ライフサイエンスコーパス: ustekinumab

1 l carcinoma developed in 1 patient receiving ustekinumab.

2 mportant molecular binding interactions with ustekinumab.

3 the PASI within 12 weeks after crossover to ustekinumab.

4 efore and after crossover from etanercept to ustekinumab.

5 oved biologic agents, such as vedolizumab or ustekinumab.

6 e may be a predictor of improved response to ustekinumab.

7 ohn's disease who participated in a trial of ustekinumab.

8 responses superior to those associated with ustekinumab.

9 , 205 to 45 mg ustekinumab, and 204 to 90 mg ustekinumab.

10 1.6-20.1); adalimumab, 13.9 (11.4-16.6); and ustekinumab, 15.1 (10.8-21.1).

11 y higher with 210 mg of brodalumab than with ustekinumab (44% vs. 22% [AMAGINE-2] and 37% vs. 19% [AM

12 psoriasis were randomly assigned to receive ustekinumab 45 mg (n=255) or 90 mg (n=256) at weeks 0 an

13 171 (67.1%) patients receiving ustekinumab 45 mg, 170 (66.4%) receiving ustekinumab 90

14 ining patients in the placebo group received ustekinumab 45 mg, which they continued at week 28 and e

15 brodalumab (210 mg or 140 mg every 2 weeks), ustekinumab (45 mg for patients with a body weight </=10

16 mg or 180-mg doses at weeks 0, 4, and 16) or ustekinumab (45 or 90 mg, according to body weight, at w

17 Subcutaneous ustekinumab, 45 mg, at weeks 0 and 4 and quarterly there

18 6 (n=76; Group 1) or placebo (weeks 0-3) and ustekinumab (63 mg) at weeks 12 and 16 (n=70; Group 2).

19 tive patients demonstrated good responses to ustekinumab (86% vs. 76%, respectively, achieved at leas

20 ing ustekinumab 45 mg, 170 (66.4%) receiving ustekinumab 90 mg, and eight (3.1%) receiving placebo ac

21 interactive voice response system to either ustekinumab (90 mg or 63 mg) every week for 4 weeks (wee

22 luated the anti-IL12/23 monoclonal antibody, ustekinumab (90 mg subcutaneous at weeks 0 and 4, then e

23 zation to receive subcutaneous injections of ustekinumab (90 mg) or placebo at weeks 8 and 16.

24 eractive voice-web response system) to 45 mg ustekinumab, 90 mg ustekinumab, or placebo at week 0, we

25 tients with Crohn's disease, the efficacy of ustekinumab, a human monoclonal antibody against interle

26 We assessed ustekinumab, a human monoclonal antibody directed agains

27 Ustekinumab, a monoclonal antibody to the p40 subunit of

28 Ustekinumab, a therapeutic agent targeting both cytokine

29 sity hospital department of dermatology with ustekinumab according to the dosing regimen approved for

30 atment with four specific drugs: etanercept, ustekinumab, adalimumab, and methotrexate.

31 We compared two biologic agents, ustekinumab (an interleukin-12 and interleukin-23 blocke

32 We treated our patient with ustekinumab, an antibody that binds the p40 subunit of i

33 thus prevents interleukin-23 signaling, and ustekinumab, an interleukin-12 and interleukin-23 inhibi

34 in 278 (54.5%) of the 510 patients receiving ustekinumab and 123 (48.2%) of the 255 receiving placebo

35 tients were randomly assigned to maintenance ustekinumab and 160 to withdrawal.

36 2 in 66.0% of patients who received 45 mg of ustekinumab and 69.2% of patients who received 90 mg of

37 rly, 65.1% of patients who received 45 mg of ustekinumab and 70.6% of patients who received 90 mg of

38 2 in 67.5% of patients who received 45 mg of ustekinumab and 73.8% of patients who received 90 mg, as

39 Ustekinumab and briakinumab, monoclonal antibodies to th

40 and 69.2% of patients who received 90 mg of ustekinumab and in 70.0% who received etanercept; 1.9%,

41 rred in six (1.2%) of 510 patients receiving ustekinumab and in two (0.8%) of 255 receiving placebo i

42 ents with adverse events were similar in the ustekinumab and placebo groups (171 of 409 [41.8%] vs 86

43 response rates for the combined groups given ustekinumab and placebo were 53% and 30% (P = .02), resp

44 in AMAGINE-2 (P=0.08 for the comparison with ustekinumab) and 27% in AMAGINE-3 (P=0.007).

