ライフサイエンスコーパス: rituximab

1 of venetoclax when given in combination with rituximab.

2 s and improves survival of mice treated with rituximab.

3 n GP2013, and 315 were assigned to reference rituximab.

4 wing treatment with the therapeutic antibody rituximab.

5 All patients were pretreated with rituximab.

6 All patients received cyclophosphamide or rituximab.

7 cluding plasma exchange, intravenous Ig, and rituximab.

8 ntravenous rituximab and 205 to subcutaneous rituximab.

9 and life-saving biological therapies such as rituximab.

10 noglobulin, plasma exchanges, and eventually rituximab.

11 efficacy and pharmacokinetic equivalence to rituximab.

12 phocytic leukaemia (CLL) in combination with rituximab.

13 the humanized anti-CD20 monoclonal antibody rituximab.

14 components and is inadequately addressed by rituximab.

15 of known poor response to bendamustine plus rituximab.

16 t pattern of relapse despite the addition of rituximab.

17 c combination consisting of bendamustine and rituximab.

18 mune retinopathy (AIR) patients treated with rituximab.

19 Sixteen AIR patients treated with rituximab.

20 d activity of venetoclax in combination with rituximab.

21 trial with the anti-CD20 monoclonal antibody rituximab.

22 profile of CT-P10 was comparable to that of rituximab.

23 equivalent efficacy and pharmacokinetics to rituximab.

24 patients while they were being treated with rituximab.

25 rienced a clinical relapse (hazard ratio for rituximab = 0.10, 95% confidence interval [CI] = 0.02-0.

26 transplant titers of 1 or more in 8 received rituximab 1 month before transplant; tacrolimus and myco

27 art SAWYER study predicted that subcutaneous rituximab 1600 mg would achieve trough serum concentrati

28 was a placebo-controlled randomized trial of rituximab (2 biweekly infusions of 1g each).

29 Compared with rituximab, 2B8T2M exhibits significantly stronger antitu

30 rituximab, 7 (50%) responded to bendamustine-rituximab (3 CR and 4 PR).

31 icenter trial, 45 eligible patients received rituximab 375 mg/m(2) day 1 and bendamustine 90 mg/m(2)

32 th continuous 28-day cycles, and intravenous rituximab 375 mg/m(2) on cycle 1, day 8, day 15, day 22,

33 ); or the same combination plus two doses of rituximab 375 mg/m(2) on days -5 and 0 (group B); or the

34 d patients with follicular lymphoma received rituximab 375 mg/m(2) on days 1, 8, 15, and 22 of cycle

35 th continuous 28-day cycles, and intravenous rituximab 375 mg/m(2) weekly during cycle 1.

36 All patients received rituximab 375 mg/m(2) weekly for 4 weeks, followed by a

37 HS patients received IVIG (2 g/kg x2 doses)/rituximab (375 mg/m x1) for desensitization with alemtuz

38 of chlorambucil (same schedule as above) and rituximab (375 mg/m(2) intravenously on day 1 of weeks 1

39 cycles, with IV dexamethasone (40 mg) and IV rituximab (375 mg/m(2)) on cycles 2 and 5, for a total t

40 Patients received six cycles of R-CHOP (rituximab [375 mg/m(2)], cyclophosphamide [750 mg/m(2)],

41 ously on days 1 and 2 for six 28-day cycles; rituximab: 375 mg/m(2) on day 1 of cycle 1, and 500 mg/m

42 rsus 22 days; P = 0.01) and to have received rituximab (44% versus 9%; P < 0.0001), bendamustine (22%

43 -inferior to those achieved with intravenous rituximab 500 mg/m(2) in patients with chronic lymphocyt

44 mong patients whose disease was sensitive to rituximab (52.6%) compared with those who were rituximab

45 iously treated with rituximab or fludarabine-rituximab, 7 (50%) responded to bendamustine-rituximab (

46 Here, we evaluated (64)Cu-rituximab, a radiolabeled antibody specifically targetin

47 prophylaxis when commencing therapy such as rituximab; a positive GM-EIA result prompts investigatio

48 with five therapies: mycophenolate mofetil, rituximab, abatacept, nilotinib, and fresolimumab.

