戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

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 ntually anti IL-12/23 neutralizing antibody (ustekinumab).
2 3.9-8.8] compared with patients positive for ustekinumab).
3 otrexate (MTX), omalizumab, upadacitinib and ustekinumab.
4 , 205 to 45 mg ustekinumab, and 204 to 90 mg ustekinumab.
5 with CD exacerbation for which she was given ustekinumab.
6 l carcinoma developed in 1 patient receiving ustekinumab.
7 mportant molecular binding interactions with ustekinumab.
8  the PASI within 12 weeks after crossover to ustekinumab.
9 efore and after crossover from etanercept to ustekinumab.
10  in the UNIFI phase 3 UC clinical studies of ustekinumab.
11 D requiring monoclonal antibody therapy with ustekinumab.
12 and guselkumab compared with vedolizumab and ustekinumab.
13 ept, golimumab, infliximab, secukinumab, and ustekinumab.
14  1.13-2.03) had lower survival compared with ustekinumab.
15 tes of patients treated with vedolizumab and ustekinumab.
16 s, 578 received vedolizumab and 544 received ustekinumab.
17 ovement" versus 29% of patients treated with ustekinumab.
18 ytes, epidermal cells, and monocytes, versus ustekinumab.
19  responses superior to those associated with ustekinumab.
20 oved biologic agents, such as vedolizumab or ustekinumab.
21 e may be a predictor of improved response to ustekinumab.
22 ohn's disease who participated in a trial of ustekinumab.
23 1.6-20.1); adalimumab, 13.9 (11.4-16.6); and ustekinumab, 15.1 (10.8-21.1).
24  adalimumab was initiated, 5405 (33.5%) with ustekinumab, 2677 (16.6%) with secukinumab, 730 (4.5%) w
25 y higher with 210 mg of brodalumab than with ustekinumab (44% vs. 22% [AMAGINE-2] and 37% vs. 19% [AM
26  psoriasis were randomly assigned to receive ustekinumab 45 mg (n=255) or 90 mg (n=256) at weeks 0 an
27 ned (bimekizumab 320 mg every 4 weeks n=321, ustekinumab 45 mg or 90 mg every 12 weeks n=163, placebo
28               171 (67.1%) patients receiving ustekinumab 45 mg, 170 (66.4%) receiving ustekinumab 90
29 ining patients in the placebo group received ustekinumab 45 mg, which they continued at week 28 and e
30 brodalumab (210 mg or 140 mg every 2 weeks), ustekinumab (45 mg for patients with a body weight </=10
31 mg or 180-mg doses at weeks 0, 4, and 16) or ustekinumab (45 or 90 mg, according to body weight, at w
32                                 Subcutaneous ustekinumab, 45 mg, at weeks 0 and 4 and quarterly there
33 6 (n=76; Group 1) or placebo (weeks 0-3) and ustekinumab (63 mg) at weeks 12 and 16 (n=70; Group 2).
34  In all, 379 patients started treatment with ustekinumab, 779 patients started treatment with etanerc
35 tive patients demonstrated good responses to ustekinumab (86% vs. 76%, respectively, achieved at leas
36 ing ustekinumab 45 mg, 170 (66.4%) receiving ustekinumab 90 mg, and eight (3.1%) receiving placebo ac
37 week 8 in patients who received subcutaneous ustekinumab (90 mg every 8 weeks; from 7.4 +/- 7.7 to 6.
38  interactive voice response system to either ustekinumab (90 mg or 63 mg) every week for 4 weeks (wee
39 luated the anti-IL12/23 monoclonal antibody, ustekinumab (90 mg subcutaneous at weeks 0 and 4, then e
40 zation to receive subcutaneous injections of ustekinumab (90 mg) or placebo at weeks 8 and 16.
41 eractive voice-web response system) to 45 mg ustekinumab, 90 mg ustekinumab, or placebo at week 0, we
42 73 [67.6%] men) were treated with open-label ustekinumab; 91 were randomized to blinded treatment.
