ライフサイエンスコーパス: abatacept

1 firming noninferiority of SC abatacept to IV abatacept.

2 5% CI 3.47-15.6) in C-peptide reduction with abatacept.

3 bal assessment was seen only with 3 mg/kg of abatacept.

4 atigue) demonstrated a treatment effect with abatacept.

5 eived placebo during year 1 were switched to abatacept.

6 dema, which were absent after treatment with abatacept.

7 als with the T-cell co-stimulation modulator abatacept.

8 ived upadacitinib, and 309 patients received abatacept.

9 provements were significantly higher for the abatacept 10 mg/kg (P = 0.006) and 30/10 mg/kg (P = 0.02

10 ry analysis suggest the potential promise of abatacept 10 mg/kg for multiple sclerosis.

11 2 in the induction trials were randomized to abatacept 10 mg/kg or placebo every 4 weeks through week

12 % in the placebo, the abatacept 3 mg/kg, the abatacept 10 mg/kg, and the abatacept 30/10 mg/kg groups

13 etes were randomly assigned (2:1) to receive abatacept (10 mg/kg, maximum 1000 mg per dose) or placeb

14 ndomly assigned (1:1) to weekly subcutaneous abatacept 125 mg or placebo for 6 months followed by a d

15 e 19%, 33%, 48%, and 42% in the placebo, the abatacept 3 mg/kg, the abatacept 10 mg/kg, and the abata

16 1.4%, 19.0%, and 20.3% of patients receiving abatacept 30, 10, and 3 mg/kg achieved a clinical respon

17 7.2%, 10.2%, and 15.5% of patients receiving abatacept 30, 10, and 3 mg/kg achieved a clinical respon

18 and 490 patients with UC were randomized to abatacept 30, 10, or 3 mg/kg (according to body weight)

19 ept 3 mg/kg, the abatacept 10 mg/kg, and the abatacept 30/10 mg/kg groups, respectively.

20 tients were assigned to treatment groups (77 abatacept, 35 placebo).

21 e treated with adalimumab (13 326 patients), abatacept (5676 patients), rituximab (5444 patients), to

22 for adalimumab, 4.46 (95% CI 3.44-5.70) for abatacept, 6.15 (95% CI 4.76-7.84) for rituximab, 5.05 (

23 monstrate mice treated with a single dose of abatacept 8 h post SEB exposure had reduced pathology co

24 Despite the known benefits of abatacept (a CTLA-4-Ig fusion protein) treatment, its pr

25 Abatacept, a co-stimulatory blocker, and rituximab, a B

26 tement in the renal community, implying that abatacept, a costimulatory inhibitor that targets B7-1,

27 t as it can enable personalized therapy with abatacept, a CTLA-4 mimetic, and inform genetic counseli

28 tic and sustained improvement in response to abatacept, a CTLA4 (cytotoxic T lymphocyte antigen-4)-im

29 Here we provide exploratory evidence that abatacept, a drug that blocks CD80/86 co-stimulation, pr

30 Abatacept, a humanized version of CTLA4Ig, has been appr

31 BACKGROUND & AIMS: The efficacy of abatacept, a selective costimulation modulator, in Crohn

32 trial to evaluate the efficacy and safety of abatacept, a selective costimulation modulator, in patie

33 and safety of upadacitinib as compared with abatacept, a T-cell costimulation modulator, in patients

34 propensity score matching to patients using abatacept, a total of 22 569 propensity score-matched pa

35 going National Institutes of Health trial of abatacept (Abatacept and Cyclophosphamide Combination: E

36 had a recent infusion of or prescription for abatacept, adalimumab, etanercept, infliximab, rituximab

37 ated with a poor clinical response following abatacept administration.

38 ercentages of patients treated with 10 mg/kg abatacept also achieved ACR50 responses (41.7% versus 20

39 Abatacept, an FDA-approved therapeutic (CTLA-4-hFc fusio

40 participants, 110 were randomly assigned to abatacept and 103 to placebo.

