ライフサイエンスコーパス: rituximab

1 tics and anti-CD20 monoclonal antibody (mAb) rituximab.

2 concurrent rituximab and less so by delayed rituximab.

3 excision, rituximab and RT, and single-agent rituximab.

4 with rheumatoid arthritis being treated with rituximab.

5 -92.6) for patients receiving ibrutinib plus rituximab.

6 etoclax-rituximab compared with bendamustine-rituximab.

7 with respect to the administration of naked rituximab.

8 t FSGS cases that fail to respond to TPE and rituximab.

9 to therapeutic plasma exchange (TPE) and/or rituximab.

10 lower, in patients receiving ibrutinib plus rituximab.

11 FL treated with frontline BR and maintenance rituximab.

12 st six cycles, or six cycles of bendamustine-rituximab.

13 -center trial of ibrutinib vs ibrutinib plus rituximab.

14 alimumab to 8.90% (CI, 5.70% to 13.52%) with rituximab.

15 -HCT AIC and B-lymphocyte function following rituximab.

16 compared to both the general population and rituximab.

17 to wild type (WT) littermates also receiving rituximab.

18 vitro complement-mediated cytotoxicity than rituximab.

19 a and lymphoma using the monoclonal antibody rituximab.

20 PMBCL) have improved with the integration of rituximab.

21 ith other immunosuppressive drugs except for rituximab.

22 tal of 163 HTX recipients were randomized to rituximab 1,000 mg intravenous or placebo on days 0 and

23 We included 4,187 first-ever initiations of rituximab, 1,620 of fingolimod, and 1,670 of natalizumab

24 re randomized to receive two doses of either rituximab (1000 mg) or saline (placebo).

25 t antithymocyte globulin (rATG; 2 mg/kg x 5)/rituximab (150 mg/m x 1; begun in 2013), alemtuzumab (20

26 influence of induction type: rATG(2mg/kg x5)/rituximab(150mg/m x1)(begun in 2013), alemtuzumab(2001-2

27 78 invasive cancers among treated patients: rituximab 33 (incidence rate [IR] per 10,000 person-year

28 le at baseline and 1 year in 86 subjects (49 rituximab, 37 placebo).

29 ntravenously days 1-5 with 8 weekly doses of rituximab 375 mg/m(2) begun either day 1 (concurrent, CD

30 g/d D1-D5) followed by two cycles of R-AraC (rituximab 375 mg/m(2) D1, cytarabine 3 g/m(2) D1 to D2).

31 otherapy consisting of two cycles of R-MBVP (rituximab 375 mg/m(2) day (D) 1, methotrexate 3 g/m(2) D

32 each 21-day cycle orally (CHP), plus either rituximab 375 mg/m(2) intravenously on day 1 of each cyc

33 icin, vincristine, and prednisolone (R-CHOP; rituximab 375 mg/m(2), cyclophosphamide 750 mg/m(2), dox

34 yclophosphamide (250 mg/m(2), days 1-3), and rituximab (375 mg/m(2) day 1 of cycle 1; 500 mg/m(2) day

35 Patients were randomized to rituximab (375 mg/m(2) IV on day 1 of weeks 1-4 and repe

36 s a single agent (n = 104), or together with rituximab (375 mg/m(2); n = 104), given weekly during cy

37 Four patients received rituximab 4 months pretransplant to prevent recurrence.

38 lotomab-satetraxetan (150 or 350 MBq/kg) and rituximab (4 x 10 mg/kg) were compared with those of sin

39 Of the 17 who received rituximab, 7 had B-lymphocyte recovery, 5 had persistent

40 Patients who received venetoclax-rituximab achieved a higher rate of PB undetectable MRD

41 Rituximab ADCC induction in Raji2R cells was 20% +/- 2%

42 Rituximab added to chemotherapy prolongs survival among

43 Rituximab added to standard LMB chemotherapy markedly pr

44 the field of CLL that, unlike chemotherapy, rituximab addition to ibrutinib does not improve progres

45 LTs decreased across the entire cohort with rituximab administration and PDX tumors that are traditi

46 Compared with CDAR, delayed rituximab after cladribine achieved lower rate (67% of 2

47 6.6%), rituximab and RT (n = 19; 3.4%), and rituximab alone (n = 15; 2.7%).

