ライフサイエンスコーパス: AMD3100

1 II, with or without CXC receptor 4 blockade (AMD3100).

2 s) in comparison with the prototype compound AMD3100.

3 s prevented by the CXCR4-specific antagonist AMD3100.

4 erminus (NT) and was completely resistant to AMD3100.

5 after pharmacologic inhibition of CXCR4 with AMD3100.

6 t highly susceptible to the CXCR4 antagonist AMD3100.

7 t for transplantation after just one dose of AMD3100.

8 using CXCR4 knockdown or the CXCR4 inhibitor AMD3100.

9 134(-)), with or without the CXCR4 inhibitor AMD3100.

10 increasing resistance to the CXCR4 inhibitor AMD3100.

11 -1 cells treated with SDF-1 and sensitive to AMD3100.

12 DF-1alpha administration also was blocked by AMD3100.

13 as blocked by the CXCR4 selective antagonist AMD3100.

14 c Envs more sensitive to the CXCR4 inhibitor AMD3100.

15 etreated with the specific CXCR4 antagonist, AMD3100.

16 its with preinjection of the CXCR4 inhibitor AMD3100.

17 2 agonist, GRObeta, and the CXCR4 antagonist AMD3100.

18 cells was often enhanced in the presence of AMD3100.

19 hydrophobic core are critical to binding of AMD3100.

20 ated by administration of a CXCR4 antagonist AMD3100.

21 a32/Delta32 CCR5 PBMCs with CXCR4 blocked by AMD3100.

22 that may induce toxicities, as observed for AMD3100.

23 that are insensitive to the CXCR4 antagonist AMD3100.

24 the presence of the CXCR4-specific inhibitor AMD3100.

25 be blocked by the CXCR4-selective antagonist AMD3100.

26 is observed when BOP is co-administered with AMD3100.

27 lization in response to the CXCR4 antagonist AMD3100.

28 inhibited by the CXCR4-specific antagonist, AMD3100.

29 of granulocyte colony-stimulating factor and AMD3100.

30 LIA1/2 and the chemokine receptor inhibitor AMD3100.

31 rapeutic agent, the small-molecule modulator AMD3100.

32 ted by application of the CXCR4-binding drug AMD3100.

33 effect was prevented by the CXCR4 antagonist AMD3100 (1 muM) and was absent in EGFP-negative stratum

34 Bis-tetraazamacrocycles such as the bicyclam AMD3100 (1) are a class of potent and selective anti-HIV

35 (4.6% +/- 1.1%) than in control animals (no AMD3100; 1.0% +/- 0.24%, P < .001).

36 eated with single subcutaneous injections of AMD3100 (5 mg/kg) or saline after ischemia/reperfusion i

37 antly more complete in AMD3100-treated mice (AMD3100: 87.0 +/- 2.6%, saline: 33.1 +/- 1.8%; P<0.0001)

38 we determined that, after mobilization with AMD3100 (a CXCR4 antagonist), HSCs exited from marrow, t

39 uates the safety and efficacy of plerixafor (AMD3100), a CXCR4 antagonist, in mobilizing hematopoieti

40 sed by post-injury injections of Plerixafor (AMD3100), a small molecule inhibitor of CXCR4.

41 ation (3-fold) was observed when plerixafor (AMD3100), a small molecule inhibitor of the CXCR-4/SDF-1

42 mokine receptor type 4 (CXCR4) antagonist 1 (AMD3100), a template with the general structure 2 was de

43 AMD3100, a bicyclam antagonist of the chemokine receptor

44 AMD3100, a competitive inhibitor of C-X-C motif chemokin

45 Administering AMD3100, a CXCL12 receptor chemokine (C-X-C motif) recep

46 ood mononuclear cells (PBMCs) mobilized with AMD3100, a CXCR4 antagonist, combined with granulocyte c

47 Treatment with AMD3100, a CXCR4 antagonist, showed the immobilization o

48 In all cases, cell death was blocked by AMD3100, a CXCR4 entry inhibitor, but not by raltegravir

49 Short-term administration of AMD3100, a CXCR4 inhibitor that mobilizes neutrophils wi

50 AMD3100, a CXCR4 inhibitor, and firategrast, an alpha4be

51 AMD3100, a CXCR4 inhibitor, PKI 166, an epidermal growth

52 tection from apoptosis, which was blocked by AMD3100, a CXCR4 inhibitor.