41 6 reactions occurred in 17 [22%] patients on abatacept and 11 reactions in six [17%] on placebo).

42 l of 118 patients were randomized to receive abatacept and 57 to receive placebo.

43 patients, 693 of 736 (94.2%) treated with SC abatacept and 676 of 721 (93.8%) treated with IV abatace

44 e randomized and treated, 86.2% receiving SC abatacept and 82% receiving SC adalimumab completed 12 m

45 Abatacept and belatacept are clinically approved agents

46 nal Institutes of Health trial of abatacept (Abatacept and Cyclophosphamide Combination: Efficacy and

47 e of costimulation through administration of abatacept and inhibitors of B7-related molecules and CD4

48 sing new agents for GVHD prophylaxis such as abatacept and JAK inhibitors with PTCy inspire hope for

49 f adverse events (AEs) was comparable in the abatacept and placebo groups (90.9% versus 91.5%), but s

50 The abatacept and placebo groups exhibited similar frequenci

51 ding halofuginone, basiliximab, alemtuzumab, abatacept and rapamycin have been proposed to be clinica

52 Abatacept and rituximab were not associated with increas

53 In the SC abatacept and SC adalimumab groups, the incidence of ser

54 The results demonstrate that SC abatacept and SC adalimumab have comparable efficacy in

55 head-to-head comparison of subcutaneous (SC) abatacept and SC adalimumab, both administered along wit

56 s factor (TNF) inhibitors (TNFi), rituximab, abatacept and tocilizumab, following TNFi failure with n

57 , AND PARTICIPANTS: Psoriasis Treatment with Abatacept and Ustekinumab: a Study of Efficacy (PAUSE),

58 sphamide, and recent pivotal trials studying abatacept and vedolizumab for GVHD prophylaxis, whereas

59 b genes interacting with approved drugs like abatacept and zoledronic acid, as well as developmental

60 as interleukin-6 antagonists (MRA), CTLA4Ig (abatacept), and anti-B cell therapy (rituximab) have alr

61 gle chain Fv (DC2219), belimumab, atacicept, abatacept, and abetimus sodium.

62 rankings between our lead molecule MEDI5265, abatacept, and belatacept, depending on which type of AP

63 reagents such as recombinant interleukin-10, abatacept, and CD3-specific antibodies are feasible as t

64 exposures, individuals initiating rituximab, abatacept, and JAKis demonstrated higher incidence rates

65 a treatment, the promising alternatives MRA, abatacept, and rituximab have been tested.

66 emulsions on the stability of BSA, lysozyme, abatacept, and trastuzumab formulations containing surfa

67 Abatacept- and vehicle-treated groups both maintained co

68 n, mice were treated for up to 16 weeks with abatacept, anti-murine TNF antibody, or vehicle.

69 -clinical phase of rheumatoid arthritis with abatacept (APIPPRA) trial, we aimed to evaluate the feas

70 were randomized at a ratio of 2:1 to receive abatacept ( approximately 10 mg/kg of body weight) or pl

71 se [ approximately 10 mg/kg] on day 1) or IV abatacept ( approximately 10 mg/kg) on days 1, 15, and 2

72 Once-monthly infusion of a fixed dose of abatacept, approximately 10 mg/kg of body weight, or pla

73 the TL and PASI scores were observed in all abatacept arms; a response according to the investigator

74 These results do not support the use of abatacept as a therapeutic strategy for targeting podocy

75 Among the 58 patients who received abatacept as either a primary or rescue therapy, sustain

76 trials evaluated the efficacy and safety of abatacept as induction (IP) and maintenance (MP) therapy

77 Patients in the IM101075 trial received abatacept at 1 of 2 different dose regimens or placebo,

78 Abatacept at a dosage of 10 mg/kg elicited an increase i

79 Patients were randomized 2:1 to receive abatacept at a fixed dose approximating 10 mg/kg by weig

80 e randomized (1:1:1:1) to receive placebo or abatacept at doses of 3 mg/kg, 10 mg/kg, or 30/10 mg/kg