43 tients with Crohn's disease, the efficacy of ustekinumab, a human monoclonal antibody against interle
44                                  We assessed ustekinumab, a human monoclonal antibody directed agains
45                                              Ustekinumab, a monoclonal antibody to the p40 subunit of
46                                              Ustekinumab, a therapeutic agent targeting both cytokine
47 ANTS: Psoriasis Treatment with Abatacept and Ustekinumab: a Study of Efficacy (PAUSE), a parallel-des
48 taneously every 4 weeks from weeks 12 to 52; ustekinumab about 6 mg/kg intravenously at week 0, then
49 sity hospital department of dermatology with ustekinumab according to the dosing regimen approved for
50 atment with four specific drugs: etanercept, ustekinumab, adalimumab, and methotrexate.
51  placebo received masked rescue therapy with ustekinumab; all other participants remained on their ra
52             We compared two biologic agents, ustekinumab (an interleukin-12 and interleukin-23 blocke
53                              The efficacy of ustekinumab, an antagonist of the p40 subunit of interle
54 ith Crohn's disease before administration of ustekinumab, an anti-IL-12/IL-23 antibody, positively co
55                  We treated our patient with ustekinumab, an antibody that binds the p40 subunit of i
56                                              Ustekinumab, an antibody to p40, blocks cytokines IL-12
57  thus prevents interleukin-23 signaling, and ustekinumab, an interleukin-12 and interleukin-23 inhibi
58 in 278 (54.5%) of the 510 patients receiving ustekinumab and 123 (48.2%) of the 255 receiving placebo
59 tients were randomly assigned to maintenance ustekinumab and 160 to withdrawal.
60 included in the analysis, with 917 receiving ustekinumab and 314 receiving secukinumab.
61 2 in 66.0% of patients who received 45 mg of ustekinumab and 69.2% of patients who received 90 mg of
62 rly, 65.1% of patients who received 45 mg of ustekinumab and 70.6% of patients who received 90 mg of
63 2 in 67.5% of patients who received 45 mg of ustekinumab and 73.8% of patients who received 90 mg, as
64  between patients receiving risankizumab and ustekinumab and a significant decrease in 2682 genes uni
65                                         Both ustekinumab and adalimumab monotherapies were highly eff
66                                              Ustekinumab and briakinumab, monoclonal antibodies to th
67  and 69.2% of patients who received 90 mg of ustekinumab and in 70.0% who received etanercept; 1.9%,
68 rred in six (1.2%) of 510 patients receiving ustekinumab and in two (0.8%) of 255 receiving placebo i
69 kin cancers) among 825 patients who received ustekinumab and no deaths and one case of cancer (testic
70 o demonstrate endoscopic differences between ustekinumab and placebo (Hedges' g = 0.743 vs 0.460).
71 everely Active Ulcerative Colitis) comparing ustekinumab and placebo for UC were processed in a compu
72 ents with adverse events were similar in the ustekinumab and placebo groups (171 of 409 [41.8%] vs 86
73        Bimekizumab was more efficacious than ustekinumab and placebo in the treatment of moderate to
74 response rates for the combined groups given ustekinumab and placebo were 53% and 30% (P = .02), resp
75 who had a response to induction therapy with ustekinumab and underwent a second randomization, the pe
76 in AMAGINE-2 (P=0.08 for the comparison with ustekinumab) and 27% in AMAGINE-3 (P=0.007).
77 dalimumab, 2 etanercept, 1 infliximab, and 1 ustekinumab) and 3 cohort studies (1 adalimumab, 1 etane
78 s, infections, specific drugs (levofloxacin, ustekinumab), and malignancy.
79 ndomly assigned-206 to placebo, 205 to 45 mg ustekinumab, and 204 to 90 mg ustekinumab.
80                                  Guselkumab, ustekinumab, and secukinumab had similar adjusted surviv
81 , adalimumab, tofacitinib 10 mg, infliximab, ustekinumab, and vedolizumab (reference), respectively.
82 lizumab], and interleukin [IL] 12 and IL-23 [ustekinumab]) and oral small molecules that inhibit janu
83 r psoriasis: adalimumab (anti-TNF-alpha) and ustekinumab (anti-IL-12/23).
84 y required, and tofacitinib, vedolizumab and ustekinumab appear to be the most promising drugs.
