ライフサイエンスコーパス: plerixafor

1 effect on mobilization induced by G-CSF with plerixafor.

2 was not in patients who received G-CSF plus plerixafor.

3 han the clinically approved CXCR4 antagonist plerixafor.

4 ization do not occur after mobilization with plerixafor.

5 induced CML-like disease with imatinib plus plerixafor.

6 t recovery was observed with the addition of plerixafor.

7 ith 5 normal subjects similarly treated with plerixafor.

8 In phase 2, 46 patients were treated with plerixafor 0.24 mg/kg/d in combination with chemotherapy

9 We investigated the effects of plerixafor (0.04 to 0.24 mg/kg) administered at 2-4 day

10 y for up to 4 days, patients received either plerixafor (240 microg/kg) or placebo subcutaneously.

11 y for up to 4 days, patients received either plerixafor (240 microg/kg) or placebo subcutaneously.

12 To target MCL-MSC interactions, we tested Plerixafor, a CXCR4 antagonist, and natalizumab, a VLA-4

13 Plerixafor, a CXCR4 antagonist, decreased fibrocyte migr

14 rticular, G-CSF, a known CXCR2 signaler, and plerixafor, a CXCR4 antagonist, have both been shown to

15 discuss recent results of trials evaluating plerixafor, a selective antagonist of CXCR4, as a mechan

16 The provision of plerixafor, a stem cell mobilizer, salvaged 5 of 10 whol

17 Plerixafor (AMD3100) and granulocyte colony-stimulating

18 s study evaluates the safety and efficacy of plerixafor (AMD3100), a CXCR4 antagonist, in mobilizing

19 HSPC mobilization (3-fold) was observed when plerixafor (AMD3100), a small molecule inhibitor of the

20 action with marrow stroma, we tested whether plerixafor, an antagonist of CXCR4, may dislodge chronic

21 stopathologic analysis, animals treated with plerixafor and G-CSF demonstrated less hepatic injury co

22 Administration of plerixafor and G-CSF following CCl4 resulted in 87% surv

23 Plerixafor and G-CSF were well tolerated and resulted in

24 Plerixafor and G-CSF were well tolerated, and significan

25 increase in circulating HSCs in response to plerixafor and G-CSF, and immunostaining suggested the i

26 A rhesus macaque model was used to compare plerixafor and G-CSF-mobilized CD34(+) cells.

27 12 hours, animals were randomized to receive plerixafor and granulocyte colony-stimulating factor (G-

28 o overview clinical experience with AMD3100 (plerixafor) and its role in stem cell mobilization.

29 F-induced mobilization while decreasing both plerixafor- and BIO5192-induced mobilization of HSPCs.

30 equestration, and support continued study of plerixafor as mechanism-based therapy in this disease.

31 The most common plerixafor-associated adverse events were GI disorders a

32 Instead, plerixafor augments the frequency of circulating neutrop

33 BTK-inhibitor ibrutinib and CXCR4-inhibitor plerixafor block SDF-1alpha-mediated CD20 upregulation.

34 fer when donor allografts are mobilized with plerixafor compared with G-CSF.

35 rket: maraviroc (CCR5) for HIV infection and plerixafor (CXCR4) for stem-cell mobilization.

36 tudy, we tested whether the CXCR4 antagonist plerixafor, differently from G-CSF, is effective in mobi

37 In contrast to G-CSF, CXCR4 inhibition via plerixafor does not result in neutrophil mobilization fr

38 ony-stimulating factor (G-CSF), BIO5192, and plerixafor enhanced mobilization by 17-fold compared wit

39 Despite much improved leukemia control, plerixafor failed to reduce leukemia burden over dasatin

40 that changing the route of administration of plerixafor from SC to IV may overcome the low stem cell

41 Plerixafor+G-CSF cells produced the highest beta-globin

42 Overall, Plerixafor+G-CSF not only allows high CD34+ cell yields

43 lating factor (G-CSF), G-CSF, Plerixafor, or Plerixafor+G-CSF were transduced with the TNS9.3.55 beta

44 encountered in all xenografted groups, with Plerixafor+G-CSF-mobilized cells achieving superior shor

45 In contrast with plerixafor, G-CSF mobilization decreased CD62L expressio

46 Eighty-nine (59%) of 150 patients in the plerixafor group and 29 (20%) of 148 patients in the pla

47 total of 106 of 148 (71.6%) patients in the plerixafor group and 53 of 154 (34.4%) patients in the p

48 One hundred thirty-five patients (90%) in plerixafor group and 82 patients (55%) in placebo group

49 nts with diabetes who received G-CSF without plerixafor had a lower probability of reaching >50/muL C

50 In addition, mice receiving plerixafor had an increased incidence of neurologic symp

51 Plerixafor has been shown to be a potentially useful tre

52 Recently, plerixafor has been used as a single agent to mobilize p

53 bilization of PBSCs from normal donors using plerixafor have been reported.

