ライフサイエンスコーパス: C225

1 up to 24 h after administration of 99mTc-EC-C225.

2 ombined poly(L-glutamic acid)-paclitaxel and C225.

3 er, tumor uptake of EGF-Cy5.5 was blocked by C225.

4 ld after pretreatment with a large excess of C225.

5 t than the uptake of unmodified (111)In-DTPA-C225.

6 n are observed when SCC cells are exposed to C225.

7 VCA420 cells to saturating concentrations of C225 (20 nM) for 7 days resulted in 40-50% growth inhibi

8 th MDA-MB-468 tumors were injected i.v. with C225 24 h before injection of EGF-Cy5.5.

9 followed by an injection of (111)In-DTPA-PEG-C225 30 min or 20 h later.

10 It was determined that the combination of C225 (5 microgram/mL) delivered simultaneously with radi

11 ombined poly(L-glutamic acid)-paclitaxel and C225 (9.84 +/- 2.51 %ID/g; P = 0.029) than in nontreated

12 Tc-labeled ethylene dicysteine (EC) C225 (EC-C225), a promising radioligand for functional tumor imag

13 atic ErbB2-overexpressing breast cancer; IMC-C225, a chimeric anti-EGFr MAb, has shown impressive act

14 This report will focus on IMC-C225, a novel monoclonal antibody that targets the EGFR.

15 Inactivation studies with C225S-alpha in the presence or absence of reductants, re

16 Inactivated C225S-alpha migrates as an 87 kDa protein and is not cov

17 n treatment with concurrent exposure to mAbs C225 and 4D5 resulted in additive anti-proliferative eff

18 Binding of EGF-Cy5.5 was blocked by C225 and by EGF.

19 In the study combining C225 and cisplatin, nine (69%) of 13 patients treated wi

20 OVCA 420 human ovarian cancer cells with mAb C225 and mAb 4D5.

21 l lines was used to study the combination of C225 and radiation.

22 rt for the ongoing clinical investigation of C225 and radiotherapy for patients with head and neck ca

23 glutamic acid)-paclitaxel and cetuximab (IMC-C225) anti-epidermal growth factor receptor antibody, th

24 The new radiopharmaceutical 99mTc-EC-C225 appears to have reasonable dosimetric properties fo

25 a human-mouse chimeric anti-EGF receptor mAb C225 are currently being investigated in clinical trials

26 cubation of the pancreatic cancer cells with C225 as well as Nitrobenzylthioinosine (NBMPR - nucleosi

27 C225 were detected in only one patient, and C225-associated toxicity was minimal.

28 he antiepidermal growth factor receptor mAb, C225 at increasing PTX:C225 ratios, producing completely

29 C225 in a phase III trial received 99mTc-EC-C225 before their 20-mg test dose or after their 400 mg/

30 inhibitor PKI166 and EGFR blocking antibody C225, both of which are used clinically to treat head an

31 riety of site-directed mutants of R1 (C462S, C225S, C754/759S, C439S, and E441Q) indicate that E441 o

32 C225 clearance did not change with repeated administrati

33 ies with two site-directed mutants, C58S and C225S, confirm that Cys-58 reacts slowly while Cys-225 r

34 rmal growth factor receptor (EGFR) antibody, C225, conjugated with heterofunctional poly(ethylene gly

35 of this study was to test an anti-EGFR MAb (C225) coupled to either the near-infrared fluorescent dy

36 ularly with Fab' fragments of cetuximab (IMC-C225), covalently linked to liposomes containing probes

37 33 and the anti-EGF receptor (EGFR) antibody C225 demonstrated that ligand-mediated activation of EGF

38 The data herein show that C225-dependent EGFR trafficking relocalizes the receptor

39 ceptor, the same kinase inhibitors stimulate C225-dependent nuclear localization of EGFR in the nucle

40 For comparison, C225 directly labeled with (111)In was also injected.

41 C225 displayed nonlinear pharmacokinetics, with antibody

42 C225 dose levels were 5, 20, 50, and 100 mg/m(2).

43 ry of 99mTc-labeled ethylene dicysteine (EC) C225 (EC-C225), a promising radioligand for functional t

44 Examination of C225 effects on radiation response in SCCs demonstrates

45 ctor receptor monoclonal antibody cetuximab (C225; Erbitux), which was recently approved for the trea

46 C225 exposure also induces apoptosis in SCC populations,

47 Western blot analysis indicates that C225 exposure induces accumulation of hypophosphorylated

48 binding changes in the already-high-affinity C225-Fab/huEGFR interface.