81 CD and 131 patients with UC who responded to abatacept at week 12 in the induction trials were random

82 Abatacept binding to CD80/CD86 induces and promotes regu

83 unction in type 1 diabetes, the finding that abatacept blunts this relationship renders the biomarker

84 Abatacept clearance increased with body weight and more

85 However, abatacept clearance was high in this population, and the

86 Abatacept + CNI/MTX may facilitate unrelated donor pool

87 For 7/8 MMUD and 8/8 MUD recipients, abatacept + CNI/MTX prophylaxis improved survival outcom

88 g FDA approval) was significantly higher for abatacept + CNI/MTX vs CNI/MTX (98% vs 75%; P = .0028).

89 For 8/8 MUDs, 2-year RFS for abatacept + CNI/MTX was numerically higher vs CNI/MTX (6

90 ns occurred in 3.8% of patients receiving SC abatacept compared to 9.1% of patients receiving SC adal

91 %), thus demonstrating the noninferiority of abatacept compared to adalimumab.

92 acept and 676 of 721 (93.8%) treated with IV abatacept completed 6 months.

93 Patients taking abatacept continued to take it.

94 MTX)-based GVHD prophylaxis, to test whether abatacept could decrease AGVHD.

95 ry signal by the CTLA4-Ig synthetic protein (abatacept) could prevent SEB-dependent pathology.

96 patient responses to CD28-ligand blockade by abatacept (CTLA-4-Ig) in conditions such as rheumatoid a

97 The selective costimulation modulator abatacept (CTLA-4Ig) binds to CD80 and CD86, blocking in

98 To describe the mechanisms of action of abatacept (CTLA4-Ig) and summarize the evidence of its e

99 Co-stimulation blockade with abatacept (CTLA4-Ig) will soon be licensed for the treat

100 Abatacept (CTLA4-Ig), etanercept (anti-TNF), or phosphat

101 Abatacept (CTLA4-Ig), the first selective T-cell costimu

102 Abatacept (cytotoxic T-lymphocyte-associated antigen 4-i

103 CTLA4-Ig/abatacept dampens activation of naive T cells by blockin

104 6-month treatment with abatacept decreases MRI inflammation, clinical symptoms,

105 The selective co-stimulation modulator abatacept demonstrated efficacy for treating rheumatoid

106 g tissues from SEB-exposed mice treated with abatacept demonstrated significantly lower levels of IL-

107 T cells in all patients after treatment with abatacept, demonstrating the effect of this drug on the

108 Abatacept did not impair the ability of mice to control

109 Abatacept did not maintain suppression of the pathogenic

110 n was 30.0% with upadacitinib and 13.3% with abatacept (difference, 16.8 percentage points; 95% CI, 1

111 hibition of CD28-mediated costimulation with abatacept does not seem to alter the inflammatory respon

112 was high in this population, and the current abatacept dosing may not achieve optimal exposure in all

113 adacitinib (15 mg once daily) or intravenous abatacept, each in combination with stable synthetic DMA

114 Abatacept effectively corrects key immune circuits in bo

115 in certain exploratory measures suggest some abatacept efficacy in patients with non-life-threatening

116 The domains of abatacept exhibit different conformational stabilities t

117 evere COVID-19 and achieved higher projected abatacept exposure had reduced mortality and a higher pr

118 cs (PK), which enabled an examination of how abatacept exposure-response relationships affected clini

119 ey are tailored for specific disease states--abatacept for autoimmune diseases and belatacept for tra

120 In this study, alternative biologics (abatacept, golimumab, and tocilizumab) were useful for t

121 ), but serious AEs (SAEs) were higher in the abatacept group (19.8 versus 6.8%).