48 IDELA improved PFS and OS compared with rituximab alone in patients with relapsed CLL.

49 0.8% after rituximab and RT, and 38.5% after rituximab alone.

50 nces were treated with anti-CD20 antibodies (rituximab) alone, resulting in improvements in estimated

51 We hypothesized that routine injection of rituximab, an anti-CD20 antibody, at the time of implant

52 Rituximab, an anti-CD20 monoclonal antibody that deplete

53 35% women) were randomly assigned, 50 to the rituximab and 47 to the placebo group.

54 After treatment with rituximab and a reduced-intensity conditioning regimen o

55 c unconjugated monoclonal Abs (mAbs) such as rituximab and Ab-induced hemolytic anemia and immune thr

56 The application to the mAbs rituximab and adalimumab illustrates the potential of ou

57 significant protective effects of both rATG/rituximab and alemtuzumab existed during the first 6 mon

58 significant protective effects of both rATG/rituximab and alemtuzumab existed during the first 6mo p

59 The prognostic effects of rATG/rituximab and alemtuzumab on ACR/severe ACR disappeared

60 The prognostic effects of rATG/rituximab and alemtuzumab on ACR/severe ACR disappeared

61 d severe ACR, the protective effects of rATG/rituximab and alemtuzumab were highly significant (P <=

62 d severe ACR, the protective effects of rATG/rituximab and alemtuzumab were highly significant(P<=0.0

63 We also discuss the role of rituximab and antiretroviral therapy.

64 compared with a fixed-duration treatment of rituximab and bendamustine in older adults with chronic

65 naging PTLD in SBTx and prompt escalation to rituximab and CTL is recommended.

66 otherapy was evaluated in iNHL refractory to rituximab and either chemotherapy or radioimmunotherapy.

67 ts from a randomized phase 2 study combining rituximab and ibrutinib vs ibrutinib alone in high-risk,

68 352 patients [80.1%] who received ibrutinib-rituximab and in 126 of 158 [79.7%] who received chemoim

69 cladribine is greatly enhanced by concurrent rituximab and less so by delayed rituximab.

70 free therapy that improves upon single-agent rituximab and may become an alternative to chemoimmunoth

71 reased risk of invasive cancer was seen with rituximab and natalizumab, compared to the general popul

72 e and the monoclonal antibodies alemtuzumab, rituximab and ocrelizumab are frequently categorized as

73 91% to 100%) and 74% (CI, 63% to 88%) in the rituximab and placebo groups, respectively, an absolute

74 icant differences at study entry between the rituximab and placebo groups.

75 (n = 47; 8.4%), observation (n = 37; 6.6%), rituximab and RT (n = 19; 3.4%), and rituximab alone (n

76 ter CT, 73.5% after observation, 80.8% after rituximab and RT, and 38.5% after rituximab alone.

77 erapy [CT]), CT, observation after excision, rituximab and RT, and single-agent rituximab.

78 onfounding is possible, and sample sizes for rituximab and tocilizumab were small.

79 rypsin-digested monoclonal antibody samples (rituximab and trastuzumab).

80 naging PTLD in SBTx and prompt escalation to rituximab and/or CTL is recommended.

81 reated with chemotherapy in combination with rituximab and/or EBRT.

82 uding teprotumumab, which reduces proptosis, rituximab (anti-CD20), which reduces inflammation, and t

83 native conformation that is not impacted by rituximab, anti-thymocyte globulin (after absorption), o

84 rs (ibrutinib), alone or in combination with rituximab, are preferred first-line therapy options for

85 f lenalidomide alone and in combination with rituximab as a first-line therapy and as a treatment of

86 ymer layer leads to the sustained release of rituximab as the crosslinkers are gradually hydrolysed,

87 ing the efficacy of treatment with ibrutinib-rituximab, as compared with standard chemoimmunotherapy

88 ilzomib, ixazomib), both in combination with rituximab, as well as BTK inhibitors (ibrutinib), alone

89 Routine use of rituximab at the time of tumor implantation may have sig

90 emdesivir in a 76-year-old woman with a post-rituximab B-cell immunodeficiency and persistent SARS-Co

91 antigen (HBsAg)-positive patients receiving rituximab-based B-cell depletion therapy.