53 ckade of CXCR4-tropic HIV virion fusion with AMD3100, a CXCR4-specific entry inhibitor, increased vir

54 cyte colony-stimulating factor (G-CSF) using AMD3100, a direct antagonist of CXCR4/stromal-derived fa

55 We found that AMD3100, a highly specific CXCR4 antagonist, directly do

56 In contrast, the bicyclam AMD3100, a nonpeptide CXCR4 ligand that did not down-mod

57 ulocyte colony-stimulating factor (G-CSF) or AMD3100, a novel CXCR4 antagonist, significantly stimula

58 rt the development and evaluation of [(64)Cu]AMD3100, a positron-emitting analogue of the stem cell m

59 AMD3100, a selective antagonist of CXCL12 that binds to

60 arly, treatment of BR5-1-derived tumors with AMD3100, a selective CXCR4 antagonist, resulted in incre

61 ated by the chemokine receptor CXCR4 because AMD3100, a selective CXCR4 inhibitor, blocked both event

62 omplished using the clinically approved drug AMD3100, a small molecule inhibitor of SDF-1/CXCR4 inter

63 1 (HIV-1) strains for their sensitivities to AMD3100, a small-molecule CXCR4 antagonist that blocks H

64 3-T8 isolate was prevented by treatment with AMD3100, a specific antagonist for CXCR4, indicating CXC

65 Finally, both AMD3100, a specific antagonist of CXCL12's G protein-cou

66 autoimmune encephalomyelitis (EAE) by using AMD3100, a specific antagonist of the CXCL12 receptor CX

67 This effect was comparable to AMD3100, a well known progenitor mobilizing agent.

68 ng plasma SDF-1 levels, the CXCR4 antagonist AMD3100 acutely promotes, while chronic AMD3100 treatmen

69 (administered intramyocardially), 5 mg/kg of AMD3100 (administered subcutaneously), or both; cardiac

70 hosphorylated (phospho)-c-kit declined after AMD3100 administration and after CXCR4 deletion.

71 AMD3100 administration failed to mobilize BM PCs in mice

72 sibly inhibits SDF-1alpha/CXCR4 binding, and AMD3100 administration mobilizes CD34(+) cells into the

73 ngraftment potential of PBMCs mobilized with AMD3100 alone, however, has remained unproven.

74 gnancies received allografts collected after AMD3100 alone.

75 Thus, we investigated whether AMD3100 also improves recovery from ischemia/reperfusion

76 AMD3100 also maintained the structural integrity of bloo

77 AMD3100 also mobilized murine long-term repopulating (LT

78 AMD3100 also promoted macrophage proliferation and phago

79 ized that a small molecule CXCR4 antagonist, AMD3100 (AMD), could augment the mobilization of bone ma

80 Antagonism of the CXCR4 pathway with AMD3100 (an SDF1/CXCR4 antagonist) inhibited MSC-induced

81 lation and bone regeneration was reversed by AMD3100, an antagonist of the chemokine receptor CXCR4 t

82 an inhibitor of attachment of gp120 to CD4, AMD3100, an inhibitor of attachment of gp120 to CXCR4, a

83 nduced migration of WT EPCs was inhibited by AMD3100, an inhibitor of CXCR4.

84 AMD3100 and alphaPD-1 significantly inhibited tumor grow

85 The affinity of AMD3100 and ALX40-4C binding to CAMs was less than to wi

86 o selectively displace the CXCR4 antagonists AMD3100 and AMD3465 from the liver.

87 Here, we evaluated the antitumor efficacy of AMD3100 and anti-PD-1 (alphaPD-1) antibody alone or in c

88 rough a previously unidentified link between AMD3100 and BM eNOS expression.

89 [MAb]), coreceptor binding (CXCR4 inhibitor AMD3100 and CCR5 inhibitor TAK-779), or fusion (T-1249),

90 Here, we show that AMD3100 and FK506 mobilization of endogenous stem cells

91 Synergy of AMD3100 and G-CSF in mobilization was due to enhanced nu

92 nds on the heterocomplex and is inhibited by AMD3100 and glycyrrhizin.

