| 包装 | 价格(元) |
| 10mM (in 1mL Ethanol) | 电议 |
| 25mg | 电议 |
| 50mg | 电议 |
| 100mg | 电议 |
Preparation Method | For competitive binding studies of CXCR4, different concentrations of Plerixafor (AMD3100) were incubated with CCRF-CEM cells and 100 pM 125I-SDF-1α in binding buffer for 3 h at 4 C.Competitive binding assays to remove unbound 125I-SDF-1αBLT1 using cold HEPES and NaCl washing were performed on CHO-S cell membranes. |
Reaction Conditions | 10-12M-10-4M Plerixafor (AMD3100) with cells for 3 hours at 4 ℃ |
Applications | Plerixafor (AMD3100) is a specific antagonist of CXCR4, is not cross-reactive with other chemokine receptors, and is not an agonist of CXCR4. |
Cell lines | CXCR4+ U2OS cells |
Preparation Method | Tumour Invasion Assay:CXCR4+ U2OS cells were trypsinized and resuspended with different concentrations of Plerixafor (AMD3100), PAMD, or rPAMD in serum-free medium for 30 min. |
Reaction Conditions | 0.3uM Plerixafor (AMD3100); 30 minutes |
Applications | When Plerixafor (AMD3100) concentration was 0.3uM, Inhibition of cell invasion with AMD3100 was 75%. |
Animal models | C57BL/6 mice with segmental bone defects |
Preparation Method | Mice were injected with PBS, IGF1, SCF, PDGF or VEGF for five consecutive days and on the 5th day, Plerixafor (AMD3100) (5 mg/kg i.p.) was injected in a volume of 100 μl in PBS. |
Dosage form | 5 mg/kg Plerixafor (AMD3100); Intraperitoneal injection |
Applications | An increased number of colony-forming MSC in the peripheral blood after injection of all compounds in a tibia fracture mouse model . However, the number and size of the colonies were highest in IGF1 plus Plerixafor (AMD3100) injected mice compared to PDGF, SCF and VEGF treated groups, in combination with Plerixafor (AMD3100). |
| 产品描述 | Plerixafor(AMD3100) is a small molecule inhibitor of CXCR4 and CXCL12-mediated chemotaxis with IC50 values of 44 nM and 5.7 nM, respectively[1].Using the CCRF CEM T-cell line that constitutively expresses CXCR4 ,Plerixafor (AMD3100) was an antagonist of SDF-1/CXCL12 ligand binding. Plerixafor (AMD3100) inhibits SDF-1 mediated GTP-binding, SDF-1 mediated calcium flux, and SDF-1 stimulated chemotaxis[1]. In U2OS cells, When Plerixafor (AMD3100) concentration was 300nM, Inhibition of cell invasion with AMD3100 was 75%[2].The cell proliferation of U87MG cells exposed to peptide R or Plerixafor (AMD3100) was evaluated.Cells treated with Plerixafor (AMD3100) showed a modest reduction in cell proliferation compared with cells stimulated with CXCL12[6]. An increased number of colony-forming MSC in the peripheral blood after injection of all compounds in a tibia fracture mouse model. However, the number and size of the colonies were highest in IGF1 plus Plerixafor (AMD3100) injected mice compared to PDGF, SCF and VEGF treated groups, in combination with Plerixafor (AMD3100).Treatment with IGF1 and Plerixafor (AMD3100) results in augmented bone growth in a mouse segmental defect model[3]. Plerixafor (AMD3100) (2 mg/kg) administration to UUO mice exacerbates renal interstitial T cell infiltration, resulting in increased production of the pro-inflammatory cytokines IL-6 and IFN-γ and decreased expression of the anti-inflammatory cytokine IL-10[4]. Both perivascular and interstitial fibrosis are significantly reduced by the CXCR4 antagonist, Plerixafor (AMD3100) at 8 weeks[5].Three adults with WHIM syndrome who received Plerixafor (Plerixafor (AMD3100)) 0.01 to 0.02 mg/kg subcutaneously twice daily for 6 months had increasing circulating white blood cells and fewer associated infections[7]. References: |
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