45 ndomly assigned-206 to placebo, 205 to 45 mg ustekinumab, and 204 to 90 mg ustekinumab.

46 y required, and tofacitinib, vedolizumab and ustekinumab appear to be the most promising drugs.

47 nd nail disease, adalimumab, etanercept, and ustekinumab are strongly recommended, and methotrexate,

48 creased rates of response and remission with ustekinumab as maintenance therapy.

49 Maintenance therapy with ustekinumab, as compared with placebo, resulted in signi

50 increased rate of response to induction with ustekinumab, as compared with placebo.

51 ce phase, 145 patients who had a response to ustekinumab at 6 weeks underwent a second randomization

52 The efficacy of ustekinumab at a dose of 45 or 90 mg was superior to tha

53 week 6 among patients receiving intravenous ustekinumab at a dose of either 130 mg or approximately

54 nts who were initially randomised to receive ustekinumab at week 0 who achieved long-term response (a

55 , then ustekinumab at week 8; or intravenous ustekinumab at week 0, then placebo at week 8.

56 s well as the superiority of brodalumab over ustekinumab at week 12 with respect to a 100% reduction

57 weeks 0 and 4, with subsequent crossover to ustekinumab at week 12.

58 ks 8-11; intravenous placebo at week 0, then ustekinumab at week 8; or intravenous ustekinumab at wee

59 then ustekinumab at weeks 8-11; subcutaneous ustekinumab at weeks 0-3, then placebo at weeks 8-11; in

60 iven subcutaneous placebo at weeks 0-3, then ustekinumab at weeks 8-11; subcutaneous ustekinumab at w

61 ere randomly assigned to receive intravenous ustekinumab (at a dose of 1, 3, or 6 mg per kilogram of

62 utaneous injections of either 45 or 90 mg of ustekinumab (at weeks 0 and 4) or high-dose etanercept (

63 The structure indicates that ustekinumab binds to the same epitope on p40 in both IL-

64 ecular and cellular evaluations conducted in ustekinumab clinical programs have provided numerous ins

65 were included in the etanercept, adalimumab, ustekinumab cohorts, respectively, and 3,421 participant

66 Although steady-state serum ustekinumab concentrations were reached by week 12, no p

67 weeks, or every 8 weeks; patients receiving ustekinumab continued to receive ustekinumab every 12 we

68 f-of-concept setting systemic treatment with ustekinumab diminished imiquimod-induced inflammation.

69 oups that received placebo or four different ustekinumab dosages at weeks 0, 1, 2, 3, 7, 11, 15, and

70 Ustekinumab doses were 27 mg, 90 mg q8w, 90 mg, or 180 m

71 fections occurred in 7 patients (6 receiving ustekinumab) during induction and 11 patients (4 receivi

72 uring induction and 11 patients (4 receiving ustekinumab) during maintenance.

73 m studies are needed to further characterise ustekinumab efficacy and safety for treatment of psoriat

74 Acitretin treatment may support ustekinumab efficacy, possibly by suppressing TH17 respo

75 ents to receive a single intravenous dose of ustekinumab (either 130 mg or approximately 6 mg per kil

76 cutaneous maintenance injections of 90 mg of ustekinumab (either every 8 weeks or every 12 weeks) or

77 1.97, and 2.49 per 100 patient-years in the ustekinumab, etanercept, adalimumab, and infliximab coho

78 s receiving ustekinumab continued to receive ustekinumab every 12 weeks, and patients receiving place

79 In the groups receiving maintenance doses of ustekinumab every 8 weeks or every 12 weeks, 53.1% and 4

80 The crystal structure of ustekinumab Fab (antigen binding fragment of mAb), in co

81 Ustekinumab Fab binds the D1 domain of the p40 subunit i

82 nt who became pregnant during treatment with ustekinumab for a refractory CD and which ended in misca

83 clude vedolizumab for ulcerative colitis and ustekinumab for Crohn's disease, which target cellular a

84 e aimed to assess the efficacy and safety of ustekinumab for psoriatic arthritis in this phase II stu

85 temic therapies, etanercept, adalimumab, and ustekinumab for the treatment of psoriasis.

