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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.
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
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
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
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
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
51 placebo received masked rescue therapy with ustekinumab; all other participants remained on their ra
54 ith Crohn's disease before administration of ustekinumab, an anti-IL-12/IL-23 antibody, positively co
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
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
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
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
77 dalimumab, 2 etanercept, 1 infliximab, and 1 ustekinumab) and 3 cohort studies (1 adalimumab, 1 etane
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
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,
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
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
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
101 s well as the superiority of brodalumab over ustekinumab at week 12 with respect to a 100% reduction
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 (
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
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
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
125 m studies are needed to further characterise ustekinumab efficacy and safety for treatment of psoriat
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
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
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
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<
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
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
163 After accounting for relevant covariates, ustekinumab had the highest first-course drug survival.
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
169 alimumab (HR = 0.93, 95% CI = 0.69-1.26), or ustekinumab (HR = 0.92, 95% CI = 0.60-1.41) compared wit
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
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
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
181 3 trial to assess the safety and efficacy of ustekinumab in patients with active psoriatic arthritis.
183 ustekinumab in patients with UC treated with ustekinumab indicated the achievement of histo-endoscopi
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
207 patients, we evaluated the impact of ADAs on ustekinumab level and clinical response as assessed by t
209 rant ELISA were associated with lower median ustekinumab levels (-0.62 mug/ml [95% CI = -1.190 to -0.
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
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
225 itinib) or intermediate efficacy medication (ustekinumab or mirikizumab) rather than a lower efficacy
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
236 3-helper T cell 17 (IL-23-TH17) pathway with ustekinumab represents an efficacious and, based on its
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
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
251 least 1 year in those receiving maintenance ustekinumab than in those withdrawn from treatment at we
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.
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
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
267 ent, lesional skin samples were taken before ustekinumab treatment and 4 and 28 weeks after treatment
272 two patients shortly after the initiation of ustekinumab treatment; both patients were withdrawn from
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;
279 79; 95% CI 1.49-2.16) vs etanercept, whereas ustekinumab was associated with a lower risk of having a
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
287 analysis showed adalimumab, secukinumab, and ustekinumab were comparable in terms of high efficacy an
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