49 ppressing agents responded to treatment with rituximab according to the lymphoma protocol (4 weekly i

50 and 274 [88%] of 313 patients with reference rituximab achieved an overall response; difference -0.40

51 g products containing the biopharmaceuticals Rituximab, Adalimumab, and Etanercept, respectively.

52 ce was performed 1, 4, and 19 h after (64)Cu-rituximab administration.

53 lso received intravenous immune globulin and rituximab after transplantation to prevent antibody rebo

54 ells (CART123); and (3) T-cell ablation with rituximab after treatment with CD20-coexpressing CART123

55 (1:1:6 ratio), with a new arm that included rituximab alone (same schedule as the combination arm) a

56 ree survival compared with bendamustine plus rituximab alone in patients with relapsed or refractory

57 of AR160 therapeutic superiority over ABX or rituximab alone.

58 Rituximab (an anti-human CD20 monoclonal antibody [mAb])

59 The present study used rituximab, an anti-CD20 antibody, to deplete B cells in

60 Treatment with rituximab, an anti-CD20 mAb that depletes B cells, has b

61 s were randomly assigned, 205 to intravenous rituximab and 205 to subcutaneous rituximab.

62 ions in 37 (44%) patients given subcutaneous rituximab and 40 (45%) patients given the intravenous do

63 ths (95% CI 34.9-45.3) with bendamustine and rituximab and 55.2 months (95% CI not evaluable) with fl

64 proved ineffective in patients treated with rituximab and chemotherapy.

65 s centers with different preferential use of rituximab and fingolimod (Stockholm, n = 156, fingolimod

66 The patients were treated with rituximab and followed up for 18 to 84 months after trea

67 ted dose of lenalidomide in combination with rituximab and idelalisib in relapsed follicular and mant

68 r antibody (anti-PLA2R-Ab) depletion in NIAT-rituximab and NIAT groups were 14 of 25 (56%) and one of

69 64.9%) and 13 of 38 (34.2%) patients in NIAT-rituximab and NIAT groups, respectively (P<0.01).

70 terquartile range, 13.0-23.0) months in NIAT-rituximab and NIAT groups, respectively.

71 B cells in multiple sclerosis (MS), such as rituximab and ocrelizumab.

72 difference in the efficacy measures between rituximab and placebo.

73 denstrom's macroglobulinaemia, refractory to rituximab and requiring treatment.

74 Supplementary administration of rituximab and total number of IVIg and PE treatments did

75 Rituximab and trastuzumab followed a similar pattern in

76 1.5 years of cessation of natalizumab, 1.8% (rituximab) and 17.6% (fingolimod) of patients experience

77 o response to regimens including cytarabine, rituximab, and autologous stem-cell transplant (ASCT).

78 phomas, in each treatment arm (chlorambucil, rituximab, and rituximab plus chlorambucil), and was con

79 mide, etoposide, doxorubicin, dexamethasone, rituximab, and the Bruton tyrosine kinase (BTK) inhibito

80 specific and clinically relevant antibodies (rituximab, anti-CD20) are non-covalently bound to the al

81 We suggest rituximab as a viable treatment option for recalcitrant

82 vailable evidence, we recommend bendamustine-rituximab as primary therapy for bulky disease, profound

83 d with the effect of a control anti-CD20 Ab (rituximab) at concentrations that triggered similar NK c

84 Lack of efficacy of rituximab, at least at this stage and severity of IgA ne

85 ulticentric Castleman disease (HIV+MCD) with rituximab-based approaches has dramatically improved sur

86 In the absence of neuropathy, a bortezomib-rituximab-based option is reasonable for relapsed or ref

87 en HIV+MCD were treated with risk-stratified rituximab-based therapy.