85  interactive web response system) to receive ustekinumab (approximately 6 mg/kg intravenously on day
86 nd nail disease, adalimumab, etanercept, and ustekinumab are strongly recommended, and methotrexate,
87 odies to TNF-alpha,alpha4beta7 integrins and Ustekinumab are the lines of treatment for UC.
88                                 We evaluated ustekinumab as 8-week induction therapy and 44-week main
89 creased rates of response and remission with ustekinumab as maintenance therapy.
90                     Maintenance therapy with ustekinumab, as compared with placebo, resulted in signi
91 increased rate of response to induction with ustekinumab, as compared with placebo.
92 ce phase, 145 patients who had a response to ustekinumab at 6 weeks underwent a second randomization
93 ek 8 among patients who received intravenous ustekinumab at a dose of 130 mg (15.6%) or 6 mg per kilo
94                              The efficacy of ustekinumab at a dose of 45 or 90 mg was superior to tha
95  week 6 among patients receiving intravenous ustekinumab at a dose of either 130 mg or approximately
96 ly more likely to respond to adalimumab than ustekinumab at all time points (most strongly at 6 month
97 with psoriasis receiving risankizumab versus ustekinumab at an early time point.
98 nts who were initially randomised to receive ustekinumab at week 0 who achieved long-term response (a
99 roup); (3) approximately 6 mg/kg intravenous ustekinumab at week 0, then 90 mg subcutaneous ustekinum
100 , then ustekinumab at week 8; or intravenous ustekinumab at week 0, then placebo at week 8.
101 s well as the superiority of brodalumab over ustekinumab at week 12 with respect to a 100% reduction
102  weeks 0 and 4, with subsequent crossover to ustekinumab at week 12.
103 file of psoriatic skin lesions compared with ustekinumab at week 4.
104  disease, showing superiority to placebo and ustekinumab at week 48 across multiple endpoints.
105 ks 8-11; intravenous placebo at week 0, then ustekinumab at week 8; or intravenous ustekinumab at wee
106 then ustekinumab at weeks 8-11; subcutaneous ustekinumab at weeks 0-3, then placebo at weeks 8-11; in
107 iven subcutaneous placebo at weeks 0-3, then ustekinumab at weeks 8-11; subcutaneous ustekinumab at w
108 ere randomly assigned to receive intravenous ustekinumab (at a dose of 1, 3, or 6 mg per kilogram of
109 utaneous injections of either 45 or 90 mg of ustekinumab (at weeks 0 and 4) or high-dose etanercept (
110                 The structure indicates that ustekinumab binds to the same epitope on p40 in both IL-
111 mparable between adalimumab, infliximab, and ustekinumab but significantly lower for etanercept.
112 e biologics included adalimumab, infliximab, ustekinumab (CD only), and vedolizumab; second-line biol
113 ecular and cellular evaluations conducted in ustekinumab clinical programs have provided numerous ins
114 were included in the etanercept, adalimumab, ustekinumab cohorts, respectively, and 3,421 participant
115 evidence supported the use of adalimumab and ustekinumab compared with certolizumab pegol and upadaci
116                  Although steady-state serum ustekinumab concentrations were reached by week 12, no p
117  weeks, or every 8 weeks; patients receiving ustekinumab continued to receive ustekinumab every 12 we
118 agnosis of CD and a claim for vedolizumab or ustekinumab (defined as the index treatment) between Jan
119 f-of-concept setting systemic treatment with ustekinumab diminished imiquimod-induced inflammation.
120 oups that received placebo or four different ustekinumab dosages at weeks 0, 1, 2, 3, 7, 11, 15, and
121                                              Ustekinumab doses were 27 mg, 90 mg q8w, 90 mg, or 180 m
122 ses in patients with psoriasis compared with ustekinumab (dual IL-12/IL-23 inhibitor), but comparativ
123 fections occurred in 7 patients (6 receiving ustekinumab) during induction and 11 patients (4 receivi
124 uring induction and 11 patients (4 receiving ustekinumab) during maintenance.