122 6 months, 28 (57%) of 49 participants in the abatacept group and 15 (31%) of 49 participants in the p

123 Four (8%) of 49 participants in the abatacept group and 17 (35%) of 49 participants in the p

124 of ACR 20 responses were 50.4 percent in the abatacept group and 19.5 percent in the placebo group (P

125 eriod, seven (6%) of 110 participants in the abatacept group and 30 (29%) of 103 participants in the

126 Five patients (0.5%) in the abatacept group and 4 patients (0.8%) in the placebo gro

127 At 1 year, 64.8% of patients in the SC abatacept group and 63.4% in the SC adalimumab group dem

128 ercent and 5.0 percent, respectively, in the abatacept group and 71.4 percent and 3.0 percent, respec

129 fidence interval [95% CI] 72.4, 86.9) in the abatacept group and 82.5% (95% CI 72.6, 92.3) in the pla

130 tients in the upadacitinib group than in the abatacept group had elevated hepatic aminotransferase le

131 months, 27 (25%) of 110 participants in the abatacept group had progressed to rheumatoid arthritis,

132 Serious infections were more frequent in the abatacept group than in the placebo group (2.9% versus 1

133 ponses were also significantly higher in the abatacept group than in the placebo group (20.3 percent

134 x months, significantly more patients in the abatacept group than in the placebo group had a clinical

135 well: 36 weeks (95% CI, 36-48 weeks) in the abatacept group vs 32 weeks (95% CI, 28-40 weeks) in the

136 ammation (25 [51%] of 49 participants in the abatacept group, 12 [24%] of 49 in the placebo group; p=

137 In the abatacept group, post hoc analysis demonstrated further

138 70 in the upadacitinib group and 5.88 in the abatacept group, the mean change at week 12 was -2.52 an

139 measures that best discriminated between the abatacept groups and placebo, and the sensitivities of t

140 trol group, compared to 22% and 24% in the 2 abatacept groups).

141 patients that received a 3-mo treatment with abatacept had an increased ability to reduce T cell func

142 Subjects treated with abatacept had an increased percentage of naive and a cor

143 At 2 years, patients taking abatacept had maintained their responses on the American

144 Although abatacept has been used to treat irAEs, it risks neutral

145 Abatacept has shown clinical efficacy in treating some a

146 Of these agents, only rituximab and abatacept have been evaluated in multiple sclerosis pati

147 [HR], 1.91; 95% CI, 1.17-3.14), followed by abatacept (HR, 1.47; 95% CI, 1.03-2.11), and JAKis (HR,

148 However, abatacept in combination with biologic background therap

149 Abatacept in combination with MTX has the potential to p

150 Abatacept in combination with synthetic DMARDs was well

151 odel that could predict clinical response to abatacept in individuals with T1D.

152 sing the same data set from a large trial of abatacept in lupus nephritis (IM101075).

153 sing data from a large, multicenter trial of abatacept in lupus nephritis, to gain insight into which

154 rationale for conducting further studies of abatacept in lupus nephritis.

155 oups and to further examine the potential of abatacept in lupus nephritis.

156 ce Network's A Cooperative Clinical Study of Abatacept in Multiple Sclerosis trial were used to exami

157 of life, prevention of structural damage) of abatacept in patients with RA who have failed to respond

158 e of B7-1 immunostaining and the efficacy of abatacept in patients with recurrent FSGS after renal tr

159 We evaluated the effect of abatacept in recent-onset type 1 diabetes.

160 12 were the superiority of upadacitinib over abatacept in the change from baseline in the DAS28-CRP a

161 iologic DMARDs, upadacitinib was superior to abatacept in the change from baseline in the DAS28-CRP a

162 e CTLA-4-immunoglobulin (Ig) fusion protein (abatacept) in a mouse model of diabetes and in individua

163 ls of IL-2 (p < 0.0001) after treatment with abatacept, indicating that T cell proliferation is the m

164 Abatacept induced partial or complete remissions of prot

165 Abatacept-induced antibodies occurred in 1.1% of SC abat

166 neficial effect continues after cessation of abatacept infusions.