54 s from the first long-term clinical trial of plerixafor in any disease, in which 3 adults with WHIM s

55 relapsed or refractory AML were treated with plerixafor in combination with mitoxantrone, etoposide,

56 and clinical efficacy of long-term, low-dose plerixafor in WHIM syndrome and support its continued st

57 These preclinical data show plerixafor, in contrast with G-CSF, does not alter the p

58 Plerixafor increased absolute lymphocyte, monocyte, and

59 nto the blood, but the mechanisms underlying plerixafor-induced neutrophilia remain poorly defined.

60 Plerixafor inhibits binding of CXCR4 to its ligand CXCL1

61 Plerixafor is a promising therapy for this condition.

62 We conclude that plerixafor is ineffective in reducing leukemia burden in

63 of combining tyrosine kinase inhibitors with plerixafor may be observed in a situation of minimal res

64 tion of transplanted T cells, the effects of plerixafor mobilization on T cells have not been well ch

65 Plerixafor mobilized CXCR4(+) cells, but no difference w

66 by BIO5192 or the combination of BIO5192 and plerixafor mobilized long-term repopulating cells, which

67 mpatibility-mismatched donors; recipients of plerixafor mobilized peripheral blood stem cells had a s

68 ed short transduction protocol of G-CSF plus plerixafor-mobilized CD34(+) cells from FA-A patients wi

69 Plerixafor-mobilized CD34(+) cells include more B-, T-,

70 Plerixafor-mobilized cells were enriched for B cells, T

71 Compared with nonmobilized T cells, plerixafor-mobilized T cells had similar phenotype, mixe

72 g, we hypothesized that the CXCR4 antagonist plerixafor (Mozobil [Genyzme Corporation], AMD3100), mig

73 Plerixafor (Mozobil) is a CXCR4 antagonist that rapidly

74 1alpha switch (54% reduction, P < 0.01) with plerixafor (Mozobil, formerly known as AMD3100) increase

75 r protein in comparison to the drug AMD3100 (Plerixafor, Mozobil).

76 ease in which transplant recipients received plerixafor or G-CSF mobilized allograft from MHC-matched

77 ollected from 3 macaques treated with G-CSF, plerixafor, or plerixafor plus G-CSF.

78 te colony-stimulating factor (G-CSF), G-CSF, Plerixafor, or Plerixafor+G-CSF were transduced with the

79 Genes up-regulated in plerixafor plus G-CSF-mobilized CD34(+) cells included m

80 T-cell miR, miR-143-5p, were up-regulated in plerixafor plus G-CSF-mobilized cells.

81 macaques treated with G-CSF, plerixafor, or plerixafor plus G-CSF.

82 Plerixafor represents a potential therapeutic agent for

83 A single subcutaneous (SC) injection of plerixafor results in rapid mobilization of hematopoieti

84 In conclusion, plerixafor results in rapid stem cell mobilization regar

85 man Tsp cells into immune-deficient mice and plerixafor therapy suggested that human Tsp cell mobiliz

86 ut diabetes (n = 10/group) were administered plerixafor to compare CD34(+) HSC mobilization; plerixaf

87 We conclude that the addition of plerixafor to cytotoxic chemotherapy is feasible in AML,

88 g analogue of the stem cell mobilizing agent plerixafor to image CXCR4 in human tumor xenografts pres

89 A total of 54% of plerixafor-treated patients reached target after one aph

90 fety of long-term administration of low-dose plerixafor treatment of patients with warts, hypogammagl

91 The optimal dose of IV plerixafor was determined to be 0.32 mg/kg.

92 rixafor to compare CD34(+) HSC mobilization; plerixafor was equally able to mobilize CD34(+) HSCs in

93 In phase 1, plerixafor was escalated to a maximum of 0.24 mg/kg/d wi

94 The most common adverse events related to plerixafor were gastrointestinal disorders and injection

95 t of the marketed CXCR4 antagonist, AMD3100 (Plerixafor), whereas both compounds exhibited similar po

96 The CXCR4 antagonist plerixafor, which is approved by the US Food and Drug Ad

97 of experiments, we tested the combination of plerixafor with dasatinib in the same as well as an atte

98 d study evaluated the safety and efficacy of plerixafor with granulocyte colony-stimulating factor (G

99 c cell precursor preferentially mobilized by plerixafor with high interferon-alpha producing ability.

100 homing assays, we demonstrate that G-CSF and plerixafor work through distinct mechanisms.

101 CXCL12 axis by the small molecule inhibitor, plerixafor, would disrupt the interaction of leukemic bl