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1  belatacept and sirolimus; six also received alefacept.
2  observed, particularly with the addition of alefacept.
3 patients treated with the CD2-targeted agent alefacept.
4 sing biomarker of early treatment effects of alefacept.
5  with chronic psoriasis received intravenous alefacept (0.025, 0.075, or 0.150 mg per kilogram of bod
6                                              Alefacept (15 mg) or placebo was administered intramuscu
7                    These data establish that alefacept activates gene expression programs in leukocyt
8                                         Thus alefacept acts as an effector molecule, mediating cognat
9                               In conclusion, alefacept administration after depletion and with tacrol
10 fter treatment, 28 patients who had received alefacept alone were clear or almost clear of psoriasis.
11                                              Alefacept, an immunomodulatory recombinant fusion protei
12 bility, 33 were randomly assigned to receive alefacept and 16 to receive placebo.
13 on that influence the biological activity of alefacept and may contribute to its efficacy and patient
14  Safety and tolerability were similar in the alefacept and placebo groups.
15  The results of a trial with a second agent, alefacept are pending public review.
16                    This study 1) establishes alefacept as a novel CD2 agonist molecule for induction
17 controlled, double-blind study, we evaluated alefacept as a treatment for psoriasis.
18                      The recombinant protein alefacept binds to CD2 on memory effector T lymphocytes,
19  months, or 15 months after the last dose of alefacept, both the 4-hour and the 2-hour C-peptide AUCs
20                                              Alefacept competitively inhibited cell bilayer adhesion
21 ng human CD2-transgenic mice and isoforms of alefacept confirmed the requirement for Fc gamma R bindi
22                                              Alefacept could be useful to preserve beta-cell function
23 Tem cells, is targeted by the fusion protein alefacept, depleting Tem cells and central memory T (Tcm
24                                      Whereas alefacept down-regulated TCRs CD3D and CD2 in responders
25            Experimentation using isoforms of alefacept engineered to have amino acid substitutions in
26                               Treatment with alefacept for 12 weeks is associated with improvement in
27 0.015 nmol/L (95% CI -0.080 to 0.110) in the alefacept group and decreased by 0.115 nmol/L (-0.278 to
28 ts were about 50% reduced (P < 0.001) in the alefacept group compared with placebo at 24 months.
29  was significantly lower at 12 months in the alefacept group than in the placebo group.
30                                       In the alefacept group, 14 (42%) participants had grade 3 or 4
31                                       In the alefacept group, 29 (88%) participants had an adverse ev
32 two weeks after treatment was greater in the alefacept groups (38, 53, and 53 percent in the groups r
33                                     However, alefacept improves psoriasis in only approximately 50% o
34        We studied the immunologic effects of alefacept in a group of psoriasis patients during treatm
35                                              Alefacept in combination with MTX may be an effective an
36        We confirmed the agonistic effects of alefacept in PBMC in vitro, which were similar to CD3/CD
37 ohort 3 recipients (n = 5) were treated with alefacept in place of basiliximab, and more intense LFA-
38  detection of the pharmacological effects of alefacept in vivo.
39                                              Alefacept is a chimeric protein combining CD58 immunoglo
40                                              Alefacept is an LFA3-Ig fusion protein that binds to CD2
41                                              Alefacept is potential future therapeutic for organ tran
42                       The CD2-depleting drug alefacept (LFA3-Ig) preserved beta cell function in new-
43 some animals also received CD2 blockade with alefacept (LFA3-Ig).
44 we show that the CD2-specific fusion protein alefacept (lymphocyte function-associated antigen-3-Ig;
45                                              Alefacept mediated maximal adhesion of CD2(+) T cells to
46                                              Alefacept mediated T cell killing by NK cells and adhesi
47 l information is needed to correctly predict Alefacept-mediated bridge formation.
48                      A mechanistic model for alefacept-mediated cell-bilayer adhesion allowed fitting
49 This population was not entirely spared from alefacept-mediated depletion in vivo or in vitro but rec
50                                              Alefacept mediates adhesion by bridging CD2 on T cells t
51 that impact Fc gamma R binding indicate that alefacept mediates cognate interactions between cells ex
52                                              Alefacept modulates the function of and selectively indu
53 % in small case series using the CD2-blocker alefacept or TNF-alpha antagonists.
54 for placebo vs 0.36 units per kg per day for alefacept; p=0.02) and the rate of hypoglycaemic events
55 e patients were randomly assigned to receive alefacept plus MTX (n = 123) or placebo plus MTX (n = 62
56 14 was achieved by 53% of patients receiving alefacept plus MTX compared with 17% of those receiving
57           At week 24, 54% of patients in the alefacept plus MTX group achieved an ACR20 response, com
58                                       In the alefacept plus MTX group, the incidence of serious adver
59 d swollen joint counts in patients receiving alefacept plus MTX were -8.0 and -6.3, respectively.
60  newly diagnosed T1D, two 12-week courses of alefacept preserved C-peptide secretion, reduced insulin
61 e primary outcome was not met, at 12 months, alefacept preserved the 4 h C-peptide AUC, lowered insul
62                              The addition of alefacept provided no additional survival benefit, but w
63 rvival in rhesus monkeys, but induction with alefacept provides no survival benefit and increases the
64                                              Alefacept reduced peripheral-blood memory effector T-lym
65 ion that included tacrolimus with or without alefacept reliably prolonged renal allograft survival in
66 r bivalently and monovalently bound forms of alefacept, respectively.
67                                              Alefacept selectively targets CD45RO+ memory effector T
68     Specifically evaluated is the ability of alefacept to activate intracellular signals mediated via
69                                 Furthermore, alefacept-treated animals demonstrated increased alloant
70                                              Alefacept treatment depleted CD4+ and CD8+ central memor
71          Furthermore, responding patients to alefacept treatment show unique patterns of gene modulat
72  effector memory CD4 T cells was specific to alefacept treatment; 2 other T cell depleting therapies,
73 ents were randomly assigned (2:1) to receive alefacept (two 12-week courses of 15 mg intramuscularly
74 blind, placebo-controlled trial, we compared alefacept (two 12-week courses of 15 mg/wk i.m., separat
75 (mean of 10.9 events per person per year for alefacept vs 17.3 events for placebo; p<0.0001) was sign
76                                    In vitro, alefacept was found to enhance CD4 effector memory T cel
77                                              Alefacept was well tolerated and nonimmunogenic.
78                           We postulated that alefacept would arrest autoimmunity and preserve residua
79  hypothesized that the immunomodulatory drug alefacept would result in targeted quantitative and qual