88 were successfully retreated at relapse with rituximab-based therapy.

89 High variability in patient outcome after rituximab-based treatment is partly explained by rituxim

90 ombination of bortezomib, dexamethasone, and rituximab (BDR) in 59 previously untreated symptomatic p

91 Clinical trials with rituximab, bendamustine, and conjugate immunotoxins will

92 results show that GP2013 represents a viable rituximab biosimilar candidate for patients with previou

93 ith rheumatoid arthritis have shown that the rituximab biosimilar CT-P10 (Celltrion, Incheon, South K

94 GP2013 is a rituximab biosimilar developed to stringent development

95 le-arm, phase 2 clinical trial, bendamustine-rituximab (BR) demonstrated an overall response rate of

96 D20 from CLL B cells, which was evident with rituximab but not obinutuzumab.

97 pond to a combination of plasma exchange and rituximab, but some die or acquire irreversible neurolog

98 Both studies were amended to remove rituximab, but two of three additional patients had grad

99 that methotrexate, cytarabine, thiotepa, and rituximab (called the MATRix regimen) is the induction c

100 lts were found when limiting the analysis to rituximab chemotherapy (OR = 0.19, 95% CI 0.11-0.32) and

101 darabine and cyclophosphamide [FC] v FC plus rituximab; CLL10: FC plus rituximab v bendamustine plus

102 roup B); or the same methotrexate-cytarabine-rituximab combination plus thiotepa 30 mg/m(2) on day 4

103 In conclusion, bendamustine-rituximab combination therapy is highly efficient, suffi

104 Desensitization with IVIG + rituximab combined with alemtuzumab induction gives HLA-

105 o target doses (200-600 mg) and then monthly rituximab commenced (375 mg/m(2) in month 1 and 500 mg/m

106 ximab-based treatment is partly explained by rituximab concentrations, and pharmacokinetic (PK) varia

107 te responders continued with four courses of rituximab consolidation every 21 days; all others receiv

108 We hypothesized that rituximab consolidation might be sufficient treatment fo

109 to progression 6 months or longer from last rituximab-containing regimen (A051202) were started with

110 ene mutations and predicts outcome following rituximab-containing regimens.

111 relapsed disease responsive to conventional rituximab-containing salvage therapy from 12 oncology-ha

112 Disease refractory to the last rituximab-containing therapy was defined as either relap

113 incristine, and prednisone (GP2013-CVP) with rituximab-CVP (R-CVP) in patients with follicular lympho

114 level of 100% and the mean levels after each rituximab cycle were calculated.

115 347 de novo DLBCL cases treated with R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, a

116 the impact of the addition of bortezomib to rituximab, cyclophosphamide, doxorubicin, vincristine, a

117 indesine, bleomycin, prednisone (R-ACVBP) or rituximab, cyclophosphamide, doxorubicin, vincristine, p

118 cohort of 142 patients with FL treated with rituximab, cyclophosphamide, vincristine, and prednisone

119 Dexamethasone-rituximab-cyclophosphamide is an alternative, particular

120 l analysis of plasma samples collected under rituximab-cyclophosphamide-doxorubicin-vincristine-predn

121 Exposure to rituximab decreased as TMTV0 increased (R(2) = 0.41, P <

122 3 mug/kg drug equivalents); combination with rituximab decreased the curative dose to 100 mug/kg (1 m

123 The levels of CD16 expression and rituximab-dependent cell cytotoxic activity of periphera

124 Treatment with rituximab depleted B cells and was well tolerated.

125 These results suggest that the IVIG + rituximab desensitization combined with alemtuzmab induc

126 our courses of immunochemotherapy induction (rituximab, dexamethasone, cytarabine, and a platinum der

127 Rituximab did not alter the level of proteinuria compare

128 (95% confidence interval [CI] 14.6-43.9) and rituximab did not increase responses.