167 R stimulation being associated with relative abatacept insensitivity.

168 hort, grade 3-4 AGVHD was 2.3% (CNI/MTX plus abatacept, intention-to-treat population), which compare

169 Abatacept is a biologic developed for inflammatory arthr

170 Abatacept is a CTLA-4-Ig fusion protein that binds to th

171 Our findings demonstrate that abatacept is a robust and potentially credible drug to p

172 Abatacept is a selective costimulation modulator, used f

173 While the mechanism of action of abatacept is fundamentally different from that of anti-T

174 The studies showed that abatacept is not efficacious for the treatment of modera

175 Therefore, abatacept is not recommended for use in combination with

176 Abatacept is superior to immunosuppressants in controlli

177 lockade of CD28 costimulation with CTLA-4-Ig/Abatacept is used to dampen effector T cell responses in

178 te reactions (mostly mild) occurred in 19 SC abatacept (IV placebo)-treated patients (2.6%) and 18 IV

179 -cell activation using CTLA4-immunoglobulin (Abatacept), led to significant increases in survival dur

180 usly reported that costimulation blockade by abatacept limits the decline of beta-cell function and t

181 -free survival plots over 24 months favoured abatacept (log-rank test p=0.044).

182 extracellular domain of CTLA4 (also known as abatacept, marketed as Orencia), demonstrated reduced le

183 Our data indicate that abatacept may stabilize beta1-integrin activation in pod

184 percentage of patients treated with 10 mg/kg abatacept met the American College of Rheumatology 20% i

185 Abatacept mimics natural CD152 and competes with CD28 fo

186 Abatacept modulates co-stimulation and prevents full T-c

187 eceive 10 mg/kg abatacept (n = 115), 2 mg/kg abatacept (n = 105), or placebo (n = 119).

188 y were randomly assigned to receive 10 mg/kg abatacept (n = 115), 2 mg/kg abatacept (n = 105), or pla

189 59% (95% CI 6.1-112) higher at 2 years with abatacept (n=73, 0.378 nmol/L) than with placebo (n=30,

190 receiving cTNFi, and 9 receiving ABT (n = 1, abatacept; n = 3, tocilizumab; n = 5, golimumab).

191 Here, we report that whereas abatacept neutralized the therapeutic effect of anti-CTL

192 therapies: mycophenolate mofetil, rituximab, abatacept, nilotinib, and fresolimumab.

193 trexate were randomized to receive 125 mg SC abatacept on days 1 and 8 and weekly thereafter (plus an

194 In addition, we did not detect an effect of abatacept on FEV1, provocative concentration of methacho

195 h year 1, suggesting an increasing effect of abatacept on the inhibition of structural damage in year

196 recurrent FSGS after transplant using either abatacept or belatacept, a B7-1 blocker with higher affi

197 ine response (by 1.49-fold [1.13-1.97]), but abatacept or JAK inhibitor decreased the vaccine respons

198 ith pre-filled syringes with coded labels of abatacept or placebo every 3 months.

199 randomly assigned in a 2:1 ratio to receive abatacept or placebo on days 1, 15, and 29 and every 28

200 Subjects were randomized 1:1 to receive abatacept or placebo, followed by a second allergen chal

201 Study patients received either abatacept or placebo, on a background of mycophenolate m

202 e and 219 patients were randomly assigned to abatacept or placebo, respectively, and 385 (89%) and 16

203 tment (P = .005) or in patients who received abatacept or sirolimus as compared with other therapies,

204 observed in animals treated with CTLA-4 Ig (abatacept) or CD28 blockade in the presence of anti-CTLA

205 nhibitor (tocilizumab) were either negative (abatacept) or were associated with high rates of adverse

206 nti-TNFs, sulfasalazine, hydroxychloroquine, abatacept, or rituximab after the incident NMSC surgery.

207 necessitating additional immunosuppressants, abatacept, or transplantation.

208 We have studied abatacept (Orencia), a fusion protein that is constructe

209 Yet, despite continued administration of abatacept over 24 months, the decrease in beta-cell func

210 Here, we performed a determination of abatacept pharmacokinetics (PK), which enabled an examin

211 ed more frequently in the subgroup receiving abatacept plus a biologic agent (22.3%) than in the othe

212 Abatacept plus calcineurin inhibitors/methotrexate (CNI/

213 .14% 1-year cumulative incidence of PJI with abatacept, predicted incidence ranged from 0.35% (CI, 0.

