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1                      Alemtuzumab (anti-CD52; Campath 1-H) depletes both host and donor T cells when u
2                           Alemtuzumab 30 mg (Campath 1-H) was used for preconditioning followed by lo
3 tored the outcome of 2,582 transplants using CAMPATH-1 (CD52) antibodies to deplete lymphocytes from
4 like many other methods of T-cell depletion, CAMPATH-1 antibodies also deplete B lymphocytes.
5                                              Campath-1 antibodies are directed against the surface an
6 ificity and antigen affinity of this pair of CAMPATH-1 antibodies for CD52.
7                                              CAMPATH-1 antibodies have a long and successful history
8 rface glycoprotein CD52, commonly called the CAMPATH-1 antigen.
9                                          The CAMPATH-1 family of antibodies are able systematically t
10 al risk of lymphoproliferative disease using CAMPATH-1 for depletion of donor lymphocytes was up to 1
11 that removed both T and B cells, such as the CAMPATH-1 monoclonal antibody or elutriation (P =.009).
12 tions were more common in patients receiving Campath 100 mg in vivo, but delayed CD4+ recovery was th
13  treated with the CD52 monoclonal antibodies CAMPATH-1G (rat IgG2b) or its humanized derivative, CAMP
14                                Murine forms, Campath-1G and Campath-1M, have been utilized extensivel
15 ntibody, the original therapeutic monoclonal CAMPATH-1G and its humanized counterpart CAMPATH-1H, int
16                                  Crystals of CAMPATH-1G have translational pseudo-symmetry.
17 bone marrow depleted with CAMPATH-1M, but no CAMPATH-1G in vivo; and (2) 459 patients reported to the
18                                        Using CAMPATH-1G to deplete residual host lymphocytes is a sim
19  in vitro depletion of the graft and an IgG (CAMPATH-1G) for in vivo depletion of the recipient befor
20                                              Campath 1H (0.3 mg/kg) was administered in four doses: P
21 noma cells (which express Ep-Cam but not the Campath 1H antigen) followed by incubation of the cells
22                      By contrast, the enzyme-Campath 1H conjugate was without effect.
23 f this research was to study the efficacy of campath 1H in combination with low-dose tacrolimus immun
24 renal allograft recipients were treated with Campath-1H (0.3 mg/kg) on days 0 and 4 postoperatively,
25                                              CAMPATH-1H (30 mg) was administered intravenously 3 time
26             Kidney transplant patients given Campath-1H (Alemtuzumab) immunodepletion therapy and lon
27                                              Campath-1H (alemtuzumab) is the most effective monoclona
28                 We evaluated the efficacy of Campath-1H (alemtuzumab; a humanized monoclonal antibody
29 -1G (rat IgG2b) or its humanized derivative, CAMPATH-1H (human immunoglobulin G1).
30 rabine (range, 4-10 courses) and 16 weeks of Campath-1H (range, 8-32 weeks) were treated.
31           The administration of alemtuzumab (Campath-1H [C1H]; Berlex Laboratories, Montville, NJ) at
32 inical trials and manageable toxicities make Campath-1H an appealing agent in the treatment of hemato
33 ransplantation from 24 patients treated with Campath-1H and sirolimus and tested for serum creatinine
34    Ten (42%) of the 24 patients treated with Campath-1H and sirolimus produced HLA antibodies.
35                                          The campath-1H antibody has activity in chronic lymphocytic
36 atients who received the lymphocytotoxic mAb CAMPATH-1H between 1991 and 1994 in the United Kingdom w
37 sults in 39 patients with T-PLL treated with CAMPATH-1H between March 1993 and May 2000.
38                                          The CAMPATH-1H binding site is highly basic; ionic interacti
39                              Analysis of the CAMPATH-1H binding site reveals that in contrast to most
40                     Prolonged treatment with CAMPATH-1H can lead to patient anti-idiotype responses w
41                                              Campath-1H causes the immune response to change from the
42                                              Campath-1H combined with fludarabine is a highly promisi
43        We present the 1.9 A structure of the CAMPATH-1H Fab complexed [corrected] with an analogue of
44                               Treatment with Campath-1H for 4 weeks led to a striking prolongation of
45      The VL domains of adjacent molecules of CAMPATH-1H form a symmetric dimer within the crystals wi
46    The infectious complications noted in the Campath-1H group were compared with a historical group o
47                   The genetically engineered Campath-1H has been utilized in the treatment of lymphom
48               These results demonstrate that Campath-1H has therapeutic efficacy on ATL in vivo in th
49 g monoclonal antibodies such as rituximab or Campath-1H in combination with fludarabine offer the opp
50                   These studies suggest that Campath-1H in conjunction with rapamycin monotherapy ret
51 ies, such as CD3 immunotoxin in primates and CAMPATH-1H in humans, has demonstrated that long-term gr
52 udy provides support for a clinical trial of Campath-1H in the treatment of patients with T-cell leuk
53        The main tumor killing mechanism with Campath-1H in vivo involves FcRgamma-containing receptor
54 t (P = 0.05), and being a child who received Campath-1H induction (P = 0.03).
55                        Patients who received Campath-1H induction did not have an increased incidence
56         In this study, we determined whether Campath-1H induction followed by sirolimus monotherapy i
57                                              Campath-1H induction for renal transplantation appears t
58                         We began using 30 mg Campath-1H intravenously for induction therapy in May 20
59                                              Campath-1H is an active drug in T-PLL patients for whom
60                       The conclusion is that CAMPATH-1H is an effective therapy in T-PLL, producing r
61                                              Campath-1H may be administered intravenously or subcutan
62 ade the infectious morbidity associated with Campath-1H more manageable.