129 A nomogram for rituximab dose needed to obtain optimal AUC according to

130 se 2 trial evaluating the efficacy of either rituximab, doxorubicin, cyclophosphamide, vindesine, ble

131 ndidate therapies, i.e., hydroxychloroquine, rituximab, eculizumab, sirolimus, and defibrotide, that

132 st that PLA2R-Ab levels are early markers of rituximab effect and that addition of rituximab to NIAT

133 Although rituximab effectively depleted B cells, it failed to red

134 Combination therapy with rituximab enhanced activity in preclinical models.

135 ge B-cell lymphoma remains suboptimal in the rituximab era.

136 ive maintenance therapy with one infusion of rituximab every 2 months, either on a short-term schedul

137 owed describing rituximab PK and calculating rituximab exposure (area under the concentration-time cu

138 r patients with TMTV0 <281 cm(3) In summary, rituximab exposure is influenced by TMTV0 and correlates

139 ume (TMTV0) on rituximab PK and of TMTV0 and rituximab exposure on outcome in patients with diffuse l

140 from 1F5 antibody (Fab'1F5), the other from Rituximab (Fab'RTX).

141 treatment with fludarabine-cyclophosphamide-rituximab (FCR) chemoimmunotherapy.

142 hed sequential treatment with four cycles of rituximab followed by four cycles of cyclophosphamide, d

143 response system to receive bendamustine plus rituximab for a maximum of six cycles (bendamustine: 70

144 isolated by culture who previously received rituximab for mucosa-associated lymphoid tissue (MALT) l

145 ver, the correct, opportune, and safe use of rituximab for this indication remains to be determined.

146 [95% CI], 19.7 to 50.5) patients in the NIAT-rituximab group and eight (21.1%; 95% CI, 8.1 to 34.0) p

147 onths, event-free survival was longer in the rituximab group than in the control group (hazard ratio,

148 verall survival at 4 years was higher in the rituximab group than in the observation group (hazard ra

149 % confidence interval [CI], 70 to 86) in the rituximab group versus 61% (95% CI, 51 to 70) in the obs

150 at 4 years was 83% (95% CI, 73 to 88) in the rituximab group versus 64% (95% CI, 55 to 73) in the obs

151 l survival was 89% (95% CI, 81 to 94) in the rituximab group versus 80% (95% CI, 72 to 88) in the obs

152 group and seven [10%] of 70 patients in the rituximab group).

153 nt in the placebo group versus 3 of 4 in the rituximab group, where these meaningful improvements wer

154 0 group and nine (13%) of 70 patients in the rituximab group.

155 INTERPRETATION: Intravenous and subcutaneous rituximab had similar efficacy and safety profiles, and

156 Rituximab had the greatest risk for HBVr (adjusted HR =

157 Although discovery of the anti-CD20 antibody rituximab has markedly improved outcomes in B-cell NHL,

158 past 5 years, as bendamustine combined with rituximab has rapidly become a standard frontline strate

159 Rituximab has shown encouraging results for the treatmen

160 The benefits of B-cell-targeted therapy with rituximab have been observed in MG; however, the duratio

161 ble) with fludarabine, cyclophosphamide, and rituximab (HR 1.643, 90.4% CI 1.308-2.064).

162 ed with increase incident of BK/CMV, whereas rituximab (HR, 0.47; 95% CI, 0.24-0.91; P = 0.02), peak

163 alisib in combination with bendamustine plus rituximab improved progression-free survival compared wi

164 nter was better in patients who had received rituximab in addition to the chemotherapy regimen (hazar

165 e the binding characteristics of the ABX and rituximab in AR160 using peptide mapping/Biacore approac

166 Is for the geometric mean ratio of CT-P10 to rituximab in AUCtau and CmaxSS were within the bounds of

167 Rituximab monotherapy and fludarabine-rituximab in combination are documented treatment option

168 Conclusion Rituximab in combination with chlorambucil demonstrated

169 ith diffuse large B-cell lymphoma (DLBCL) is rituximab in combination with cyclophosphamide, doxorubi

170 dies warrant further investigation of (64)Cu-rituximab in EAE models and consideration of use in MS p

171 ity of subcutaneous rituximab to intravenous rituximab in follicular lymphoma and to provide efficacy

172 f combining idelalisib with lenalidomide and rituximab in patients with relapsed mantle cell lymphoma

173 Randomized trials of rituximab in primary membranous nephropathy (PMN) have n

174 are needed to further explore the utility of rituximab in the management of AIR.