214 n 8.16% risk for hospitalized infection with abatacept, predicted risk from propensity-weighted model

215 Abatacept produced significant clinical and functional b

216 on rates, consistent with the established IV abatacept profile.

217 SC abatacept provides efficacy and safety comparable with t

218 Within both cell types, abatacept reduced the proportion of activated cells expr

219 All abatacept regimens resulted in improved MRI, HAQ, and SF

220 data expand upon the mechanism of action of abatacept reported in other autoimmune diseases and iden

221 ere the first biological agents, followed by abatacept, rituximab, and tocilizumab.

222 New administration of adalimumab, abatacept, rituximab, tocilizumab, or tofacitinib.

223 Abatacept's colloidal stability was studied by measuring

224 t clear and warrant further investigation of abatacept's mode of action.

225 Abatacept's safety profile in combination with DMARDs al

226 V placebo)-treated patients (2.6%) and 18 IV abatacept (SC placebo)-treated patients (2.5%).

227 its TCR-driven activation, thereby promoting abatacept sensitivity.

228 as mice exposed to SEB and also treated with abatacept showed no weight loss for the duration of the

229 Abatacept significantly potentiated regulatory B cell re

230 ontinuous 24-month costimulation blockade by abatacept significantly slows the decline of beta-cell f

231 Co-stimulation modulation with abatacept slowed reduction in beta-cell function over 2

232 Abatacept statistically significantly reduced disease ac

233 At 1 year, abatacept statistically significantly slowed the progres

234 anced the inhibition of T cell activation by abatacept, strongly inhibiting T cell activation driven

235 this study, we show that the extent to which abatacept suppresses T cell activation is influenced by

236 sults of this study suggest that 10 mg/kg of abatacept, the approved dosage for rheumatoid arthritis

237 In patients treated with SC abatacept, the frequency of discontinuations due to AEs

238 HSCT and abatacept therapy gave rise to similar probabilities of

239 proteomic abnormalities were reversed after abatacept therapy; notably, gene signatures derived from

240 For patients treated with 10 mg/kg abatacept, there were also statistically significant and

241 ransplantation, was rationally designed from abatacept to bind with more avidity to CD86, providing t

242 of adding T-cell costimulation blockade with abatacept to calcineurin inhibitor (CNI)/methotrexate (M

243 ell stimulation via the TCR, synergized with abatacept to inhibit T cell activation.

244 int for determining the noninferiority of SC abatacept to IV abatacept was the proportion of patients

245 -4.2, 4.8]), confirming noninferiority of SC abatacept to IV abatacept.

246 Adding abatacept to our routine GVHD prophylaxis reduced the in

247 as rheumatoid arthritis in combination with abatacept to promote the efficacy of treatment.

248 Adding abatacept to URD HCT was safe, reduced AGVHD, and improv

249 of subcutaneous forms of existing therapies (abatacept, tocilizumab), as well as newer-generation mon

250 In post hoc analyses, the proportions of abatacept-treated and placebo-treated patients with a BI

251 were 67.0% and 4.2%, respectively, in the SC abatacept-treated group and 65.2% and 4.9%, respectively

252 gen-induced eosinophilic inflammation in the abatacept-treated group compared with placebo (17.71% +/

253 and 65.2% and 4.9%, respectively, in the IV abatacept-treated group, with comparable frequencies of

254 ements were comparable between the SC and IV abatacept-treated groups.

255 % (95% confidence interval 72.6, 79.0) of IV abatacept-treated patients achieved an ACR20 response (e

256 pt-induced antibodies occurred in 1.1% of SC abatacept-treated patients and 2.3% of IV abatacept-trea

257 smallest detectable change) was 84.8% for SC abatacept-treated patients and 88.6% for SC adalimumab-t

258 Abatacept-treated patients had a similar incidence of ad

259 % (95% confidence interval 72.9, 79.2) of SC abatacept-treated patients versus 75.8% (95% confidence

260 SC abatacept-treated patients and 2.3% of IV abatacept-treated patients.

261 sis revealed control of T-cell activation in abatacept-treated patients.