92 rden grade 1-3a FL received obinutuzumab- or rituximab-based chemotherapy induction.

93 tandard of care for first-line treatment and rituximab-based regimens for second-line treatment.

94 Intravenous immunoglobulins (IVIg) and rituximab-based regimens were the most effective therapi

95 In patients responding to rituximab-bendamustine, median response duration was not

96 We find that the rituximab binding affinity depends sensitively and nonmo

97 everse rituximab resistance; it can increase rituximab binding and ADCC activity in vitro and can syn

98 Results: Rituximab binding in Raji2R cells was 36% +/- 5% of that

99 rvival (PFS) compared with bendamustine plus rituximab (BR) in patients with relapsed or refractory c

100 Rituximab can clear MRD, but long-term results are unkno

101 er after prephase treatment was 33.3% in the rituximab-chemotherapy group and 24.2% in the chemothera

102 nfidence interval [CI], 89.1 to 96.7) in the rituximab-chemotherapy group and 82.3% (95% CI, 75.7 to

103 Events were observed in 10 patients in the rituximab-chemotherapy group and in 28 in the chemothera

104 Approximately twice as many patients in the rituximab-chemotherapy group as in the chemotherapy grou

105 Eight patients in the rituximab-chemotherapy group died (4 deaths were disease

106 age with PMBCL treated with curative intent rituximab-chemotherapy were identified.

107 (PFS) benefit for fixed-duration venetoclax-rituximab compared with bendamustine-rituximab in relaps

108 ontinued benefit was observed for venetoclax-rituximab compared with bendamustine-rituximab.

109 hylactic NA therapy in patients who received rituximab-containing chemotherapy.

110 riers with hematological cancer who received rituximab-containing chemotherapy.

111 sk subtypes in patients treated with R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, a

112 The preferred treatment is abbreviated rituximab, cyclophosphamide, doxorubicin, vincristine, a

113 the outcome of PMBCL primarily treated with rituximab, cyclophosphamide, doxorubicin, vincristine, a

114 The use of R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, a

115 in, and rituximab (DA-EPOCH-R) with standard rituximab, cyclophosphamide, doxorubicin, vincristine, a

116 tially received one 21-day cycle of standard rituximab, cyclophosphamide, doxorubicin, vincristine, a

117 , half of them treated with R-CHOP biweekly (rituximab, cyclophosphamide, doxorubicin, vincristine, a

118 The classifier was not prognostic for rituximab, cyclophosphamide, doxorubicin, vincristine, p

119 mpared with a historical cohort treated with rituximab, cyclophosphamide, vincristine, and prednisone

120 clophosphamide, vincristine, prednisone, and rituximab (DA-EPOCH-R) may obviate the need for highly d

121 cristine, cyclophosphamide, doxorubicin, and rituximab (DA-EPOCH-R) with standard rituximab, cyclopho

122 ly 560 mg ibrutinib, 375 mg/m(2) intravenous rituximab day 1 of cycles 1 to 6, and 10, 15, 20, or 25

123 FS after completion of 2 years of venetoclax-rituximab demonstrate the feasibility of this regimen.

124 eated with immunosuppressive therapies, with rituximab demonstrating the most robust therapeutic resp

125 ration rate at time of biopsy, glomerulitis, rituximab, diabetes, v score, allograft glomerulopathy,

126 prednisone) and the other half with R-ACVBP (rituximab, doxorubicin, cyclophosphamide, vindesine, ble

127 ront-line, and all 13 patients not receiving rituximab during reinduction died.

128 domly assigned to 2 years of venetoclax plus rituximab during the first six cycles, or six cycles of

129 Outcomes for FL in the rituximab era are encouraging, with ~80% of patients hav

130 Their outcomes in the rituximab era are not fully defined.

131 In the rituximab era, none of the clinical risk scores identifi

132 United States of limited-stage DLBCL in the rituximab era, with the best NCTN results in this diseas

133 known of their causes of death (CODs) in the rituximab era.

