ライフサイエンスコーパス: panitumumab

1 cific treatment (chemotherapy, radiation, or panitumumab).

2 cific treatment (chemotherapy, radiation, or panitumumab).

3 clinical approval of the drugs cetuximab and panitumumab.

4 led to its targeting by using Cetuximab and Panitumumab.

5 tor receptor (EGFR) antibodies cetuximab and panitumumab.

6 monoclonal antibodies, such as cetuximab or panitumumab.

7 b and fluorescein 5(6)-isothiocyanate (FITC) panitumumab.

8 decane-N,N',N'',N'''-tetraacetic acid (DOTA)-panitumumab.

9 fractionation RT plus the anti-EGFR antibody panitumumab.

10 lidated in a cohort of patients treated with panitumumab.

11 as significant reduction in recurrences with panitumumab.

12 fractionation RT plus the anti-EGFR antibody panitumumab.

13 signed to arm B received either cetuximab or panitumumab.

14 K-Ras alterations based on the responses to panitumumab.

15 analysed for interaction with the effect of panitumumab.

16 mab, 26 received trifluridine-tipiracil plus panitumumab, 13 received irinotecan plus cetuximab, and

17 scertained in 427 (92%) of 463 patients (208 panitumumab, 219 BSC).

18 ction rate was improved with the addition of panitumumab (33.3% v 12.1%; P = .02).

19 bevacizumab and chemotherapy with or without panitumumab 6 mg/kg every 2 weeks.

20 rtive care in study 20020408 with or without panitumumab 6.0 mg/kg once every 2 weeks.

21 received sotorasib (960 mg, once daily) plus panitumumab (6 mg kg(-1), once every 2 weeks).

22 to receive sotorasib 960 mg (daily, orally)-panitumumab (6 mg/kg every 2 weeks, intravenous infusion

23 infusion), sotorasib 240 mg (daily, orally)-panitumumab (6 mg/kg every 2 weeks, intravenous infusion

24 us, with a permuted block method) to receive panitumumab (6 mg/kg once every 2 weeks) or cetuximab (i

25 ours were randomly assigned (1:1) to receive panitumumab (6 mg/kg; every 2 weeks with the first 6 wee

26 diotherapy plus panitumumab (three cycles of panitumumab 9 mg/kg every 3 weeks administered with radi

27 in the IrPan group also received intravenous panitumumab 9 mg/kg every 3 weeks.

28 abine 1000 mg/m(2) per day on days 1-21, and panitumumab 9 mg/kg on day 1).

29 emoradiotherapy (three cycles of intravenous panitumumab 9.0 mg/kg every 3 weeks plus cisplatin 75 mg

30 Evaluation of the immunogenicity of panitumumab, a fully human anti-epidermal growth factor

31 Panitumumab, a fully human antibody against the epiderma

32 Panitumumab, a fully human antibody targeting the epider

33 We aimed to compare panitumumab, a fully human monoclonal antibody against E

34 Panitumumab, a fully human monoclonal antibody targeting

35 Panitumumab, a fully human monoclonal antibody targeting

36 Panitumumab, a human monoclonal antibody that binds to t

37 on of 28 patients receiving monotherapy with panitumumab, a therapeutic anti-EGFR antibody.

38 of detecting 10 ng/ml positive control anti-panitumumab Ab.

39 arate immunoassays for the detection of anti-panitumumab Abs.

40 in expression showed the highest (64)Cu-DOTA-panitumumab accumulation, whereas SQB20 tumors with the

41 GFR expression showed the lowest (64)Cu-DOTA-panitumumab accumulation.

42 ) patients treated with modified FOLFOX plus panitumumab achieved RECIST response (odds ratio 0.87, 9

43 This trial evaluated panitumumab added to bevacizumab and chemotherapy (oxali

44 clonal immunoglobulin gamma2 (IgG2) antibody panitumumab against human epidermal growth factor recept

45 asure the specificity of radiolabeled (89)Zr-panitumumab (an EGFR antibody) in vivo using patient-der

46 viral oncogene homolog)-G12C inhibitor, and panitumumab, an epidermal growth factor receptor (EGFR)

47 vival was 10.4 months (95% CI 9.4-11.6) with panitumumab and 10.0 months (9.3-11.0) with cetuximab (H

48 (73%) patients treated with mFOLFOXIRI plus panitumumab and 165 (76%) patients treated with modified

49 toxicity occurred in 62 (13%) patients given panitumumab and 48 (10%) patients given cetuximab.

50 of whom began study treatment: 499 received panitumumab and 500 received cetuximab.