262 ertook this study to determine the effect of abatacept treatment in a murine model of chronic M tuber

263 Abatacept treatment increased thymic output and expansio

264 is trial were used to examine the effects of abatacept treatment on the frequency and transcriptional

265 Furthermore, we show that abatacept treatment significantly alters the frequencies

266 function, and HRQOL observed after 1 year of abatacept treatment were maintained through 2 years of t

267 These changes were significantly affected by abatacept treatment, which drove the peripheral contract

268 ectively decreased in participants following abatacept treatment.

269 anges were reversed following termination of abatacept treatment.

270 Studies of a co-stimulation blocker (abatacept), tumor necrosis factor inhibitor (infliximab)

271 Importantly, abatacept uncouples the relationship between changes in

272 cells in rheumatoid arthritis was CTLA4-Ig (abatacept), use of this biologic is now expanding to oth

273 19.8 to 36.7 percentage points]), 39.9% for abatacept versus 16.8% for placebo (difference, 23.0 per

274 25.1 to 41.7 percentage points]), 48.3% for abatacept versus 18.2% for placebo (difference, 30.1 per

275 ACR 50, and ACR 70 responses were 67.9% for abatacept versus 39.7% for placebo (difference, 28.2 per

276 1 year, the responses increased to 73.1% for abatacept versus 39.7% for placebo (difference, 33.4 per

277 8 to 38.5 percentage points]), and 28.8% for abatacept versus 6.1% for placebo (difference, 22.7 perc

278 0 to 31.1 percentage points]), and 19.8% for abatacept versus 6.5% for placebo (difference, 13.3 perc

279 8-HLA-mismatched URD) comparing CNI/MTX plus abatacept versus CNI/MTX CIBMTR controls.

280 In 8/8s, grade 3-4 AGVHD was 6.8% (abatacept) versus 14.8% (placebo) (P = .13, hazard ratio

281 increase in infections (32 [42%] patients on abatacept vs 15 [43%] on placebo) or neutropenia (seven

282 All-cause 28-day mortality was 11.0% for abatacept vs 15.1% for placebo (odds ratio [OR], 0.62 [9

283 In CD-MP, 23.8% vs 11.1% of abatacept vs placebo patients were in remission at week

284 UC-MP, 12.5% vs 14.1% of patients receiving abatacept vs placebo were in remission at week 52.

285 During treatment, abatacept was associated with improvements in pain score

286 transplant, treatment with the B7-1 blocker abatacept was associated with proteinuria remission.

287 Abatacept was associated with significant reductions in

288 Abatacept was found to be well tolerated and safe over t

289 ths, the decrease in beta-cell function with abatacept was parallel to that with placebo after 6 mont

290 The costimulation modifier abatacept was shown to be effective and relatively well

291 ing the noninferiority of SC abatacept to IV abatacept was the proportion of patients in each group m

292 lities that are highly pH dependent, whereas abatacept was weakly colloidally unstable at pH 6 or 7.5

293 Abatacept was well tolerated with few serious infectious

294 neration, higher avidity variant of CTLA4Ig (abatacept), was approved by the Food and Drug Administra

295 dy, the T-cell costimulation blockade agent, abatacept, was safe and effective in preventing acute gr

296 were randomly assigned to receive 125 mg SC abatacept weekly or 40 mg SC adalimumab biweekly, both g

297 SC abatacept will provide additional treatment options, suc

298 8/8-HLA-matched URD), comparing CNI/MTX plus abatacept with CNI/MTX plus placebo, and a single-arm st

299 In total, 29 patients received abatacept with favorable responses and the overall survi

300 ficacy and safety comparable with that of IV abatacept, with low immunogenicity and high retention ra