125 m studies are needed to further characterise ustekinumab efficacy and safety for treatment of psoriat
126              Acitretin treatment may support ustekinumab efficacy, possibly by suppressing TH17 respo
127  to receive an intravenous induction dose of ustekinumab (either 130 mg [320 patients] or a weight-ra
128 ents to receive a single intravenous dose of ustekinumab (either 130 mg or approximately 6 mg per kil
129 cutaneous maintenance injections of 90 mg of ustekinumab (either every 12 weeks [172 patients] or eve
130 cutaneous maintenance injections of 90 mg of ustekinumab (either every 8 weeks or every 12 weeks) or
131 pha antagonists, vedolizumab, tofacitnib, or ustekinumab, either as monotherapy or in combination (wi
132 crosis factor-a antagonists, vedolizumab, or ustekinumab, either as monotherapy or in combination (wi
133  1.97, and 2.49 per 100 patient-years in the ustekinumab, etanercept, adalimumab, and infliximab coho
134                           New treatment with ustekinumab, etanercept, and methotrexate.
135 for psoriasis and started new treatment with ustekinumab, etanercept, or methotrexate.
136 g patients assigned to 90 mg of subcutaneous ustekinumab every 12 weeks (38.4%) or every 8 weeks (43.
137 2 +/- 4.2; P < .0001) but not in those given ustekinumab every 12 weeks (from 6.1 +/- 5.7 to 7.2 +/-
138 s receiving ustekinumab continued to receive ustekinumab every 12 weeks, and patients receiving place
139 S from baseline) at week 44 if they received ustekinumab every 8 weeks (50% in the randomized mainten
140 ogic improvement continued in patients given ustekinumab every 8 weeks (from 7.1 +/- 6.2 to 5.2 +/- 4
141 tekinumab at week 0, then 90 mg subcutaneous ustekinumab every 8 weeks from week 8 to week 40 (usteki
142 In the groups receiving maintenance doses of ustekinumab every 8 weeks or every 12 weeks, 53.1% and 4
143                     The crystal structure of ustekinumab Fab (antigen binding fragment of mAb), in co
144                                              Ustekinumab Fab binds the D1 domain of the p40 subunit i
145 crossed over such that all patients received ustekinumab for 52 weeks.
146 nt who became pregnant during treatment with ustekinumab for a refractory CD and which ended in misca
147 clude vedolizumab for ulcerative colitis and ustekinumab for Crohn's disease, which target cellular a
148 e aimed to assess the efficacy and safety of ustekinumab for psoriatic arthritis in this phase II stu
149 temic therapies, etanercept, adalimumab, and ustekinumab for the treatment of psoriasis.
150                        In 1 phase 2 trial of ustekinumab for treatment of psoriatic arthritis, joint
151 p had an IGA response versus 87 (53%) in the ustekinumab group (risk difference 30 [95% CI 22-39]; p<
152 oup had PASI90 versus 81 (50%) of 163 in the ustekinumab group (risk difference 35 [95% CI 27-43]; p<
153              29 (15%) of 191 patients in the ustekinumab group and 46 (24%) of 195 in the adalimumab
154 t randomisation (49 for placebo; 50 for each ustekinumab group).
155 inumab every 8 weeks from week 8 to week 40 (ustekinumab group); or (4) intravenous placebo every 4 w
156  18-mg and 90-mg risankizumab groups and the ustekinumab group, 5 patients (12%), 6 patients (15%), a
157 oup vs 32 weeks (95% CI, 28-40 weeks) in the ustekinumab group.
158 nkizumab groups, as compared with 18% in the ustekinumab group.
159 Crohn's disease, those receiving intravenous ustekinumab had a significantly higher rate of response
160  and 70.6% of patients who received 90 mg of ustekinumab had cleared or minimal disease according to
161 ompared to infliximab, patients treated with ustekinumab had significantly higher costs.
162         Patients with an initial response to ustekinumab had significantly increased rates of respons
163    After accounting for relevant covariates, ustekinumab had the highest first-course drug survival.
164  vedolizumab and 11.6% of patients receiving ustekinumab had undergone a CD-related surgery.
165                   A differential response to ustekinumab has been confirmed in HLA-C*06:02-positive v
166  of cytokines, such as IL-12 and IL-23 using ustekinumab, has proven effective in randomized studies
167 was lower for secukinumab when compared with ustekinumab (hazard ratio [HR] 0.66, 95% confidence inte
168 of discontinuation was comparable to that of ustekinumab (HR 0.95, 95% CI 0.61-1.49).