134 owever, the benefit remains uncertain in the rituximab era.

135 chemotherapy, stem-cell transplantation, or rituximab, except for IRRs for humoral deficiency, which

136 with lymphopenia, BK-related infections and rituximab exposure in addition to the previously mention

137 Fludarabine, cyclophosphamide, and rituximab (FCR) can improve disease-free survival for yo

138 irst-line fludarabine, cyclophosphamide, and rituximab (FCR) have prolonged progression-free survival

139 ent recommendation was reinduction including rituximab from the early 2000s followed by blood stem ce

140 ted of reduction of immunosuppression (RIS), rituximab (from 2000), cytotoxic T-lymphocyte (CTL) ther

141 before transplantation, 9 of 10 treated with rituximab front-line, and all 13 patients not receiving

142 are stable under sialidase catalysis and the rituximab glycoform with a sialylated complex-type biant

143 35.1% in the placebo group and 26.0% in the rituximab group (difference, 9.2 percentage points [95%

144 event developed in 12 patients (24%) in the rituximab group (with 9 infectious serious adverse event

145 At 24 months, 39 patients (60%) in the rituximab group and 13 (20%) in the cyclosporine group h

146 ith IGHV mutation was 87.7% in the ibrutinib-rituximab group and 88.0% in the chemoimmunotherapy grou

147 events occurred in 11 patients (17%) in the rituximab group and in 20 (31%) in the cyclosporine grou

148 and of greater magnitude and duration in the rituximab group than in the cyclosporine group.

149 randomization (354 patients to the ibrutinib-rituximab group, and 175 to the chemoimmunotherapy group

150 erobic threshold improvement was seen in the rituximab group, only but this was not associated with f

151 Rituximab had some evidence of a beneficial effect on al

152 Lenalidomide-rituximab has been demonstrated to be an effective chemo

153 Budesonide, ciclosporin, and rituximab have shown potential in modifying the disease

154 all survival remain superior to bendamustine-rituximab (hazard ratio, 0.16 [95% CI, 0.12 to 0.23]; an

155 d ratio [HR] = 1.53, 95% CI = 0.98-2.38) and rituximab (HR = 1.68, 95% CI = 1.00-2.84).

156 cause of superior efficacy of the IDELA-plus-rituximab (IDELA/R) arm.

157 ve HIV-NHLs, using dose-adjusted EPOCH (plus rituximab if CD20+), alone or with 300 mg vorinostat, ad

158 se 1 inhibitor (itacitinib) or chemotherapy (rituximab, ifosfamide, carboplatin, and etoposide).

159 L cell lines and to act synergistically with rituximab in a rituximab-sensitive NHL animal model.

160 Patients were randomly assigned to receive rituximab in combination with either IDELA 150 mg twice

161 t of effective retroviral therapy and use of rituximab in HHV8-MCD have improved outcomes in HHV8-MCD

162 been complemented by the anti-CD20 antibody rituximab in moderate and severe disease.

163 guably, the success of B cell depletion with rituximab in open-label clinical trials, the approval of

164 ents from lenalidomide and lenalidomide with rituximab in patients with follicular lymphoma treated i

165 b (IDELA) plus rituximab versus placebo plus rituximab in patients with relapsed chronic lymphocytic

166 g approved in the United States for use with rituximab in patients with relapsed/refractory follicula

167 Although the efficacy of rituximab in primary MN is now well established, no rand

168 Whereas the efficacy of rituximab in primary MN is now well established, no rand

169 ty as a single agent and in combination with rituximab in relapsed or refractory diffuse large B-cell

170 etoclax-rituximab compared with bendamustine-rituximab in relapsed/refractory chronic lymphocytic leu

171 4) or without (R-CHOP-14) intensification of rituximab in the first 4 cycles.