175 To evaluate the durability of response to rituximab in the treatment of acetylcholine receptor aut

176 vant, evidence-based practice parameters for rituximab in the treatment of MG.

177 combination of idelalisib, lenalidomide, and rituximab in these trials is excessively toxic, and thes

178 kinase delta inhibitor, to bendamustine plus rituximab in this population.

179 the cytotoxicity of ABX and CD20 affinity of rituximab in vitro.

180 30 mg orally 3 times weekly, with or without rituximab, in 40 patients with relapsed or refractory de

181 ponse with the combination of venetoclax and rituximab including 25 (51%) of 49 patients who achieved

182 e disorder (PTLD) and identified response to rituximab induction as a prognostic factor for overall s

183 OP consolidation on the basis of response to rituximab induction is feasible, safe, and effective.

184 Response to rituximab induction remained a prognostic factor for ove

185 for patients with a complete response after rituximab induction.

186 tion, were treated with four weekly doses of rituximab induction.

187 DLBCL patients who received four 375 mg/m(2) rituximab infusions every 2 weeks in combination with ch

188 gement during the 18-month interval included rituximab infusions, cyclophosphamide/methylprednisolone

189 after treatment initiation, coinciding with rituximab infusions.

190 red with the rate of visual decline prior to rituximab initiation (P = .005).

191 visual decline was significantly less after rituximab initiation compared with the rate of visual de

192 Rates of VA change before vs after rituximab initiation were compared with mixed-model line

193 yes had stable or improved VA 6 months after rituximab initiation.

194 Bendamustine plus rituximab is a standard of care for the management of pa

195 Intravenous rituximab is the standard of care in B-cell non-Hodgkin

196 Immunotherapy using mAbs, such as rituximab, is an established means of treating hematolog

197 t lack of additional clinical benefit to the rituximab-lenalidomide doublet, further investigation of

198 udarabine and mitoxantrone) regimens without rituximab maintenance as initial therapy for patients wi

199 [CVP]), every 3 weeks during induction, then rituximab maintenance every 8 weeks.

200 Routine rituximab maintenance should be avoided.

201 Rituximab maintenance therapy after transplantation prol

202 We investigated whether rituximab maintenance therapy at a dose of 375 mg per sq

203 Rituximab maintenance therapy has been shown to improve

204 we randomly assigned 240 patients to receive rituximab maintenance therapy or to undergo observation

205 Rituximab monotherapy and fludarabine-rituximab in combi

206 positive for PLA2R1-Ab randomly allocated to rituximab (n=29) or antiproteinuric therapy alone (n=29)

207 ssigned 176 patients to receive subcutaneous rituximab (n=88) or intravenous rituximab (n=88); 134 (7

208 subcutaneous rituximab (n=88) or intravenous rituximab (n=88); 134 (76%) patients comprised the pharm

209 Rituximab (odds ratio = 9.52; P = 0.001), and high-dose

210 travenous infusions of 375 mg/m(2) CT-P10 or rituximab on day 1 of eight 21-day cycles.

211 herapy with NIAT and 375 mg/m(2) intravenous rituximab on days 1 and 8 (n=37) or NIAT alone (n=38).

212 Positive effect of rituximab on proteinuria remission occurred after 6 mont

213 isation algorithm to 375 mg/m(2) intravenous rituximab or 1400 mg subcutaneous rituximab, plus chemot

214 lapse less than 12 months since last dose of rituximab or failure to achieve at least a minor respons

215 Among 14 patients previously treated with rituximab or fludarabine-rituximab, 7 (50%) responded to

216 is finding in patients with CLL treated with rituximab or obinutuzumab in vivo.