169 alimumab (HR = 0.93, 95% CI = 0.69-1.26), or ustekinumab (HR = 0.92, 95% CI = 0.60-1.41) compared wit
170 ; adalimumab: HR = 1.26, 95% CI = 0.86-1.84; ustekinumab: HR = 1.22, 95% CI = 0.75-1.99).
171 tekinumab (if in the placebo group) or 90 mg ustekinumab (if in the 45 mg group).
172 red masked early-escape and were given 45 mg ustekinumab (if in the placebo group) or 90 mg ustekinum
173 40 subunit of the cytokines IL-12 and IL-13 (ustekinumab), IL-17 (secukinumab, ixekizumab, bimekizuma
174 tor alpha inhibitors, interleukin (IL)-17Ai, ustekinumab, IL-23i, dupilumab, or apremilast.
175  cross-over trial of the clinical effects of ustekinumab in 104 patients with moderate-to-severe Croh
176 eous injections or 1 intravenous infusion of ustekinumab in 27 patients who were primary or secondary
177                                 We evaluated ustekinumab in adults with moderate-to-severe Crohn's di
178 n of the HLA-C*06:02 allele with response to ustekinumab in large cohorts of patients from the phase
179 fety of Brodalumab Compared With Placebo and Ustekinumab in Moderate to Severe Plaque Psoriasis in Su
180 orts of patients from the phase 3 studies of ustekinumab in moderate-to-severe psoriasis.
181 3 trial to assess the safety and efficacy of ustekinumab in patients with active psoriatic arthritis.
182               Data from the UNIFI program of ustekinumab in patients with UC treated with ustekinumab
183 ustekinumab in patients with UC treated with ustekinumab indicated the achievement of histo-endoscopi
184                                              Ustekinumab induced a clinical response in patients with
185                                              Ustekinumab induced and maintained significantly higher
186                                              Ustekinumab-induced remissions suggest that T cells play
187                                              Ustekinumab induces and maintains histologic improvement
188 Study to Evaluate the Safety and Efficacy of Ustekinumab Induction and Maintenance Therapy in Partici
189 he mean GHAS was significantly reduced after ustekinumab induction treatment (from 10.4 +/- 7.0 to 7.
190 reported across treatment cohorts, including ustekinumab, infliximab, adalimumab, etanercept, and non
191 , and joint disease, adalimumab, etanercept, ustekinumab, infliximab, methotrexate, apremilast, and g
192 cribe unique observations about IL-12p35 and ustekinumab interactions with p40 that account for its d
193                                              Ustekinumab is a fully human monoclonal antibody (mAb) t
194                                              Ustekinumab is a fully human monoclonal antibody against
195                                              Ustekinumab is a human monoclonal antibody that binds to
196                                              Ustekinumab is a human monoclonal antibody that inhibits
197                                              Ustekinumab is a monoclonal antibody against the p40 sub
198                                              Ustekinumab is a relatively new pharmacotherapy and in a
199                                     Although ustekinumab is an effective therapy for moderate to seve
200                                              Ustekinumab is an effective treatment for psoriasis, but
201          The fully human monoclonal antibody ustekinumab is an efficacious treatment for moderate-to-
202                                              Ustekinumab is approved for psoriasis and psoriatic arth
203                                              Ustekinumab is currently being explored for the treatmen
204                                              Ustekinumab is generally well tolerated but does not sho
205        One of the first to enter the clinic, ustekinumab, is a human monoclonal antibody (mAb) that b
206              Subsequent to the generation of ustekinumab, it was discovered that IL-23 also contains
207 patients, we evaluated the impact of ADAs on ustekinumab level and clinical response as assessed by t
208  part of this variation by reducing the free ustekinumab level.
209 rant ELISA were associated with lower median ustekinumab levels (-0.62 mug/ml [95% CI = -1.190 to -0.
210                                  Circulating ustekinumab levels were measured using an ELISA.
211                                 Subcutaneous ustekinumab maintained remission in patients who had a c
212 provements occurred in patients who received ustekinumab maintenance therapy every 8 weeks.