172 rapy with fludarabine, cyclophosphamide, and rituximab, in patients with previously untreated chronic

173 Rituximab induces complete remission off therapy in 90%

174 visceral (P = 0.0009 and P < 0.000001), rATG/rituximab induction (P < 0.000001 and P < 0.01), and ale

175 Type MMV or MV(P=0.0009 and <0.000001), rATG/rituximab induction(P<0.000001 and 0.01), and alemtuzuma

176 e globulin, or rabbit antithymocyte globulin/rituximab) induction (P = 0.004), and liver inclusion (L

177 Biannual rituximab infusions over 18 months effectively maintain

178 Extended therapy with biannual rituximab infusions over 18 months was associated with a

179 Rituximab injection was added to the standard PDX engraf

180 Early rituximab intensification during R-CHOP-14 does not impr

181 This randomized trial assessed whether rituximab intensification during the first 4 cycles of R

182 nsistently higher after the incorporation of rituximab into DLBCL treatments.

183 prednisone, with (R-CHOP) or without (CHOP) rituximab is the standard first-line treatment for aggre

184 Rituximab is used for desensitization and antibody-media

185 hieved remission in 50% (n = 18), additional rituximab led to remission in 25% (n = 9), and the remai

186 tion treatment and were randomly assigned to rituximab maintenance (n = 505) or observation (n = 513)

187 Rituximab maintenance after induction immunochemotherapy

188 tion < 5%) but more prominent in patients on rituximab maintenance after R-FC, in whom grade 3-4 leuk

189 ata cutoff, median PFS was 10.5 years in the rituximab maintenance arm compared with 4.1 years in the

190 Prolongation of rituximab maintenance beyond 2 years is effective and sa

191 ce was seen in patients randomly assigned to rituximab maintenance or observation (hazard ratio, 1.04

192 The excellent results of R-CHOP followed by rituximab maintenance until progression for older patien

193 After R-FC, rituximab maintenance was associated with an unexpectedl

194 Toxicity of rituximab maintenance was low after R-CHOP (grade 3-4 le

195 58% and 32% of patients treated with R-CHOP, rituximab maintenance was still ongoing 2 and 5 years fr

196 s provided by 607 patients (59.6%) of 1,018 (rituximab maintenance, n = 309; observation, n = 298).

197 g on efficacy and safety of long-term use of rituximab maintenance.

198 -Hodgkin lymphoma (NHL) who are treated with rituximab may develop resistant disease, often associate

199 B-cell depletion with rituximab may therefore be noninferior to treatment with

200 Whether pretransplant rituximab modifies the course of recurrence requires add

201 motherapy (16%), combined modality (12%), or rituximab monotherapy (4%).

202 Rituximab monotherapy (R-Mono) in unselected patients ha

203 In total, 77 patients were allocated to rituximab monotherapy and 77 to the combination (47% poo

204 ars, respectively, when randomly assigned to rituximab (n = 87), compared with 1.9 years (P < .001) a

205 eously [SC], n = 68; IFN-beta-1b SC, n = 41; rituximab, n = 31; tocilizumab, n = 44) and followed dur

206 ifference in risk of invasive cancer between rituximab, natalizumab, and the general population but a

207 methyl fumarate, teriflunomide, natalizumab, rituximab, ocrelizumab) or injectable (interferon-beta,

208 , and who started the high-efficacy therapy (rituximab, ocrelizumab, mitoxantrone, alemtuzumab, or na

209 y of polatuzumab vedotin in combination with rituximab or obinutuzumab and cyclophosphamide, doxorubi

210 2 inhibitor, venetoclax, in combination with rituximab or obinutuzumab and cyclophosphamide, doxorubi

211 man patients were more commonly treated with rituximab or other immunosuppressants (63%).

212 Rituximab or placebo infusion every 6 months for 18 mont

213 atacept, adalimumab, etanercept, infliximab, rituximab, or tocilizumab before surgery.

214 B-cell depletion using several infusions of rituximab over 12 months was not associated with clinica

215 s of overall survival also favored ibrutinib-rituximab over chemoimmunotherapy (98.8% vs. 91.5% at 3

216 ng plasmapheresis, pulse steroids, IVIG, and rituximab (P = ns).

