ライフサイエンスコーパス: AMD3100

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

2 its with preinjection of the CXCR4 inhibitor 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 is observed when BOP is co-administered with AMD3100.

16 etreated with the specific CXCR4 antagonist, 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 a32/Delta32 CCR5 PBMCs with CXCR4 blocked by AMD3100.

21 lization in response to the CXCR4 antagonist 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 ated by administration of a CXCR4 antagonist AMD3100.

26 inhibited by the CXCR4-specific antagonist, AMD3100.

27 of granulocyte colony-stimulating factor and AMD3100.

28 LIA1/2 and the chemokine receptor inhibitor AMD3100.

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

30 be blocked by the CXCR4-selective antagonist AMD3100.

31 s) in comparison with the prototype compound AMD3100.

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

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

34 (4.6% +/- 1.1%) than in control animals (no AMD3100; 1.0% +/- 0.24%, P < .001).

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

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

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

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

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

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

41 AMD3100, a bicyclam antagonist of the chemokine receptor

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

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

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

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

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

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

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

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

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

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

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

53 AMD3100, a selective antagonist of CXCL12 that binds to

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

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

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

57 1 (HIV-1) strains for their sensitivities to AMD3100, a small-molecule CXCR4 antagonist that blocks H

58 3-T8 isolate was prevented by treatment with AMD3100, a specific antagonist for CXCR4, indicating CXC

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

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

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

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

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

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

65 AMD3100 administration failed to mobilize BM PCs in mice

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

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

68 gnancies received allografts collected after AMD3100 alone.

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

70 AMD3100 also mobilized murine long-term repopulating (LT

71 AMD3100 also promoted macrophage proliferation and phago

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

109 AMD3100 caused a rapid and statistically significant inc

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

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

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

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

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

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

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

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

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

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

120 AMD3100 did not show efficacy when administered 14 days

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

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

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

124 AMD3100 enhanced sensitivity of MM cell to multiple ther

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

142 AMD3100 induced rapid mobilization of mouse and human HP

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

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

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

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

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

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

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

150 The AMD3100-inhibitable fraction of adhesion reflected CXCR4

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

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

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

154 AMD3100 is a bicyclam molecule that selectively and reve

155 AMD3100 is a CXCR4 antagonist that induces rapid mobiliz

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

171 >/=20 weeks) induced impairment of G-CSF- or AMD3100-mobilization (P < 0.01, n = 8).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

199 -9/-2 inhibitor SB-3CT, the CXCR4 antagonist AMD3100, or a combination of both drugs.

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

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

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

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

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

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

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

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

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

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

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

211 AMD3100 prevents monoclonal antibody 12G5 from binding t

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

213 AMD3100 prolongs BM progenitor mobilization and improves

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

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

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

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

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

219 This AMD3100-resistant replication was also sensitive to vMIP

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

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

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

223 AMD3100 safely and rapidly mobilizes stem cells in patie

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

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

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

227 Mechanistically, AMD3100 significantly inhibited Akt phosphorylation and

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

256 AMD3100 upregulated BM levels of endothelial nitric oxid

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

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

259 AMD3100 was recently FDA-approved for stem cell mobiliza

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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