51 PFS in the WT KRAS group was 12.3 weeks for panitumumab and 7.3 weeks for BSC.

52 emission tomography (PET) imaging ([(89)Zr]-panitumumab and [(89)Zr]-pertuzumab) was used to charact

53 Median OS was 34.2 and 24.3 months in the panitumumab and bevacizumab arms, respectively (HR, 0.62

54 0.63; 95% CI, 0.39 to 1.02; P = .058) in the panitumumab and bevacizumab arms, respectively.

55 The anti-EGFR monoclonal antibodies panitumumab and cetuximab are effective in patients with

56 median PFS was 10.0 and 11.4 months for the panitumumab and control arms, respectively (HR, 1.27; 95

57 ival was 19.4 months and 24.5 months for the panitumumab and control arms, respectively.

58 etween therapeutic efficacy of cetuximab and panitumumab and EGFR expression level as determined by i

59 sociated with the use of the EGFR inhibitors panitumumab and erlotinib.

60 as confirmed by ex vivo immunostaining using panitumumab and fluorescein 5(6)-isothiocyanate (FITC) p

61 y poor in patients who received single-agent panitumumab and had right-sided tumors (median PFS, 7.7

62 n changes from baseline for sotorasib 960 mg-panitumumab and sotorasib 240 mg-panitumumab (both vs in

63 1 ((111)In)- and iodine 125 ((125)I)-labeled panitumumab and trastuzumab, respectively.

64 en used to radiolabel an anti-EGFR antibody, Panitumumab, and injected into mice bearing colon cancer

65 countries), including the mAbs cetuximab and panitumumab, and the small molecule TKIs gefitinib, erlo

66 nti-RTK antibodies (immuno-PET) onartuzumab, panitumumab, and trastuzumab to monitor MET, EGFR, and H

67 Photoimmunotherapy was performed by binding panitumumab (anti-HER1)-IR700 to HER1-positive tumor cel

68 onal antibodies (mAbs) such as cetuximab and panitumumab are promising; however, most studies indicat

69 3, and 4 of KRAS and NRAS), PFS favored the panitumumab arm (HR, 0.65; 95% CI, 0.44 to 0.96; P = .02

70 The ORR of the mFOLFOXIRI plus panitumumab arm exceeded 75% and was higher when compare

71 RAS analyses showed adverse outcomes for the panitumumab arm in both wild-type and mutant groups.

72 nce of improved efficacy was observed in the panitumumab arm of the irinotecan cohort.

73 platin patients showed worse efficacy in the panitumumab arm.

74 -treated mice that did not receive unlabeled panitumumab as a blocking control for AB-36, AB-37, and

75 ractionation RT (70 Gy/35 over 6 weeks) plus panitumumab at 9 mg/kg intravenous for 3 doses (arm B).

76 ractionation RT (70 Gy/35 over 6 weeks) plus panitumumab at 9 mg/kg intravenous for 3 doses (arm B).

77 aracterize the targeting potential of (89)Zr-panitumumab at different lesion sites.

78 n is available regarding the localization of panitumumab at primary and metastatic lesions.

79 asib 960 mg-panitumumab and sotorasib 240 mg-panitumumab (both vs investigator's choice), respectivel

80 (89)Zr-panitumumab can play a vital role in patient stratificat

81 Panitumumab cannot replace cisplatin in the combined tre

82 Targeted therapies (bevacizumab or panitumumab) combined with standard chemotherapy reduced

83 towards reduced recurrences with FOLFOX plus panitumumab compared with FOLFOX (12% versus 21%, hazard

84 rall survival showed a trend in favor of the panitumumab-containing arm (hazard ratio for death, 0.67

85 nd G12V positively associated with OS in the panitumumab-containing arm.

86 Patients receiving panitumumab-containing therapy were randomly assigned 1:

87 ere randomly assigned 1:1 to modified FOLFOX/panitumumab (control group) or mFOLFOXIRI/panitumumab (e

88 , these analyses suggest that sotorasib plus panitumumab could represent a valuable new treatment in

89 Sotorasib-panitumumab demonstrated acceptable safety with promisin

90 Panitumumab did not enhance the benefit from NAC.

91 nt chemotherapy backbone in combination with panitumumab does not provide additional benefit in terms

92 onally be sub-randomised 1 : 1 to FOLFOX +/- panitumumab during the preoperative phase.

93 study, sotorasib (KRAS(G12C) inhibitor) plus panitumumab (EGFR inhibitor) significantly prolonged pro

94 gained FDA approval in oncology (cetuximab, panitumumab, erlotinib, gefitinib and lapatinib).