93 and peripheral blood stem cells mobilized by AMD3100 and granulocyte colony-stimulating factor in pat

94 hemokine (C-X-C motif) receptor 4 antagonist AMD3100 and granulocyte colony-stimulating factor mobili

95 ident cells), whereas blockade of CXCR4 with AMD3100 and inhibition of alpha4beta1(VLA4) integrin or

96 to injury sites using the combined effect of AMD3100 and low-dose FK-506 (AF) can reduce the adhesion

97 ndogenous stem cell mobilization produced by AMD3100 and low-dose tacrolimus is able to reduce by 25%

98 tivity only when combined with sorafenib and AMD3100 and not when combined with sorafenib alone.

99 However, the combination of AMD3100 and sorafenib did not significantly change cytot

100 , produced by a pharmacologic combination of AMD3100 and tacrolimus, leads to faster and better-quali

101 hypothesized that maternal administration of AMD3100 and/or firategrast prior to IUHCT would mobilize

102 Animals receiving AMD3100 and/or with the genotype CCR2(-/-) failed to dem

103 Plerixafor (AMD3100) and granulocyte colony-stimulating factor (G-CS

104 mobilization by CXCR4 antagonists, including AMD3100, and for the trafficking of HSCs during steady-s

105 ized sequentially with the CXCR4 antagonist, AMD3100, and G-CSF.

106 inhibitable by the CXCR4-specific antagonist AMD3100, and replication was abrogated in a novel CXCR4(

107 Inhibitors (T22, AMD3100, and Sch-C) that block fusion by binding chemoki

108 fibrosis after 3 days of AngII, and AngII + AMD3100 animals showed exacerbated fibrocyte infiltratio

109 stabilizes the oligomeric structure, whereas AMD3100, another well-characterized CXCR4 antagonist, do

110 AMD3100 appears to be a safe and effective agent for the

111 uation is necessary before the random use of AMD3100 as a new entry inhibitor in patients harboring S

112 Studies are underway testing AMD3100 as an adjunct to chemotherapy in patients with r

113 cells were inhibited by the CXCR4 antagonist AMD3100 as well as knockdown of either CXCR4 or CXCR7.

114 When PeP3(b) mice were treated with AMD3100 at 2 hours before the transplantation of 4 x 10(

115 Donors (N = 25) were treated with AMD3100 at a dose of 240 mug/kg by subcutaneous injectio

116 Finally, blockade of CXCL12 with AMD3100 attenuated the exaggerated fibrosis observed in

117 ti-CXCR4 antibodies and the CXCR4 antagonist AMD3100 blocked HIV-1 gp120 binding to CXCR4-PMPLs.

118 e R5X4 and X4 HIV-1 isolates can utilize the AMD3100-bound conformation of CXCR4, with the efficiency

119 ced by HIV-1 NL4-3 is completely reversed by AMD3100, but not SDF-1 alpha, although SDF-1 alpha alone

120 nd CCR5 antibodies or by the CXCR4 inhibitor AMD3100, but not the fusion inhibitor T20.

121 ized by the pharmacological CXCR4 antagonist AMD3100, but the other components of the SDF-1-CXCR4 sig

122 okine receptor type 4 (CXCR4) by plerixafor (AMD3100) can decrease regulatory T (T(reg))-cell intratu

123 AMD3100 caused a rapid and statistically significant inc

124 nduced progenitor-cell mobilization, and Shh-AMD3100 combination therapy for treatment of surgically

125 Searching for mechanisms, we found that AMD3100 combined with low-dose tacrolimus mobilized incr

126 as a 228.8-fold increase of HSC with FL/GCSF/AMD3100 compared with AMD3100 treatment alone.

127 lates that exhibited plateau effects: as the AMD3100 concentration was increased, virus infection and

128 xP3(+) Tregs were efficiently mobilized with AMD3100-containing regimens, with as much as a 4.0-fold

129 Our results indicate that AMD3100 could be a potentially useful therapy for the tr

130 These results suggest that AMD3100 could be used to target the CXCR4-CXCL12 axis to

131 stitution in TFF2(-/-) mice was inhibited by AMD3100 (CXCR4 receptor antagonist).