213 ek 44 (all P < .05) in patients who received ustekinumab maintenance therapy.
214 thritis, our case series raises concern that ustekinumab may unmask or aggravate joint disease in sel
215 , etanercept, intralesional corticosteroids, ustekinumab, methotrexate sodium, and acitretin are reco
216                         We report 4 cases of ustekinumab monotherapy for plaque psoriasis that result
217 re enrolled and randomly assigned to receive ustekinumab (n=191) or adalimumab (n=195).
218 population and received mirikizumab (n=579), ustekinumab (n=287), or placebo (n=199).
219 etanercept (n=1,098), infliximab (n=96), and ustekinumab (n=450) were available.
220 9; adalimumab, n = 538; etanercept, n = 104; ustekinumab, n = 597).
221 were randomized to receive an anti-IL-12/23 (ustekinumab, n=50), anti-tumor necrosis factor-a (TNF-al
222 -controlled trial to determine the effect of ustekinumab on aortic vascular inflammation (AVI) measur
223                  We evaluated the effects of ustekinumab on histologic CD activity in an analysis of
224          No increased risk was observed with ustekinumab or etanercept.
225 itinib) or intermediate efficacy medication (ustekinumab or mirikizumab) rather than a lower efficacy
226 etin, adalimumab, etanercept, infliximab, or ustekinumab or phototherapy for psoriasis.
227 were more frequent with brodalumab than with ustekinumab or placebo.
228 were re-randomised at week 40 to maintenance ustekinumab or withdrawal from treatment until loss of r
229 dication (eg, tofacitinib, upadacitinib, and ustekinumab) or an intermediate-efficacy medication (eg,
230 response system) to 45 mg ustekinumab, 90 mg ustekinumab, or placebo at week 0, week 4, and every 12
231 mab, vedolizumab, tofacitinib, upadacitinib, ustekinumab, ozanimod, etrasimod, risankizumab, and guse
232 -line treatment with adalimumab (p < 0.001), ustekinumab (p < 0.001) and vedolizumab (p < 0.017), sho
233 as compared with 40% (16 of 40 patients) for ustekinumab (P<0.001); the percentage of patients with a
234 6.6%, 34.1%, and 39.7% for 1, 3, and 6 mg of ustekinumab per kilogram, respectively, as compared with
235                        Absence of detectable ustekinumab regardless of ADA status correlated with poo
236 3-helper T cell 17 (IL-23-TH17) pathway with ustekinumab represents an efficacious and, based on its
237 mab, vedolizumab, golimumab, adalimumab, and ustekinumab, respectively.
238 ty evidence supported the use of adalimumab, ustekinumab, risankizumab, guselkumab, and upadacitinib,
239  use of infliximab, adalimumab, vedolizumab, ustekinumab, risankizumab, mirikizumab, and guselkumab,
240 ecommends the use of infliximab, adalimumab, ustekinumab, risankizumab, mirikizumab, guselkumab, or u
241 cation (infliximab, adalimumab, vedolizumab, ustekinumab, risankizumab, mirikizumab, or guselkumab) r
242 rscore the need for further investigation of ustekinumab's effects on psoriatic arthritis.
243                                       No new ustekinumab safety signals were observed.
244                                  Adalimumab, ustekinumab, secukinumab, guselkumab, ixekizumab.
245                                              Ustekinumab seems to be efficacious for the treatment of
246  her abdominal symptoms mildly improved with ustekinumab, she developed new bilateral lower extremity
247  with anti-TNF alpha agents, vedolizumab and ustekinumab should be favoured over anti-TNF alpha agent
248            The patient with PRP who received ustekinumab showed regression of skin lesions after 2 we
249                                              Ustekinumab significantly improved active psoriatic arth
250                                              Ustekinumab significantly reduced signs and symptoms of
251  least 1 year in those receiving maintenance ustekinumab than in those withdrawn from treatment at we
252 ropenia were higher with brodalumab and with ustekinumab than with placebo.
253 zed the two IgG1 antibodies, briakinumab and ustekinumab, that have similar Fc parts but different te
254  cases, psoriasis improved dramatically with ustekinumab therapy while psoriatic arthritis flared.