95 OX/panitumumab (control group) or mFOLFOXIRI/panitumumab (experimental group) up to 12 cycles, follow

96 Overall survival was 26.0 months in the panitumumab-FOLFOX4 group versus 20.2 months in the FOLF

97 ments in overall survival were observed with panitumumab-FOLFOX4 therapy.

98 sion-free survival and overall survival with panitumumab-FOLFOX4 treatment, which was consistent with

99 ogression-free survival was 10.1 months with panitumumab-FOLFOX4 versus 7.9 months with FOLFOX4 alone

100 a lack of response in patients who received panitumumab-FOLFOX4.

101 Randomized Trial of EOC +/- Panitumumab for Advanced and Locally Advanced Esophagoga

102 obtained from mice coinjected with 0.1 mg of panitumumab for blocking the target.

103 s ((177)Lu-NT-AuNP) were constructed without panitumumab for comparison.

104 nstrates the potential of (86)Y-CHX-A''-DTPA-panitumumab for quantitative noninvasive PET of HER1-exp

105 ''-diethylenetriaminepentaacetic acid (DTPA)-panitumumab for quantitative PET of HER1-expressing carc

106 ing the beta-particle emitter (177)Lu and to panitumumab for targeting epidermal growth factor recept

107 ptides to capture Bevacizumab, Rituximab, or Panitumumab from diluted (25%) serum.

108 grade 3-4 hypomagnesaemia was higher in the panitumumab group (35 [7%] vs 13 [3%]).

109 42%] of 89 patients in the radiotherapy plus panitumumab group), dysphagia (20 [32%] vs 36 [40%]), an

110 herapy group and 90 in the radiotherapy plus panitumumab group).

111 oup and 51% (40-62) in the radiotherapy plus panitumumab group.

112 34%) of 89 patients in the radiotherapy plus panitumumab group.

113 randomized controlled trials of cetuximab or panitumumab have evaluated outcomes for patients with me

114 itinib, erlotinib, cetuximab, lapatinib, and panitumumab have less systemic side-effects than traditi

115 The potential utility of (89)Zr-panitumumab in assessing HER1 status in distant metastas

116 mparing FOLFIRINOX + Panitumumab vs FOLFOX + Panitumumab in Metastatic Colorectal Cancer Patients Str

117 101 master protocol evaluated sotorasib plus panitumumab in patients with chemotherapy-refractory KRA

118 ndicating that the low uptake of (64)Cu-DOTA-panitumumab in SQB20 tumors was not due to the loss of E

119 small-animal PET studies with (64)Cu-labeled panitumumab in xenografts derived from 3 cell lines of h

120 The Raman studies detect large panitumumab-induced differences in vitro in cells harbor

121 Anti-epidermal growth factor receptor (EGFR) panitumumab-IR700 was used for targeting EGFR-expressing

122 cer cell line (2LMP-Luc) in combination with panitumumab-IRDye 700DX (pan-IR700) was used to validate

123 e detection are of particular interest, with panitumumab-IRDye800 as a major candidate in current stu

124 Intratumoral distribution of panitumumab-IRDye800 correlated with near-infrared fluor

125 get-to-background ratios peaked at 14 h post panitumumab-IRDye800 infusion, reaching 19.5 in vivo and

126 xpression were imaged in vivo after systemic panitumumab-IRDye800 injection to assess its tumor-speci

127 Tumor specific uptake of panitumumab-IRDye800 provided remarkable contrast and a

128 were enrolled in a clinical trial evaluating panitumumab-IRDye800CW for surgical guidance (NCT0241588

129 ted the safety of an antibody-dye conjugate (panitumumab-IRDye800CW) as primary outcome.

130 tly-labeled, tumor-targeting contrast agent, panitumumab-IRDye800CW, to facilitate the identification

131 b plus avelumab, trifluridine-tipiracil plus panitumumab, irinotecan plus cetuximab, or panitumumab m

132 gand model in a randomized clinical trial of panitumumab, irinotecan, and ciclosporin in colorectal c

133 otecan plus ciclosporin, and irinotecan plus panitumumab (IrPan) groups.

134 Panitumumab is a fully human monoclonal antibody that ta

135 Panitumumab is an anti-HER1 monoclonal antibody approved

136 toma PDX tumor xenografts, we believe (89)Zr-panitumumab is an attractive target for pre-surgical ima

137 Our findings show that panitumumab is non-inferior to cetuximab and that these

138 ided more accurate information about (111)In-panitumumab localization in the tumor, as the tumor was

139 The PFS benefit of FU plus LV added to panitumumab maintenance, reported in the study, was inde

140 day on days 1-21) or modified-dose EOC plus panitumumab (mEOC+P; epirubicin 50 mg/m(2) and oxaliplat

141 AS/NRAS/BRAF wild-type tumors, cetuximab and panitumumab (monoclonal antibodies to the epithelial gro

142 Panitumumab monotherapy efficacy in mCRC is confined to

143 ollected in a phase III mCRC trial comparing panitumumab monotherapy to best supportive care (BSC).