86 In 1 phase 2 trial of ustekinumab for treatment of psoriatic arthritis, joint

87 t randomisation (49 for placebo; 50 for each ustekinumab group).

88 18-mg and 90-mg risankizumab groups and the ustekinumab group, 5 patients (12%), 6 patients (15%), a

89 nkizumab groups, as compared with 18% in the ustekinumab group.

90 Crohn's disease, those receiving intravenous ustekinumab had a significantly higher rate of response

91 and 70.6% of patients who received 90 mg of ustekinumab had cleared or minimal disease according to

92 Patients with an initial response to ustekinumab had significantly increased rates of respons

93 After accounting for relevant covariates, ustekinumab had the highest first-course drug survival.

94 A differential response to ustekinumab has been confirmed in HLA-C*06:02-positive v

95 of cytokines, such as IL-12 and IL-23 using ustekinumab, has proven effective in randomized studies

96 alimumab (HR = 0.93, 95% CI = 0.69-1.26), or ustekinumab (HR = 0.92, 95% CI = 0.60-1.41) compared wit

97 ; adalimumab: HR = 1.26, 95% CI = 0.86-1.84; ustekinumab: HR = 1.22, 95% CI = 0.75-1.99).

98 tekinumab (if in the placebo group) or 90 mg ustekinumab (if in the 45 mg group).

99 red masked early-escape and were given 45 mg ustekinumab (if in the placebo group) or 90 mg ustekinum

100 cross-over trial of the clinical effects of ustekinumab in 104 patients with moderate-to-severe Croh

101 eous injections or 1 intravenous infusion of ustekinumab in 27 patients who were primary or secondary

102 We evaluated ustekinumab in adults with moderate-to-severe Crohn's di

103 n of the HLA-C*06:02 allele with response to ustekinumab in large cohorts of patients from the phase

104 orts of patients from the phase 3 studies of ustekinumab in moderate-to-severe psoriasis.

105 3 trial to assess the safety and efficacy of ustekinumab in patients with active psoriatic arthritis.

106 Ustekinumab induced a clinical response in patients with

107 Ustekinumab-induced remissions suggest that T cells play

108 reported across treatment cohorts, including ustekinumab, infliximab, adalimumab, etanercept, and non

109 , and joint disease, adalimumab, etanercept, ustekinumab, infliximab, methotrexate, apremilast, and g

110 cribe unique observations about IL-12p35 and ustekinumab interactions with p40 that account for its d

111 Ustekinumab is a fully human monoclonal antibody (mAb) t

112 Ustekinumab is a fully human monoclonal antibody against

113 Ustekinumab is a human monoclonal antibody that binds to

114 Ustekinumab is a human monoclonal antibody that inhibits

115 Ustekinumab is a monoclonal antibody against the p40 sub

116 Ustekinumab is a relatively new pharmacotherapy and in a

117 The fully human monoclonal antibody ustekinumab is an efficacious treatment for moderate-to-

118 Ustekinumab is approved for psoriasis and psoriatic arth

119 Ustekinumab is generally well tolerated but does not sho

120 One of the first to enter the clinic, ustekinumab, is a human monoclonal antibody (mAb) that b

121 Subsequent to the generation of ustekinumab, it was discovered that IL-23 also contains

122 Subcutaneous ustekinumab maintained remission in patients who had a c

123 thritis, our case series raises concern that ustekinumab may unmask or aggravate joint disease in sel

124 , etanercept, intralesional corticosteroids, ustekinumab, methotrexate sodium, and acitretin are reco

125 We report 4 cases of ustekinumab monotherapy for plaque psoriasis that result

126 etanercept (n=1,098), infliximab (n=96), and ustekinumab (n=450) were available.

