
220 eeks (arm 1), or MTX (same dosage as arm 1), etanercept placebo, and prednisolone placebo (arm 2).
221 onses at weeks 39 and 52 to receive 25 mg of etanercept plus methotrexate (combination-therapy group)
222 centile points) and in patients treated with etanercept plus methotrexate at years 1, 2, and 3 (2.4,
223 ne added to methotrexate, was noninferior to etanercept plus methotrexate in patients with rheumatoid
224  results indicate that combined therapy with etanercept plus methotrexate may be beneficial in patien
225                                              Etanercept plus methotrexate was the only combination th
226 rexate or biologic therapy received 50 mg of etanercept plus methotrexate weekly for 52 weeks (open-l
227 r systemic JIA treated with etanercept only, etanercept plus methotrexate, or methotrexate only.
228 e, sulfasalazine, and hydroxychloroquine) or etanercept plus methotrexate.
229 tis within 1 year of combined treatment with etanercept plus methotrexate.
230 one (0.8 mg/kg/week, maximum dose 50 mg), or etanercept plus MTX for 3 years in an open-label, nonran
231 00 patient-years in the MTX, etanercept, and etanercept plus MTX groups, respectively).
232 ts were enrolled in the MTX, etanercept, and etanercept plus MTX groups, respectively.
233 -term studies and suggest that etanercept or etanercept plus MTX has an acceptable safety and effecti
234 4, 10.0, and 13.0 percentile points) and the etanercept-plus-methotrexate group (2.9, 6.9, and 8.4 pe
235 p (range 9.6-13.8 percentile points) and the etanercept-plus-methotrexate group (range 2.1-5.2 percen
236 ho had a remission while receiving full-dose etanercept-plus-methotrexate therapy, continuing combina
237 rthritis who had a remission while receiving etanercept-plus-methotrexate therapy.
238 groups received infliximab post-reperfusion; etanercept pre-reperfusion and at postoperative days (PO
239                                              Etanercept production was verified from the conditioned
240 - and O-glycans and O-glycosylation sites in etanercept provides a basis for future studies addressin
241              Psoriasis patients treated with etanercept rapidly decrease cutaneous IL-17C levels, sug
242     At week 36, after 24 weeks of open-label etanercept, rates of PASI 75 were 68% and 65% for patien
243                                              Etanercept reduces symptoms and serum levels of inflamma
244 nd MMP12 cleaved infliximab, adalimumab, and etanercept, releasing a 32-kilodalton Fc monomer.
245  by intravitreal injection of bevacizumab or etanercept, respectively.
246 iopharmaceuticals Rituximab, Adalimumab, and Etanercept, respectively.
247   Treatment with the combination of MTX plus etanercept resulted in a statistically significant radio
248 nt of Nlrp3A350V mice with the TNF inhibitor etanercept resulted in all pups surviving to adulthood,
249                                              Etanercept significantly reduced disease severity in chi
250 ith infliximab (TNF monoclonal antibody) and etanercept (soluble TNF receptor) therapy.
251 uggest that the acceptable safety profile of etanercept therapy is maintained for up to 8 years in th
252 Given concern about a drug-induced eruption, etanercept therapy was discontinued and the cutaneous fi
253                  Adalimumab therapy, but not etanercept therapy, induces a potent and stable Treg cel
254 the increase was unaltered after 12 weeks of etanercept therapy.
255 metric assay, prior to and after 12 weeks of etanercept therapy.
256 nditions and following the administration of etanercept (TNF-alpha inhibitor; 1 mg Kg(-1)).
257 reating animals with anti-inflammatory drugs etanercept (TNFalpha inhibitor), anakinra (IL-1 receptor
258 and p38MAPK, while TNFalpha inhibition (with etanercept), TNFalpha gene ablation, or p38 inhibition,
259 udies of ixekizumab compared with placebo or etanercept to assess the safety and efficacy of specific
260 derwent a second randomization to placebo or etanercept to investigate the effects of withdrawal and
261  The efficacy and safety of a crossover from etanercept to ustekinumab were evaluated after week 12.
262 were similar before and after crossover from etanercept to ustekinumab.
263                                Compared with etanercept, tofacitinib showed a wider spectrum of cardi
264 fected with recombinant minicircles encoding etanercept (trade name, Enbrel), which is a tumour necro
265 t percentiles from baseline were observed in etanercept-treated patients at year 3 (4.8 percentile po
266  Treg cell number, function, or phenotype in etanercept-treated patients, and Th17 responses remained
267 y greater improvements in WPAI-PSO scores vs etanercept-treated patients: UNCOVER-2: presenteeism, wo
268     TNF(-/-) and TNF-R1(-/-) mice as well as Etanercept-treated WT mice displayed enhanced intratumor
269 erventions (SI-control; n=5) or with EXN and etanercept treatment (SI-EXN; n=4).
270 riasis genes were reversed after 3 months of etanercept treatment in patients who responded to treatm
271                                              Etanercept treatment of old mice reversed these changes,
272                                              Etanercept treatment significantly attenuated the total
273                              With all of the etanercept treatment strategies, blocking of TNFalpha si
274  (72%) entered the fourth year of continuous etanercept treatment, and 26 patients (45%) entered the
275   Randomisation was stratified by history of etanercept treatment, with a block size of three.
276                                              Etanercept treatment, with or without methotrexate, may
277 luated to determine the long-term outcome of etanercept treatment.
278 observed during the Wegener's Granulomatosis Etanercept Trial (WGET), which included 180 patients wit
279          In this retrospective analysis of 2 etanercept trials, disease activity was calculated at ba
280 parably shortly after initiation of MTX plus etanercept, triple therapy, and MTX monotherapy among pa
281 s in mean cholesterol levels in the MTX plus etanercept, triple therapy, and MTX monotherapy arms.
282 d: 31 following infliximab use, 15 following etanercept use, and 2 following adalimumab use.
283 Investigative Examination of Secukinumab vs. Etanercept Using Two Dosing Regimens to Determine Effica
284 ponse to treatment with four specific drugs: etanercept, ustekinumab, adalimumab, and methotrexate.
285 t nail, skin, and joint disease, adalimumab, etanercept, ustekinumab, infliximab, methotrexate, aprem
286 , -5.87 [CI, -15.59 to 3.85]; P = 0.23), and etanercept vs. saline (mean difference, 10.29 [CI, 0.55
287 with moderate to severe alcoholic hepatitis, etanercept was associated with a significantly higher mo
288            We confirmed that self-reproduced etanercept was biologically active in vitro.
289 pth characterization of the glycosylation of etanercept was carried out using liquid chromatography/m
290                                              Etanercept was first treated with peptide N-glycosidase
291 re-randomised from placebo to tildrakizumab; etanercept was given twice weekly in part 1 of reSURFACE
292       The reporting rates for infliximab and etanercept were compared with the background rate of mal
293                      The reporting rates for etanercept were elevated above background for lymphomas
294                  Infliximab, adalimumab, and etanercept were incubated with mucosal homogenates from
295   Compared to adalimumab, patients receiving etanercept were more likely to discontinue therapy (haza
296 lity rates of patients receiving placebo and etanercept were similar on an intention-to-treat basis (
297 a and pharmacological blockade of TNF-alpha (Etanercept) were also performed.
298 proaches, whether triple therapy or MTX plus etanercept, were similar.
299 onsidered in these patients in preference to etanercept, which seems to be associated with lower rate
300     Blocking of TNFalpha was performed using etanercept, which was administered subcutaneously at a d

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