217 th the membrane dye PKH67 and opsonized with rituximab or obinutuzumab, we observed that a mean of 50

218 n B-cell PTLD, treatment stratification into rituximab or rituximab plus CHOP consolidation on the ba

219 unosuppression and antibody removal, without rituximab or splenectomy, can achieve long-term outcomes

220 second-line immunotherapy (cyclophosphamide, rituximab, or both).

221 tment with thrombopoietin receptor agonists, rituximab, or mycophenylate, which pose known or unknown

222 ease progression, relapse, death, allergy to rituximab, or severe infection) after transplantation am

223 (64)Cu-rituximab PET signal in brain regions ranged between 1.7

224 detected in the CNS of EAE mice using (64)Cu-rituximab PET.

225 partment population model allowed describing rituximab PK and calculating rituximab exposure (area un

226 line total metabolic tumor volume (TMTV0) on rituximab PK and of TMTV0 and rituximab exposure on outc

227 treatment arm (chlorambucil, rituximab, and rituximab plus chlorambucil), and was confirmed in the v

228 21 days; all others received four courses of rituximab plus CHOP chemotherapy every 21 days.

229 , treatment stratification into rituximab or rituximab plus CHOP consolidation on the basis of respon

230 ohort of 110 patients uniformly treated with rituximab plus cyclophosphamide, doxorubicin, vincristin

231 plete remission unconfirmed after first-line rituximab plus cyclophosphamide, doxorubicin, vincristin

232 ge DLBCL to evaluate the benefit of RT after rituximab plus cyclophosphamide, doxorubicin, vincristin

233 We hypothesized that rituximab plus cyclophosphamide, doxorubicin, vincristin

234 e, vincristine, and prednisone) with R-CHOP (rituximab plus cyclophosphamide, doxorubicin, vincristin

235 completion of front-line therapy with either rituximab plus cyclophosphamide, doxorubicin, vincristin

236 nd overall survival in patients treated with rituximab plus cyclophosphamide, doxorubicin, vincristin

237 gned a randomized phase III trial to compare rituximab plus cyclophosphamide, doxorubicin, vincristin

238 h sofosbuvir/ledipasvir and chemotherapy (14 rituximab plus cyclophosphamide, doxorubicin, vincristin

239 Purpose The FOLL05 trial compared R-CVP (rituximab plus cyclophosphamide, vincristine, and predni

240 icin, vincristine, and prednisone) and R-FM (rituximab plus fludarabine and mitoxantrone) regimens wi

241 d prednisone (R-CHOP)-14 (eight cycles) with rituximab plus high-dose sequential chemotherapy (R-HDS)

242 ntravenous rituximab or 1400 mg subcutaneous rituximab, plus chemotherapy (six-to-eight cycles of cyc

243 ednisone, fludarabine, cyclophosphamide, and rituximab presented with progressive multifocal neurolog

244 tuximab (52.6%) compared with those who were rituximab refractory (16.7%) (P = .04).

245 mia, new treatment options for patients with rituximab-refractory disease are an important clinical n

246 and safety of ibrutinib in a population with rituximab-refractory disease.

247 ice for patients who had heavily pretreated, rituximab-refractory Waldenstrom's macroglobulinaemia.

248 s therapies was four (IQR 2-6), and all were rituximab-refractory.

249 2 weeks after treatment to determine whether rituximab resets early B cell tolerance checkpoints.

250 as markedly improved outcomes in B-cell NHL, rituximab resistance remains an important obstacle to su

251 sulted in a significant tumor control in the rituximab-resistant A20-huCD20 tumors.

252 Rituximab (RTX) has been the hallmark anti-CD20 mAb for

253 Rituximab (RTX) is frequently considered as its "ancesto

254 Rituximab (Rtx) may be a safer alternative.

255 a known off target of the anti-CD20 antibody rituximab (RTX).