63  on ATL in vivo in that the life span of the Campath-1H treatment group was comparable with that of m
64 plantation were expanded, and induction with Campath-1H was introduced.
65 urvival of mice receiving 4 weeks of 4 mg/kg Campath-1H was significantly longer than that of the gro
66                 We report the combination of Campath-1H with fludarabine in patients with CLL refract
67 safety, and clinical benefit of alemtuzumab (Campath-1H) for patients with relapsed or refractory B-c
68                                 Alemtuzumab (Campath-1H) induction with tacrolimus monotherapy has be
69 ither conventional treatment or alemtuzumab (Campath-1H) induction.
70                                 Alemtuzumab (Campath-1H) is a humanized IgG1 monoclonal antibody that
71                                 Alemtuzumab (Campath-1H) is a humanized monoclonal antibody (Ab) dire
72                     Alemtuzumab (MabCampath, Campath-1H) is a lymphocyte-depleting monoclonal antibod
73                     Alemtuzumab (MabCampath, Campath-1H) is a potent lymphocyte-depleting monoclonal
74                                 Alemtuzumab (Campath-1H) is a powerful antilymphocyte antibody that p
75 g humanized monoclonal antibody alemtuzumab (Campath-1H) is highly effective in the treatment of earl
76 chanism of action of alemtuzumab (anti-CD52; Campath-1H) remains unclear.
77 te maintenance corticosteroids, alemtuzumab (Campath-1H) was used as induction therapy in first cadav
78 d anti-leukocyte (CD52) monoclonal antibody (Campath-1H), has illuminated mechanisms that underlie th
79 ntation patients who received a alemtuzumab (Campath-1H)-based induction protocol for the incidence o
80 e anti-CD52 monoclonal antibody alemtuzumab (Campath-1H).
81 lysis to evaluate the safety and efficacy of Campath-1H, an anti-CD52 humanized monoclonal antibody,
82 hat binds to the tumor antigen Ep-Cam, or to Campath-1H, an antibody that binds to the T and B cell a
83  treated with fludarabine, cyclophosphamide, CAMPATH-1H, and CD34-selected HSCT (8 million CD34+ dono
84                     We combined alemtuzumab (Campath-1H, Berlex Laboratories, Montville, NJ) and tacr
85 nsisted of the humanized monoclonal antibody CAMPATH-1H, fludarabine, and melphalan.
86 nal CAMPATH-1G and its humanized counterpart CAMPATH-1H, into which the six complementarity-determini
87                          The humanized form, Campath-1H, is currently the focus of many clinical tria
88   In an early assessment, the combination of Campath-1H, low dosing of tacrolimus and mycophenolate m
89                                 Alemtuzumab (Campath-1H, Millennium Pharmaceuticals, Cambridge, MA) i
90  = 51), and group 3b (April 2001 to present, Campath-1H, n = 18) was 44%/32%, 52%/38%, 83%/60%, and 4
91 he first antibody to undergo "humanisation", CAMPATH-1H, permits treatment with limited patient anti-
92        Nonmyeloablative allogeneic SCT after CAMPATH-1H-containing conditioning is a relatively safe
93 ar leukocytes and monocytes are required for Campath-1H-mediated tumor killing in vivo.
94                              The most common Campath-1H-related adverse events were acute reactions d
95 f acute rejection, the latest 2 treated with Campath-1H.
96 induction rate with the human CD52 antibody, CAMPATH-1H.
97 pates in only two main-chain interactions in CAMPATH-1H.
98 re and for 18 months after a single pulse of Campath-1H.
99 the humanised anti-CD52 monoclonal antibody, Campath-1H.
100 ined the efficacy and safety of alemtuzumab (Campath-1H; Burroughs Wellcome, United Kingdom) in patie
101 ion, which had been frequent in the historic CAMPATH-1M group (31%), was largely overcome in the trea
102                                      An IgM (CAMPATH-1M) was used for in vitro depletion of the graft
103 ients who received bone marrow depleted with CAMPATH-1M, but no CAMPATH-1G in vivo; and (2) 459 patie
104                 Murine forms, Campath-1G and Campath-1M, have been utilized extensively in allogeneic
105 esponses to donor antigen were equal between Campath and control groups.
106 es to authentic TGN1412 but only modestly to Campath and not to control antibodies such as Herceptin,
107 ys also do not fully delineate mild (such as Campath) and severe (such as TGN1412) cytokine storm-ind
108 ty allograft recipients T-cell depleted with Campath antibodies were evaluated for respiratory virus
109 ty antibodies, broad-specificity antibodies, Campath antibodies, elutriation, and lectins.
110                   Alemtuzumab (MabCampath or Campath; Genzyme, Cambridge, MA) is a CD52-specific mono
111                                 However, the Campath group displayed a greater response to third part
112        Eight of the 49 (16%) patients in the Campath group had an infectious complication, compared t
113                                              CAMPATH monoclonal antibodies were used for T-cell deple
114 oglobulin, and Rituximab (three patients) or Campath (one patient), AMR was treated with laparoscopic
115                          Interestingly, more Campath patients (4 of 15) than control patients (0 of 8
116 g humanized monoclonal antibody alemtuzumab (Campath [registered trade mark]) significantly reduced t
117          We examined the T-cell responses of Campath-treated transplant patients on monotherapy versu

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