144 d irinotecan plus cetuximab, and 27 received panitumumab monotherapy) were included in the current an

145 r without bevacizumab, 1 patient (0.4%) with panitumumab monotherapy, and 3 (1%) with immune checkpoi

146 lecting patients with mCRC as candidates for panitumumab monotherapy.

147 s panitumumab, irinotecan plus cetuximab, or panitumumab monotherapy.

148 960 mg-panitumumab (n=53), sotorasib 240 mg-panitumumab (n=53), and investigator's choice (n=54).

149 andomly assigned to receive sotorasib 960 mg-panitumumab (n=53), sotorasib 240 mg-panitumumab (n=53),

150 rmal growth factor receptor (EGFR) inhibitor panitumumab on cell lines expressing wild-type Kirsten-R

151 We tested whether the effect of panitumumab on progression-free survival (PFS) differed

152 ed patients who received one or more dose of panitumumab or cetuximab, analysed per allocated treatme

153 uld also be randomly assigned 1:1 to receive panitumumab or not during NAC.

154 otecan doublets with or without bevacizumab, panitumumab, or cetuximab; and 1 (0.4%) with irinotecan

155 Panitumumab (P) is a fully human, immunoglobulin G2 mono

156 expressing EGFR and HER2, using PA- labeled panitumumab (pan) and trastuzumab (tra), respectively.

157 dies daclizumab (Dac), trastuzumab (Tra), or panitumumab (Pan).

158 a median follow-up of 46 months, the PFS of panitumumab plus accelerated-fractionation RT was not su

159 a median follow-up of 46 months, the PFS of panitumumab plus accelerated-fractionation RT was not su

160 y (three cycles of cisplatin 100 mg/m(2)) or panitumumab plus chemoradiotherapy (three cycles of intr

161 oradiotherapy group vs 35 [40%] of 87 in the panitumumab plus chemoradiotherapy group), mucosal infla

162 in the chemoradiotherapy group and 87 in the panitumumab plus chemoradiotherapy group).

163 group and in 37 (43%) of 87 patients in the panitumumab plus chemoradiotherapy group.

164 emoradiotherapy group and 61% (50-71) in the panitumumab plus chemoradiotherapy group.

165 e randomly assigned at a one-to-one ratio to panitumumab plus mFOLFOX6 or bevacizumab plus mFOLFOX6.

166 ysis, we assessed the efficacy and safety of panitumumab plus oxaliplatin, fluorouracil, and leucovor

167 tment with the anti-EGFR monoclonal antibody panitumumab plus the standard-of-care trifluridine-tipir

168 Of 62 included patients, 31 received panitumumab plus trifluridine-tipiracil (19 [61.3%] male

169 s 4.0 months (95% CI, 2.8-5.3 months) in the panitumumab plus trifluridine-tipiracil arm vs 2.5 month

170 ts obtaining prolonged clinical benefit with panitumumab plus trifluridine-tipiracil compared with tr

171 Patients were randomized 1:1 to receive panitumumab plus trifluridine-tipiracil or trifluridine-

172 cil and folinic acid (FU/FA) with or without panitumumab (Pmab) after Pmab + mFOLFOX6 induction withi

173 ed PANAMA trial investigated the efficacy of panitumumab (Pmab) when added to maintenance therapy wit

174 or biochemotherapy (bevacizumab, cetuximab, panitumumab, ramucirumab, or aflibercept, started within

175 prospectively stratified design, restricting panitumumab randomisation to patients with KRAS wild-typ

176 atients in the irinotecan-vs-irinotecan with panitumumab randomization, 331 had sufficient tumor tiss

177 PFS was similar and OS was improved with panitumumab relative to bevacizumab when combined with m

178 The successful development of panitumumab represents a milestone for mice engineered w

179 Panitumumab retained 105.7% (81.9-129.5) of the effect o

180 al antibody (MoAb) therapy with cetuximab or panitumumab (see Note).

181 dermal growth factor inhibitor (cetuximab or panitumumab) should not be used in mCRC.

182 grade 3-4 infusion reactions was lower with panitumumab than with cetuximab (one [<0.5%] patient vs

183 ression of either AREG or EREG would predict panitumumab therapy benefit in RAS-wt patients; and low

184 ligand expression is a predictive marker for panitumumab therapy benefit on PFS in RAS wt patients; c

185 Currently, panitumumab therapy should be limited to patients with w

186 13 mCRC tumors are unlikely to benefit from panitumumab therapy.