256 Rituximab's lack of efficacy could be due to a considera

257 The addition of rituximab (S0014) to combined-modality therapy did not m

258 d on the basis of improved response rates in rituximab-sensitive disease.

259 spreading at baseline and were treated with rituximab showed reversal of epitope spreading at month

260 The health-related costs associated with the rituximab strategy were lower than the TNF inhibitor str

261 broad potency, and potential to combine with rituximab suggest that SGN-CD19B may offer unique clinic

262 In patients eligible for bendamustine plus rituximab, the addition of ibrutinib to this regimen res

263 Despite the use of rituximab, the risk of developing HHV8-associated lympho

264 Rituximab therapy appears to be an effective option in p

265 In this trial, rituximab therapy did not significantly improve renal fu

266 nsplantation recipients with recurrent FSGS, rituximab therapy may be a recommended treatment for cas

267 reatment, 32 years [age range, 2-77 years]), rituximab therapy resulted in a mean (SE) 0.79 (0.15) (9

268 After depletion by rituximab, they show earlier and higher repopulation tha

269 with OA-MCL might be improved by addition of rituximab to chemotherapy treatment.

270 a median follow-up of 7.4 years, addition of rituximab to chlorambucil led to significantly better EF

271 Overall, the addition of rituximab to corticosteroid and CsA appeared to be safe

272 rial to test the efficacy of the addition of rituximab to corticosteroids (CSs) and cyclosporine A (C

273 rmacokinetic non-inferiority of subcutaneous rituximab to intravenous rituximab in follicular lymphom

274 ers of rituximab effect and that addition of rituximab to NIAT does not affect safety.

275 of IgA nephropathy, may reflect a failure of rituximab to reduce levels of specific antibodies assign

276 Adding rituximab to the ALL chemotherapy protocol improved the

277 A 33% decrease was seen after cycle 1 of rituximab treatment (100% vs 67%; P = .004); 20% after c

278 t group and 63 (92.6%) of 68 patients in the rituximab treatment group (4.3%; one-sided 97.5% CI -4.2

279 10 treatment group and 56 (80%) of 70 in the rituximab treatment group.

280 ot decrease to a significant degree over the rituximab treatment period.

281 p of 47 (range, 18-81) months since the last rituximab treatment.

282 patients, and one patient remitted following rituximab treatment.

283 ollicular helper (Tfh) cells decreased after rituximab treatment.

284 mmunostaining verified that increased (64)Cu-rituximab uptake in CNS tissues corresponded with elevat

285 ution results revealed notably higher (64)Cu-rituximab uptake in the brain and spinal cord of huCD20t

286 In the era of widespread rituximab use for Waldenstrom's macroglobulinaemia, new

287 the Fc region of hydrogen peroxide-stressed Rituximab, using a single, commercially available softwa

288 ide [FC] v FC plus rituximab; CLL10: FC plus rituximab v bendamustine plus rituximab) were analyzed a

289 ase 2 dose of venetoclax in combination with rituximab was 400 mg.

290 Lenalidomide plus rituximab was felt to be a safe and promising backbone b

291 Rituximab was introduced either immediately (N = 6) or a

292 A further course of rituximab was required for 4 patients as a result of FSG

293 tio of geometric least squares means (CT-P10/rituximab) was 102.25% (90% CI 94.05-111.17) for AUCtau

294 icin, vincristine, and prednisone (CHOP) +/- rituximab were used.

295 CLL10: FC plus rituximab v bendamustine plus rituximab) were analyzed according to MRD assessed in pe

296 not compromise the anti-lymphoma activity of rituximab when given with chemotherapy.

297 okinetic equivalence of CT-P10 compared with rituximab, when used in combination with cyclophosphamid

298 first case of a patient with DH treated with rituximab who achieved complete clinical and serological

299 er 1.73 m(2), to receive standard therapy or rituximab with standard therapy.

300 ange within 4 weeks before randomisation, or rituximab within 6 months before screening, were exclude