255                                   Open-label ustekinumab therapy, though associated with a modest dec
256 tration and is enriched in non-responders to ustekinumab therapy.
257 y innate and T-cell-derived cytokines during ustekinumab therapy.
258  or serious adverse events in patients given ustekinumab through week 8 compared with placebo.
259  patients with CD, the treatment sequence of ustekinumab to infliximab was associated with the highes
260 rmediate-efficacy medication (eg, golimumab, ustekinumab, tofacitinib, filgotinib, and mirikizumab) r
261 ecrosis factor biologic agents, vedolizumab, ustekinumab, tofacitinib, methotrexate, and corticostero
262                                         More ustekinumab-treated (87 of 205 [42.4%] in the 45 mg grou
263 43 patients were randomized, and at week 12, ustekinumab-treated patients had a -18.65% (95% confiden
264 (78%) placebo-treated patients and 170 (85%) ustekinumab-treated patients, with infections most commo
265 ne (2%) placebo-treated patient and six (3%) ustekinumab-treated patients.
266 following brodalumab treatment compared with ustekinumab treatment (anti-IL-23/-IL-12).
267 ent, lesional skin samples were taken before ustekinumab treatment and 4 and 28 weeks after treatment
268                                              Ustekinumab treatment did not show a significant reducti
269                                              Ustekinumab treatment induced sustained remissions in al
270                                              Ustekinumab treatment is currently ongoing in all 4 pati
271                    At the end of 52 weeks of ustekinumab treatment, there was no change in AVI compar
272 two patients shortly after the initiation of ustekinumab treatment; both patients were withdrawn from
273           Despite early results of a phase 2 ustekinumab trial suggesting efficacy for both plaque ps
274 iximab and adalimumab vs etanercept, whereas ustekinumab users had lower risk of having a serious inf
275 as compared with the MES for differentiating ustekinumab vs placebo treatment response and agreement
276 d 348 maintenance patients, CDS was lower in ustekinumab vs placebo users at week 8 (141.9 vs 184.3;
277 nt in a greater proportion of patients given ustekinumab vs placebo.
278                                              Ustekinumab was also evaluated as subcutaneous maintenan
279 79; 95% CI 1.49-2.16) vs etanercept, whereas ustekinumab was associated with a lower risk of having a
280                               Thus, although ustekinumab was designed to target IL-12, it also modula
281                                              Ustekinumab was more effective than placebo for inducing
282 ependent increase in serum concentrations of ustekinumab was recorded.
283 condary nonresponders), clinical response to ustekinumab was significantly greater than the group giv
284 Median time to relapse from the last dose of ustekinumab was similar between groups as well: 36 weeks
285 The incidence of serious adverse events with ustekinumab was similar to that with placebo.
286 es at week 8 to subcutaneous and intravenous ustekinumab were 43% and 54%, respectively.
287 analysis showed adalimumab, secukinumab, and ustekinumab were comparable in terms of high efficacy an
288 and safety of a crossover from etanercept to ustekinumab were evaluated after week 12.
289 val = 1.24-2.83), whereas patients receiving ustekinumab were more likely to persist (hazard ratio =
290  to discontinue therapy, whereas patients on ustekinumab were more likely to persist (HR 0.48; 95% CI
291  8 weeks after administration of intravenous ustekinumab were randomly assigned again to receive subc
292 which the 397 patients who had a response to ustekinumab were randomly assigned to receive subcutaneo
293 gic exposure, upadacitinib, tofacitinib, and ustekinumab were ranked highest for achieving remission.
294 tudy and a phase II study of risankizumab vs ustekinumab) were analyzed by using histopathology, immu
295 t the p40 subunit of interleukins 12 and 23, ustekinumab, were used to treat patients with relapsing-
296 treated a series of 4 patients with GPP with ustekinumab, which was applied on an outpatient basis ac
297 een HLA-C*06:02 and drug type (adalimumab or ustekinumab) while accounting for potentially confoundin
298 oriasis (adalimumab, etanercept, infliximab, ustekinumab) with the possibility to switch between trea
299 oriasis molecular signature in lesions after ustekinumab withdrawal, and serum IL-19 levels increased
300 onide and subsequently continued to tolerate ustekinumab without recurrence of LCV.

 
Page Top