132 Optimal HSC mobilization was observed when AMD3100 (day 10) was coadministered with Flt3 ligand (FL

133 In the intervention mode, AMD3100 delivery commenced 14 days after laser induction

134 topoietic stem cells mobilized by GRObeta or AMD3100 demonstrate superior engraftment and contributio

135 hibiting CXCR4 signaling with the antagonist AMD3100 did not affect protein homeostasis in atrophying

136 cell mobilization with the CXCR4 antagonist AMD3100 did not alter the donor T cell's ability to indu

137 AMD3100 did not show efficacy when administered 14 days

138 ent receptor of CXCL12, by administration of AMD3100 diminished the protective impact of 4MU in adopt

139 Mice treated with AMD3100 display a partial inhibition of skeletal regrowt

140 In addition, AMD3100 disrupts the interaction between mouse and human

141 AMD3100 enhanced sensitivity of MM cell to multiple ther

142 lls isolated after treatment with G-CSF plus AMD3100 expressed a phenotype that was characteristic of

143 s, and demonstrate the clinical potential of AMD3100 for HSC mobilization.

144 either alone or in combination with G-CSF or AMD3100 for mobilization of hematopoietic stem and proge

145 he use of the SDF-1/CXCL12-CXCR4 antagonist, AMD3100 for mobilization of hematopoietic stem and proge

146 The bicyclam AMD3100 (formula weight 830) blocks HIV-1 entry and memb

147 showed low cardiac toxicity but, contrary to AMD3100, gave maximum nonlethal doses of around 2.0 mg/k

148 s macaque model to determine the impact that AMD3100 has on lymphocyte mobilization, both alone and i

149 ule" imaging agents based on T140, FC131 and AMD3100 have been extensively studied.

150 e agonist, T140, and a weak partial agonist, AMD3100, identified by alanine scanning mutants, were sp

151 emokine (CXC motif) ligand 12) and inhibitor AMD3100 identify CXCR4 as a functional ubiquitin recepto

152 ism of CXC-chemokine receptor 4 (CXCR4) with AMD3100 improves cardiac performance after myocardial in

153 e bone marrow (BM), and the CXCR4 antagonist AMD3100 improves recovery from coronary ligation injury

154 CXCR4 inhibition, using AMD3100 in combination with sorafenib treatment, prevent

155 assessing the safety and clinical effects of AMD3100 in patients with multiple myeloma (MM) and non-H

156 n, which was blocked by pretreated EPCs with AMD3100 in vitro.

157 Moreover, AMD3100 increased mobilization of MM cells to the circul

158 with plerixafor (Mozobil, formerly known as AMD3100) increased circulating diabetic PC numbers (6.8

159 AMD3100 induced rapid mobilization of mouse and human HP

160 te that the S1P(1) agonist SEW2871 increases AMD3100-induced HSC and progenitor cell mobilization.

161 rylation in the aorta, and it prevented VEGF/AMD3100-induced mobilization of Flk-1(+)/Sca-1(+) cells

162 ing of intramyocardial Shh gene transfer and AMD3100-induced progenitor-cell mobilization improves ca

163 eness of Sonic hedgehog (Shh) gene transfer, AMD3100-induced progenitor-cell mobilization, and Shh-AM

164 s of Shh gene therapy could be improved with AMD3100-induced progenitor-cell mobilization.

165 We report that the CXCR4 inhibitor AMD3100 induces disruption of the interaction of MM cell

166 In MIN6 beta-cells, a CXCR4 antagonist (AMD3100) induces apoptosis, increases reactive oxygen sp

167 The AMD3100-inhibitable fraction of adhesion reflected CXCR4

168 Treatment with the CXCR4 antagonist AMD3100 inhibited cyclin D1 expression and maximal tumor

169 The mTOR inhibitor rapamycin, but not AMD3100, inhibited growth of AML tumor xenografts.

170 importantly, Lip-NLCs loaded with IR780 and AMD3100 (IR780-AMD-Lip-NLCs) exhibited enhanced anti-tum

171 AMD3100 is a bicyclam molecule that selectively and reve

172 AMD3100 is a CXCR4 antagonist that induces rapid mobiliz

173 These data show that AMD3100 is a potent and rapid mobilizer of angiogenic ce

174 While no longer under clinical development, AMD3100 is a useful tool with which to probe interaction

175 FL/GCSF/AMD3100 is an efficient treatment to maximally mobilize

176 enhanced mobilization observed using BOP and AMD3100 is recapitulated in a humanized NODSCIDIL2Rgamma