187 during radiotherapy) or to radiotherapy plus panitumumab (three cycles of panitumumab 9 mg/kg every 3

188 The utility of PET and MRI using (89)Zr-panitumumab to assess the status of HER1 in distant meta

189 The addition of panitumumab to bevacizumab and oxaliplatin- or irinoteca

190 Addition of panitumumab to EOC chemotherapy does not increase overal

191 to assess addition of the anti-EGFR antibody panitumumab to epirubicin, oxaliplatin, and capecitabine

192 Adding panitumumab to irinotecan did not improve the overall su

193 Our aim was to assess the addition of panitumumab to irinotecan in pretreated advanced colorec

194 PICCOLO trial, which tested the addition of panitumumab to irinotecan therapy in patients with KRAS

195 The addition of panitumumab to mFOLFOXIRI in patients with RAS WT metast

196 ies should determine whether the addition of panitumumab to mFOLFOXIRI prolongs survival.

197 mised phase II trial testing the addition of panitumumab to neoadjuvant FOLFOX compared with FOLFOX a

198 ment in TTR from the addition of neoadjuvant panitumumab to perioperative FOLFOX in RAS/BRAF-wt LACC.

199 cinoma of the head and neck, the addition of panitumumab to standard fractionation radiotherapy and c

200 epidermal growth factor receptor antagonist panitumumab to treat advanced colorectal cancer--was dev

201 This trial investigated the addition of panitumumab to triplet chemotherapy with fluorouracil/fo

202 as significantly greater in tumors of (89)Zr-panitumumab-treated mice that did not receive unlabeled

203 expanded subclones before the initiation of panitumumab treatment.

204 e factor for PFS or OS in patients receiving panitumumab treatment.

205 cycles, followed by fluorouracil/-leucovorin/panitumumab until disease progression.

206 At 2 days after injection, the mean (111)In-panitumumab uptake of 29.6% injected dose (ID) per gram

207 uptake of 13.6% ID/g +/- 1.0 and the (125)I-panitumumab uptake of 7.4% ID/g +/- 1.2 (P = .0006 and P

208 /4 adverse events in the oxaliplatin cohort (panitumumab v control) included skin toxicity (36% v 1%)

209 as awaited the recent regulatory approval of panitumumab (Vectibix), a fully human antibody directed

210 bound Neu5Gc in cetuximab (Erbitux) but not panitumumab (Vectibix).

211 We assessed the efficacy and toxicity of panitumumab versus cetuximab in these patients.

212 e II Randomized Study Comparing FOLFIRINOX + Panitumumab vs FOLFOX + Panitumumab in Metastatic Colore

213 FS was 3.2 [2.7-8.1] months (irinotecan with panitumumab) vs 4.0 [2.7-7.5] months (irinotecan); HR, 0

214 S was 8.3 [4.0-11.0] months (irinotecan with panitumumab) vs 4.4 [2.8-6.7] months (irinotecan alone);

215 mor uptake in mice coinjected with 0.1 mg of panitumumab was 9.3 +/- 1.5, 8.8 +/- 0.9, and 10.0 +/- 1

216 FOLFOX plus panitumumab was associated with higher rates of grade 3

217 Panitumumab was conjugated to CHX-A''-DTPA and radiolabe

218 Panitumumab was discontinued after a planned interim ana

219 Panitumumab was dual-labeled with the fluorophore IRDye

220 ponent with the largest spectral response to panitumumab was lipid droplets, but this effect was not

221 AB-39 AB-53), the biodistribution of (89)Zr-panitumumab was measured 120 h post-injection and was re

222 or the primary analysis of overall survival, panitumumab was non-inferior to cetuximab (Z score -3.19

223 Panitumumab was not associated with increased pathologic

224 (86)Y-CHX-A''-DTPA-panitumumab was routinely prepared with a specific activ

225 al arm (modified FOLFOXIRI [mFOLFOXIRI] plus panitumumab) was considered active if the ORR was >= 75%

226 Response rates to panitumumab were 17% and 0%, for the WT and mutant group

227 pproved monoclonal antibodies, cetuximab and panitumumab, which displaced each other and displayed no

228 are the monoclonal antibodies cetuximab and panitumumab, which prevent epidermal growth factor recep

229 We aimed to compare chemoradiotherapy plus panitumumab with chemoradiotherapy alone in patients wit

230 was demonstrated by coinjection of 0.1 mg of panitumumab with the radioimmunoconjugate.

231 ober, 2011, trial recruitment was halted and panitumumab withdrawn.