217 patients, 174 (90%) completed the venetoclax-rituximab phase and 130 (67%) completed 2 years of venet

218 kidney transplantation after DES with IVIG + rituximab +/- PLEX (plasma exchange) +/- tocilizumab.

219 me, to receive R-pola or R-pina (375 mg/m(2) rituximab plus 2.4 mg/kg ADCs) every 21 days until disea

220 s, focusing on the long-term outcomes of the rituximab plus bendamustine and rituximab plus fludarabi

221 Rituximab plus bendamustine therapy resulted in response

222 B-cell PTLD treated initially with R-Mono or Rituximab plus CHOP (R-CHOP).

223 Immunochemotherapy with rituximab plus cyclophosphamide, doxorubicin, vincristin

224 at randomized responding patients to R-CHOP (rituximab plus cyclophosphamide, doxorubicin, vincristin

225 ositive patients had inferior outcomes after rituximab plus cyclophosphamide, doxorubicin, vincristin

226 orth America who were uniformly treated with rituximab plus cyclophosphamide, doxorubicin, vincristin

227 hosphamide, vincristine, prednisone; n = 45, rituximab plus cyclophosphamide, doxorubicin, vincristin

228 nts treated from 1998 to 2009 with frontline rituximab plus cyclophosphamide, doxorubicin, vincristin

229 ge FL requiring systemic treatment (n = 138, rituximab plus cyclophosphamide, vincristine, prednisone

230 comes of the rituximab plus bendamustine and rituximab plus fludarabine regimens.

231 Rituximab plus fludarabine therapy seems to carry a high

232 re, open-label, phase 2 study was to compare rituximab plus pola (R-pola) or pina (R-pina) in patient

233 To determine whether rituximab provides added benefit to ibrutinib, we conduc

234 The integration of rituximab (R) into cyclophosphamide, doxorubicin, vincri

235 acy of BCL-2 inhibitor venetoclax (VEN) plus rituximab (R), and VEN plus bendamustine (B) and R, vs B

236 owever, patients treated with ibrutinib plus rituximab reached their remissions faster and achieved s

237 This distance is required for improving rituximab recognition, and in agreement with the known r

238 romising potential therapy for patients with rituximab-refractory EBV-associated lymphoma after trans

239 The ibrutinib-rituximab regimen resulted in progression-free survival

240 ilotomab-satetraxetan may be used to reverse rituximab resistance in NHL.

241 ab-satetraxetan has the potential to reverse rituximab resistance; it can increase rituximab binding

242 Methods: The rituximab-resistant Raji2R and the parental Raji cell li

243 )Zr-DFO-N-suc-cetuximab and (89)Zr-DFO-N-suc-rituximab, respectively, which are similar to isolated y

244 )Zr-DFO-N-suc-cetuximab and (89)Zr-DFO-N-suc-rituximab, respectively.

245 Potential selection bias based on previous rituximab response and tolerance.

246 n variable region (IGHV) mutation, ibrutinib-rituximab resulted in better progression-free survival t

247 tion of Cardiac Allograft Vasculopathy Using Rituximab [Rituxan] Therapy in Cardiac Transplantation;

248 Rituximab (RTX) has been in clinical use for two decades

249 We describe outcomes in response to rituximab (RTX) versus cyclophosphamide (CYC) and plasma

250 uring weeks 12-15 in responding patients) or rituximab (same schedule) in combination with lenalidomi

251 d to act synergistically with rituximab in a rituximab-sensitive NHL animal model.

252 to up-regulate CD20 expression in different rituximab-sensitive NHL cell lines and to act synergisti

253 n Raji2R cells was 36% +/- 5% of that in the rituximab-sensitive Raji cells.

254 elpful in limiting disease progression, with rituximab showing efficacy in retinopathy refractory to

255 Addition of lenalidomide to rituximab significantly improved CR/CRu rates, PFS, and

256 )Zr-DFO-N-suc-cetuximab and (89)Zr-DFO-N-suc-rituximab suitable for clinical use.

257 3 or higher were less common with ibrutinib-rituximab than with chemoimmunotherapy (in 37 patients [

258 ), with either cyclophosphamide (P = .01) or rituximab therapy (P = .001).