177 Treatment with stem cell factor/AMD3100 led to a greater increase in circulating Flk-1(+

178 sed adhesion of WM cells to stromal cells by AMD3100 led to increased sensitivity of these cells to c

179 f the CXCR4 receptor in normal thymocytes by AMD3100 led to the retention of mature T cells in the th

180 m the infected CD4+ cells in the presence of AMD3100 maintained an unchanged envelope genotype and an

181 We investigated whether AMD3100 may accelerate diabetes-impaired wound healing t

182 tive against GVHD, our results indicate that AMD3100 may mobilize a GVHD-protective T-cell repertoire

183 Direct antagonism of CXCR4 by AMD3100 may provide a more rapid and possibly less toxic

184 In addition, mobilization with AMD3100 may provide a safer preparative approach for HSC

185 Thus SDF-1, but not the smaller molecule AMD3100, may interfere at multiple points with the bindi

186 fundamental differences in the mechanism of AMD3100-mediated and G-CSF-mediated hematopoietic stem c

187 Not all of the AMD3100-mediated effects evolved through CXCR4 antagonis

188 AMD3100-mediated inhibition of CXCL12 function reduced t

189 t plerixafor (Mozobil [Genyzme Corporation], AMD3100), might be an effective treatment.

190 >/=20 weeks) induced impairment of G-CSF- or AMD3100-mobilization (P < 0.01, n = 8).

191 or antagonist, PESLAN-1, increased G-CSF- or AMD3100-mobilization of WBCs and LSKs, compared to the u

192 d in vivo angiogenic potential compared with AMD3100-mobilized CACs.

193 More AMD3100-mobilized CD34(+) cells are in the G(1) phase of

194 Thus, AMD3100-mobilized CD34(+) cells represent an alternative

195 In vivo gene marking levels obtained with AMD3100-mobilized CD34(+) cells were better than those o

196 In this study, AMD3100-mobilized CD34(+) cells were phenotypically anal

197 We show engraftment of transduced AMD3100-mobilized CD34(+) cells with Neo(R) gene marked

198 in increased basal WBCs, decreased basal and AMD3100-mobilized LSK cells, and had no effect on G-CSF.

199 adiation (TBI) before infusion of autologous AMD3100-mobilized PBMCs (median CD34 cell count, 3.9 x 1

200 re given 920 cGy TBI followed by infusion of AMD3100-mobilized PBMCs (median CD34 cell dose, 4.7 x 10

201 We therefore studied AMD3100-mobilized PBMCs in a canine model.

202 In summary, both autologous and allogeneic AMD3100-mobilized PBMCs led to prompt and durable engraf

203 luate the long-term engraftment potential of AMD3100-mobilized PBMCs, 5 dogs were given 920 cGy TBI f

204 Overall, these results indicate that AMD3100 mobilizes a population of hematopoietic stem cel

205 ion; (2) firategrast treatment alone or with AMD3100 mobilizes endogenous HSCs from the FL and result

206 When mice received weekly injections of AMD3100 on 3 consecutive weeks and marrow cells were tra

207 BM eNOS expression abolished the benefit of AMD3100 on sca1(+)/flk1(+) cell mobilization without alt

208 sis of antagonists revealed that exposure to AMD3100 or ALX40-4C induced G protein activation by CXCR

209 or pretreatment with the specific antagonist AMD3100 or an anti-CXCR4 antibody.

210 get cells at 25 degrees C in the presence of AMD3100 or C34, prior to incubation at 37 degrees C, the

211 ne, cotreatment with PS and CXCR4 antagonist AMD3100 or FC-131 synergistically induced apoptosis of c

212 Mice injected with AMD3100 or G-CSF demonstrated transient increased S1P le

213 Compared with baseline, treatment with AMD3100 or G-CSF increased the number of blood CACs 10.0

214 Administration of AMD3100 or G-CSF to mice with deficiencies in either S1P

215 Mobilization induced by G-CSF, AMD3100 or ischemia was evaluated by flow cytometric enu

216 cells, which was again attenuated by either AMD3100 or knockdown of CXCR4 or CXCR7.

