ライフサイエンスコーパス: plerixafor

1 f the FDA-approved CXCR4 antagonist AMD3100 (plerixafor).

2 han the clinically approved CXCR4 antagonist plerixafor.

3 (G-CSF) and the additional administration of Plerixafor.

4 ssion and has to be considered in the use of Plerixafor.

5 vercome by targeting CXCR4 with FDA-approved plerixafor.

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

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

8 ization do not occur after mobilization with plerixafor.

9 induced CML-like disease with imatinib plus plerixafor.

10 t recovery was observed with the addition of plerixafor.

11 ith 5 normal subjects similarly treated with plerixafor.

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

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

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

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

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

17 Plerixafor, a CXCR4 antagonist, decreased fibrocyte migr

18 not receive G-CSF were treated with low-dose plerixafor, a CXCR4 antagonist, for 19 to 52 months.

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

20 Plerixafor, a hematopoietic stem cell mobilization agent

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

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

23 Plerixafor (AMD3100) and granulocyte colony-stimulating

24 f C-X-C chemokine receptor type 4 (CXCR4) by plerixafor (AMD3100) can decrease regulatory T (T(reg))-

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

26 can be reversed by post-injury injections of Plerixafor (AMD3100), a small molecule inhibitor of CXCR

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

28 utic benefit of CXCR4 antagonists, only one, plerixafor (AMD3100), which blocks the ligand-binding si

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

30 M who each received 12 months treatment with plerixafor and 12 months treatment with granulocyte CSF

31 therapy; and groups B (n = 4) and C (n = 4), plerixafor and bortezomib combinations.

32 udy revealed anticipated effects of combined plerixafor and bortezomib on BMPCs, an acceptable safety

33 BM aspirates varied depending on the dose of plerixafor and bortezomib.

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

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

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

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

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

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

40 12 hours, animals were randomized to receive plerixafor and granulocyte colony-stimulating factor (G-

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

42 Transient rash occurred on plerixafor, and bone pain was more common on G-CSF.

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

44 were also desensitized with daratumumab and plerixafor (anti-CXCR4).

45 Plerixafor application was performed either continuously

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

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

48 The application of plerixafor attenuates chronic rejection in aortic allogr

49 Instead, plerixafor augments the frequency of circulating neutrop

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

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

52 c effects of rapamycin (mTOR inhibition) and plerixafor (CXCR4 antagonist) for T(reg) cell induction.

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

54 4 signaling pharmacologically and found that plerixafor decreases fibrosis, alleviates solid stress,

55 Noteworthy, this was accompanied by a plerixafor-dependent plasmacytoid dendritic cells-(pDCs)

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

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

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

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

60 cyte colony-stimulating factor and 1 dose of plerixafor, followed by the collection of mobilized cell

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

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

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

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

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

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

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

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

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

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

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

72 Plerixafor has been shown to be a potentially useful tre

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

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

75 of a subset of large wart areas occurred on plerixafor in 5 of 7 patients with major wart burdens at

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

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

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

79 on of the specific CXCR4 antagonist AMD3100 (plerixafor) in mice rapidly and transiently corrected T

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

81 Plerixafor increased absolute lymphocyte, monocyte, and

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

83 ion of the small-molecule inhibitor AMD3100 (plerixafor) induces an integrated immune response that i

84 Plerixafor inhibits binding of CXCR4 to its ligand CXCL1

85 Plerixafor is a promising therapy for this condition.

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

87 Injection of repeated low-dose plerixafor is the most effective application form in the

88 The CXCR4 inhibitor, plerixafor, is a more rapid mobilizer, yet not potent en

89 ether mobilization of bone marrow cells with Plerixafor led to a breakdown of the outer blood-retina

90 Even though Plerixafor liberates HSPCs and mature immune cells from

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

92 hermore, in vivo pDC-depletion abrogated the plerixafor-mediated T(reg) cell number increase and redu

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

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

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

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

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

98 cy, and toxicology of HBB gene correction in plerixafor-mobilized CD34(+) cells from healthy and SCD

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

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

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

102 The CXCR4 antagonist plerixafor mobilizes leukocytes to the blood; however, i

103 ere enrolled into 3 groups: group A (n = 4), plerixafor monotherapy; and groups B (n = 4) and C (n =

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

105 Plerixafor (Mozobil) is a CXCR4 antagonist that rapidly

106 1alpha switch (54% reduction, P < 0.01) with plerixafor (Mozobil, formerly known as AMD3100) increase

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

108 examine the effects of the CXCR4 antagonist, plerixafor, on PC BM residence; its safety profile (alon

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

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

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

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

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

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

115 Plerixafor represents a potential therapeutic agent for

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

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

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

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

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

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

122 m cells were found in the bone marrow of all plerixafor-treated mice.

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

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

125 l and PC levels increased in the blood after plerixafor treatment.

126 tive immunotherapeutic target in addition to plerixafor treatment.

127 for D-RVd and 9.4 x 106/kg for RVd, although plerixafor use was more common with D-RVd.

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

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

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

131 In exploratory endpoints, plerixafor was noninferior to G-CSF for maintaining neut

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

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

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

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

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

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

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

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