49 intravenously with 100-fold excess of native C225, followed by an injection of (111)In-DTPA-PEG-C225

50 tion of poly(L-glutamic acid)-paclitaxel and C225, followed by intravenous injection of (111)In-DTPA-

51 ration of the EGFR antagonist cetuximab (IMC-C225) for 2 weeks beginning at birth in CNPase-hEGFR mic

52 C225 given in combination with cisplatin has biologic ac

53 C225 has dose-dependent pharmacokinetics, and doses that

54 udied the combination of cetuximab (Erbitux, C225; ImClone Systems, New York, NY) with either gefitin

55 patients who had been randomized to receive C225 in a phase III trial received 99mTc-EC-C225 before

56 he tumor-to-blood ratios of (111)In-DTPA-PEG-C225 in A431 and MDA-MB-468 xenografts were about 3 fold

57 Exposure to C225 in culture inhibits SCC proliferation in a time-dep

58 aluated the pharmacokinetics and toxicity of C225 in patients with advanced tumors overexpressing EGF

59 i-EGF receptor monoclonal antibody cetuximab/C225 in PTEN-deficient cancer cells, we exposed MDA468 b

60 antly reduced the uptake of (111)In-DTPA-PEG-C225 in the liver.

61 growth factor receptor) antibody cetuximab (C225)- induced EGFR internalization in pancreatic cancer

62 Nanoconjugation uniformly enhanced C225-induced EGFR endocytosis in PANC-1, AsPC-1, and Mia

63 pendent receptor dimerization may facilitate C225-induced receptor trafficking.

64 The monoclonal antibody C225 interacts with the ectodomain of the epidermal grow

65 nism, which also involves interaction of the C225-internalized receptor with the Sec61 translocon wit

66 C225 is a human-to-murine chimeric monoclonal antibody t

67 C225 is an anti-EGFr monoclonal antibody that inhibits r

68 C225 is one of the cysteines in RNR's active site that s

69 Ultimately, IMC-C225 may prove to become a valuable contributor in the t

70 n A431 tumor xenografts, the tumor uptake of C225 modified with PEG was not significantly different t

71 Incubation of the C225S mutant of the R1 subunit of ribonucleotide reducta

72 , however, with the pyrene maleimide-labeled C225S mutant.

73 e histological stage of the lesions when the C225-N,N'-di-carboxypentyl-indodicarbocyanine-5,5'-disul

74 l growth factor receptor monoclonal antibody C225 on proliferation, cell cycle phase distribution, ap

75 Two preparations of PEG-modified C225, one with 20% and the other with 60% amine substitu

76 he growth inhibition of OVCA420 cells by mAb C225 or 4D5 was associated with an increased G1 cell pop

77 nt with humanized anti-EGF receptor antibody C225 or anti-human epidermal growth factor receptor-2 (H

78 -Cy5.5, or the anti-EGFr monoclonal antibody C225 or EGF followed by EGF-Cy5.5 and examined under a f

79 ell cycle regulators induced by mAb 4D5, mAb C225 or the combination of the two mAbs could be reverse

80 utamic acid)-paclitaxel, monoclonal antibody C225, or a combination of poly(L-glutamic acid)-paclitax

81 humanized anti-EGF receptor (EGFR) antibody C225, or anti-human epidermal growth factor receptor-2 (

82 er their 400 mg/m2 loading dose of unlabeled C225 (patients 1/3/5 and 2/4/6, respectively).

83 hibitor (PD153035) or an anti-EGFR antibody (C225), PLCgamma-1 activation was abrogated indicating th

84 nografts were not significantly different in C225-pretreated mice than in nonpretreated mice.

85 apoptotic events, thereby indirectly linking C225/radiation-induced regulation of STAT-3 protein to a

86 factor receptor mAb, C225 at increasing PTX:C225 ratios, producing completely soluble conjugates.

87 C225 represents a promising growth-inhibitory agent that

88 ) revealed that all excited pyrene labels on C225 residues can form excimers with pyrenes of adjacent

89 , [1'-(2)H]-F(2)CDP was studied with wt- and C225S-RNR by 9 and 140 GHz EPR spectroscopy.

90 hese findings indicate that (111)In-DTPA-PEG-C225 selectively localized to the tumors expressing high

91 PEG-modification of C225 significantly reduced its liver uptake, resulting i

92 Blocking EGFR by pretreatment with native C225 significantly reduced the uptake of (111)In-DTPA-PE

93 Antibodies such as IMC-C225 specifically target EGF receptors, whereas tyrosine

94 late nuclear accumulation of the receptor in C225-treated cells and does not provoke receptor dimeriz

95 Flow cytometry analysis demonstrates that C225 treatment induces accumulation of cells in G1, whic

96 head and neck or non-small-cell lung cancer, C225 was further escalated to 200 and 400 mg/m(2).

97 In addition, (111)In-DTPA-PEG-C225 was injected into mice with EGFR-positive MDA-MB-46

98 Antibodies against C225 were detected in only one patient, and C225-associa

99 The conjugates, (111)In-DTPA-PEG-C225, were injected intravenously into nude mice with EG

100 ere clearly visualized with (111)In-DTPA-PEG-C225, whereas tumors of the MDA-MB-435 xenograft, which

101 agments included Fab' fragments derived from C225, which binds both EGFR and EGFRvIII, or novel anti-

102 In the study combining C225 with cisplatin, limited to patients with either hea