217 tin receptor-deficient mice and treated with AMD3100 or saline.

218 e or in combination with a CXCR4 antagonist (AMD3100) or hedgehog inhibitor (GDC-0449) displays reduc

219 -9/-2 inhibitor SB-3CT, the CXCR4 antagonist AMD3100, or a combination of both drugs.

220 intraperitoneal injections of normal saline, AMD3100, or anti-SDF-1 antibody from postnatal day 1 to

221 Using a specific inhibitor of CxCR4, AMD3100, our results indicate that blocking this recepto

222 view is to overview clinical experience with AMD3100 (plerixafor) and its role in stem cell mobilizat

223 ous infusion of the small-molecule inhibitor AMD3100 (plerixafor) induces an integrated immune respon

224 ed to that of the marketed CXCR4 antagonist, AMD3100 (Plerixafor), whereas both compounds exhibited s

225 e receptor protein in comparison to the drug AMD3100 (Plerixafor, Mozobil).

226 ested the hypotheses that the combination of AMD3100 plus granulocyte colony-stimulating factor (G-CS

227 These findings suggest that AMD3100 preserves cardiac function after myocardial infa

228 Compared with control animals, injecting AMD3100-pretreated EPCs resulted in a larger infarct vol

229 CXCR4 inhibition using AMD3100 prevented PW1(+) cells differentiation into SMC

230 eptor (C-X-C receptor type 4 or CXCR4) using AMD3100 prevented the polarization toward an immunosuppr

231 Thus, AMD3100 prevents CXCR4 functioning as both a HIV-1 co-re

232 AMD3100 prevents monoclonal antibody 12G5 from binding t

233 cells in the lung, although neither RNAi nor AMD3100 prolonged overall survival in mice with experime

234 AMD3100 prolongs BM progenitor mobilization and improves

235 conclusion, a single topical application of AMD3100 promoted wound healing in diabetic mice by incre

236 pc3(-/-) mice, the specific CXCR4 antagonist AMD3100 rapidly reversed neutropenia.

237 Overall, specifically blocking CxCR4 using AMD3100 reduced a number of pathological parameters rela

238 Supporting that model, AMD3100 reduces death caused by gp120 or by gp120/sCD4.

239 he R5X4 HIV-1 isolate DH12 was necessary for AMD3100 resistance and could confer this property on two

240 This AMD3100-resistant replication was also sensitive to vMIP

241 ment of leukemic mice with chemotherapy plus AMD3100 resulted in decreased tumor burden and improved

242 Combination treatment with G-CSF and AMD3100 resulted in the earliest and most complete recov

243 AMD3100 reversibly inhibits SDF-1alpha/CXCR4 binding, an

244 AMD3100 safely and rapidly mobilizes stem cells in patie

245 locking experiments with the CXCR4 inhibitor AMD3100 showed that the later D36 1999 isolate could inf

246 Studies using TAK-779 and AMD3100 showed that two highly M-tropic isolates entered

247 otubes, whereas normal myotubes treated with AMD3100 showed time- and dose-dependent reductions in di

248 Mechanistically, AMD3100 significantly inhibited Akt phosphorylation and

249 Treatment of allergic mice with AMD3100 significantly reduced airway hyperreactivity, pe

250 in AA mice, using CXCR4(-/-) splenocytes or AMD3100, significantly reduced BM infiltration of T cell

251 nocytes mobilized into the blood by G-CSF or AMD3100 stimulate angiogenesis at sites of ischemia thro

252 Our results indicate that, unlike G-CSF, AMD3100 substantially mobilizes both B and T lymphocytes

253 CXCR4 with RNAi, or the specific antagonist AMD3100, substantially delayed the growth of 4T1 cells i

254 man PBMC even in the presence of TAK-779 and AMD3100, suggesting that it might use an undefined, alte

255 n the presence of a potent CXCR4 antagonist (AMD3100) suggests that STRL33 can be used as a corecepto

256 AMD3100 synergized with G-CSF to mobilize murine LTR cel

257 aging data, confirmed the ability of [(64)Cu]AMD3100 to image CXCR4 expression.