127 9; adalimumab, n = 538; etanercept, n = 104; ustekinumab, n = 597).

128 were randomized to receive an anti-IL-12/23 (ustekinumab, n=50), anti-tumor necrosis factor-a (TNF-al

129 No increased risk was observed with ustekinumab or etanercept.

130 etin, adalimumab, etanercept, infliximab, or ustekinumab or phototherapy for psoriasis.

131 were more frequent with brodalumab than with ustekinumab or placebo.

132 were re-randomised at week 40 to maintenance ustekinumab or withdrawal from treatment until loss of r

133 response system) to 45 mg ustekinumab, 90 mg ustekinumab, or placebo at week 0, week 4, and every 12

134 as compared with 40% (16 of 40 patients) for ustekinumab (P<0.001); the percentage of patients with a

135 6.6%, 34.1%, and 39.7% for 1, 3, and 6 mg of ustekinumab per kilogram, respectively, as compared with

136 3-helper T cell 17 (IL-23-TH17) pathway with ustekinumab represents an efficacious and, based on its

137 rscore the need for further investigation of ustekinumab's effects on psoriatic arthritis.

138 No new ustekinumab safety signals were observed.

139 Ustekinumab seems to be efficacious for the treatment of

140 The patient with PRP who received ustekinumab showed regression of skin lesions after 2 we

141 Ustekinumab significantly improved active psoriatic arth

142 Ustekinumab significantly reduced signs and symptoms of

143 least 1 year in those receiving maintenance ustekinumab than in those withdrawn from treatment at we

144 ropenia were higher with brodalumab and with ustekinumab than with placebo.

145 zed the two IgG1 antibodies, briakinumab and ustekinumab, that have similar Fc parts but different te

146 cases, psoriasis improved dramatically with ustekinumab therapy while psoriatic arthritis flared.

147 Open-label ustekinumab therapy, though associated with a modest dec

148 y innate and T-cell-derived cytokines during ustekinumab therapy.

149 or serious adverse events in patients given ustekinumab through week 8 compared with placebo.

150 More ustekinumab-treated (87 of 205 [42.4%] in the 45 mg grou

151 (78%) placebo-treated patients and 170 (85%) ustekinumab-treated patients, with infections most commo

152 ne (2%) placebo-treated patient and six (3%) ustekinumab-treated patients.

153 ent, lesional skin samples were taken before ustekinumab treatment and 4 and 28 weeks after treatment

154 Ustekinumab treatment did not show a significant reducti

155 Ustekinumab treatment induced sustained remissions in al

156 Ustekinumab treatment is currently ongoing in all 4 pati

157 two patients shortly after the initiation of ustekinumab treatment; both patients were withdrawn from

158 Despite early results of a phase 2 ustekinumab trial suggesting efficacy for both plaque ps

159 Ustekinumab was also evaluated as subcutaneous maintenan

160 Thus, although ustekinumab was designed to target IL-12, it also modula

161 ependent increase in serum concentrations of ustekinumab was recorded.

162 condary nonresponders), clinical response to ustekinumab was significantly greater than the group giv

163 es at week 8 to subcutaneous and intravenous ustekinumab were 43% and 54%, respectively.

164 analysis showed adalimumab, secukinumab, and ustekinumab were comparable in terms of high efficacy an

165 and safety of a crossover from etanercept to ustekinumab were evaluated after week 12.

166 val = 1.24-2.83), whereas patients receiving ustekinumab were more likely to persist (hazard ratio =

167 to discontinue therapy, whereas patients on ustekinumab were more likely to persist (HR 0.48; 95% CI

168 which the 397 patients who had a response to ustekinumab were randomly assigned to receive subcutaneo

169 t the p40 subunit of interleukins 12 and 23, ustekinumab, were used to treat patients with relapsing-

170 treated a series of 4 patients with GPP with ustekinumab, which was applied on an outpatient basis ac

171 oriasis (adalimumab, etanercept, infliximab, ustekinumab) with the possibility to switch between trea