259 s well as with cyclophosphamide (P=0.01) and rituximab therapy (P=0.001).

260 tients experienced drug-free remission after rituximab therapy and none of them had relapse (median f

261 tion of Cardiac Allograft Vasculopathy Using Rituximab Therapy in Cardiac Transplantation [Clinical T

262 3) with established EBV-PTLD, who had failed rituximab therapy, with third-party EBV-CTLs.

263 ranged from 0.35% (CI, 0.11% to 1.12%) with rituximab to 3.67% (CI, 1.69% to 7.88%) with tocilizumab

264 The addition of rituximab to intensive chemotherapy improves outcomes in

265 emia to compare the addition of six doses of rituximab to standard lymphomes malins B (LMB) chemother

266 pecially with recent regulatory approvals of rituximab, trastuzumab, and bevacizumab biosimilars, it

267 Rituximab treatment of early PGNMID recurrence is effect

268 ti-ADAMTS13 autoantibodies, as well as after rituximab treatment, suggesting a role for anti-ADAMTS13

269 6-104 (median, 78) months after last delayed rituximab treatment.

270 Cs and CCAs, appear to benefit the most from rituximab treatment.

271 for at least 3 months to receive intravenous rituximab (two infusions, 1000 mg each, administered 14

272 acy compared to the targeting with anti-CD20 rituximab, two experimental anti-CD19 antibodies and non

273 rm results are unknown and optimal timing of rituximab undefined.

274 match >= 3 (pOR = 1.83 [1.06, 3.17], I= 0%), rituximab use (pOR =3.03 (1.82, 5.04); I =0%) and polycl

275 MURANO study, fixed-duration venetoclax plus rituximab (VenR) resulted in improved progression-free s

276 change in PAV at 12 months was +6.8 +/- 8.2% rituximab versus +1.9 +/- 4.4% placebo (p = 0.0019).

277 Mortality at 12 months was 3.4% rituximab versus 6.8% placebo (p = 0.47); there were no

278 , phase III study of idelalisib (IDELA) plus rituximab versus placebo plus rituximab in patients with

279 -to-rejection (P = 0.01 and P = 0.003), rATG/rituximab was additionally associated with a consistentl

280 oss-due-to-rejection(P=0.01 and 0.003), rATG/rituximab was additionally associated with a consistentl

281 When use of cyclophosphamide or rituximab was compared with all other treatments, the ri

282 The patient being treated with rituximab was diagnosed postmortem and the pathology fin

283 tic role for B cells in functional recovery, rituximab was given to human CD20(+) (hCD20(+)) transgen

284 Rituximab was mainly used at relapses (11 [33%]).

285 xpected increase in coronary artery PAV with rituximab was observed during the first year in HTX reci

286 Conclusions: Rituximab was safe over the 12-month study period but sh

287 The combination of ibrutinib, HD-MTX, and rituximab was tolerated with an acceptable safety profil

288 )Zr-DFO-N-suc-cetuximab and (89)Zr-DFO-N-suc-rituximab were all more than 90% according to instant th

289 -remitting MS patients receiving 1,000 mg of rituximab were included.

290 suppressive treatment such as infliximab and rituximab, were invited to participate in the study when

291 phoma in a xenograft model as effectively as rituximab, which is a standard treatment for B cell lymp

292 the time of diagnosis and 10 (50%) received rituximab, which was started before the use of ACTH gel.

293 t observed among those patients treated with rituximab who had remission; however, follow-up duration

294 The combination of rituximab with 350 MBq/kg (177)Lu-lilotomab-satetraxetan

295 Our aim was to determine whether rituximab with azathioprine or mycophenolate mofetil imp

296 Survival after a regimen combining rituximab with continuous-infusion chemotherapy followed

297 ons of PDX were implanted with 406 receiving rituximab with implantation.

298 treatment with intravenous immune globulin + rituximab with or without plasma exchange were tested fo

299 Six patients required anti-CD20 therapy (rituximab) with complete resolution of EBV related sympt

300 Here, we show that the encapsulation of rituximab within a crosslinked zwitterionic polymer laye