258 Administration of AMD3100 to leukemic mice induced a 1.6-fold increase in

259 ons of granulocyte-colony-stimulating factor/AMD3100 to mobilize HSPCs from the bone marrow (BM) into

260 ransplantation, demonstrating the ability of AMD3100 to mobilize true long-term repopulating hematopo

261 alpha (SDF-1 alpha), or a CXCR4 antagonist, AMD3100, to CXCR4 inhibits infection of CD4(+) T cells b

262 he soluble inhibitors, soluble CD4 (sCD4) or AMD3100, to delineate the role of CD4 and CXCR4 receptor

263 ll molecule competitive antagonist of CXCR4, AMD3100, to examine the interaction of mouse APL cells w

264 erence between the donor cell engraftment of AMD3100-treated and control recipients.

265 he cytokine profile that was observed in the AMD3100-treated animals.

266 d closure was significantly more complete in AMD3100-treated mice (AMD3100: 87.0 +/- 2.6%, saline: 33

267 eft ventricular function were greater in the AMD3100-treated mice at week 4.

268 sca1(+)/flk1(+) cells endured for 7 days in AMD3100-treated mice compared with just 1 day in the sal

269 infarct area to area at risk were smaller in AMD3100-treated mice than in mice administered saline, a

270 nferring a significant survival advantage to AMD3100-treated mice.

271 ith more rapid revascularization observed in AMD3100-treated mice.

272 se of HSC with FL/GCSF/AMD3100 compared with AMD3100 treatment alone.

273 Furthermore, AMD3100 treatment failed to prevent infection of known C

274 Interestingly, AMD3100 treatment had no inhibitory role in the infectio

275 nist AMD3100 acutely promotes, while chronic AMD3100 treatment inhibits, mobilization of pro-angiogen

276 l factor increased phospho-c-kit levels, and AMD3100 treatment suppressed SDF-1-induced, but not SCF-

277 n administered starting from 5 days post-LI, AMD3100 treatment was ineffective.

278 ) cells into T helper cells was increased by AMD3100 treatment.

279 AMD3100 upregulated BM levels of endothelial nitric oxid

280 On day 7 after treatment, AMD3100 was associated with higher circulating EPC and m

281 In db/db mice, mobilization by G-CSF or AMD3100 was either increased or unaffected (P < 0.05, n

282 The optimal dose of AMD3100 was found to be 5.0 mg/kg.

283 AMD3100 was recently FDA-approved for stem cell mobiliza

284 Following laser treatment, hydrophilic AMD3100 was released from the aqueous liposome chamber a

285 In the prevention mode, a CXCR4 antagonist (AMD3100) was delivered via an osmotic pump 1 day after l

286 most virus strains was completely blocked by AMD3100, we identified several R5X4 and X4 isolates that

287 Once saturating concentrations of AMD3100 were achieved, further inhibition was not observ

288 a function of time of addition of C34 and of AMD3100 were equivalent, indicating that engagement of g

289 l counts observed at 4 and 6 hours following AMD3100 were higher in the 240 microg/kg group (19.3 +/-

290 ) cells, and the cardioprotective effects of AMD3100 were retained in eNOS-knockout mice that had bee

291 When PBMC mobilized by FL/GCSF/AMD3100 were transplanted into recipients conditioned no

292 antagonist TAK-779 and the CXCR4 antagonist AMD3100, were examined for their inhibitory effects on R

293 t at inhibiting it than the CXCR4 antagonist AMD3100, which is more than 100 times weaker at inhibiti

294 + and HCO3 secretion were largely blunted by AMD3100, which selectively blocks the SDF1 receptor CXCR

295 Administration of AMD3100, which specifically blocks binding of SDF-1 to i

296 S, which blocks entry via CCR5 and CCR3, and AMD3100, which targets CXCR4.

297 ctural basis for the interaction of T140 and AMD3100 with CXCR4 confirms that the mechanisms used by

298 h an inhibitor of SDF-1alpha receptor CXCR4 (AMD3100) with LI significantly delayed tumor regrowth.

299 cells, more efficiently than the marketed 1 (AMD3100) with subcutaneous administration at the same do

300 nhibitory activities albeit a lower K(B) for AMD3100, with the 1(R,R) isomer being second in potency.