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    Plerixafor 8HCl (AMD3100)
    Plerixafor 8HCl (AMD3100)

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    This product is for research use only, not for human use. We do not sell to patients.
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    InvivoChem Cat #: V1487
    CAS #: 155148-31-5Purity ≥98%

    Description: Plerixafor 8HCl (formerly JM-3100; AMD-3100; SDZ-SID-791; JLK-169; SID-791; JM-2987; MOZOBIL), the hydrochloride salt of Plerixafor, is a specific chemokine receptor CXCR4 antagonist used as an immunostimulant to mobilize hematopoietic stem cells in cancer patients into the bloodstream. In inhibits CXCR4 and CXCL12-mediated chemotaxis with IC50s of 44 nM and 5.7 nM in cell-free assays, respectively.  

    References: J Immunol. 2009 Sep 1;183(5):3204-11; J Invest Dermatol. 2012 Mar;132(3 Pt 1):711-20.

    Related CAS #: 155148-31-5 (HCl)   110078-46-1 (free base)  

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    Molecular Weight (MW)794.47
    CAS No.155148-31-5
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO:<1 mg/mL
    Water: 100 mg/mL (125.9 mM)
    Ethanol: <1 mg/mL
    Solubility (In vivo)Saline: 30 mg/mL  
    SynonymsJM 3100 8HCl; AMD3100; JM 3100; AMD-3100; JM3100; JM-3100; AMD 3100; SDZ-SID-791; JLK-169; SID-791; JM-2987; Plerixafor HCl; MOZOBIL.

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    In Vitro

    In vitro activity: Plerixafor inhibits CXCL12-mediated chemotaxis with a potency lightly better than its affinity for CXCR4. Plerixafor also antagonizes SDF-1/CXCL12 ligand binding with an IC50 of 651 nM. Plerixafor inhibits SDF-1 mediated GTP-binding, SDF-1 mediated calcium flux and SDF-1 stimulated chemotaxis with IC50 of 27 nM, 572 nM and 51 nM, respectively. Plerixafor does not inhibit calcium flux against cells expressing CXCR3, CCR1, CCR2b, CCR4, CCR5 or CCR7 when stimulated with their cognate ligands, nor does Plerixafor inhibit receptor binding of LTB4. Plerixafor does not, on its own, induce a calcium flux in the CCRF–CEM cells, which express multiple GPCRs including CXCR4, CCR4 and CCR7.

    Cell Assay: Plerixafor 8HCl showed to inhibit I-SDF-1 ligand binding to CCRF–CEM T-lymphoblastoid cells which express CXCR4. Plerixafor 8HCl has shown to block CXCR4 activation, SDF-1 mediated calcium flux and SDF-1 mediated chemotaxis with IC50 values of 27.3, 572 and 51 nM, respectively.

    In VivoA single topical application of Plerixafor promotes wound healing in diabetic mice by increasing cytokine production, mobilizing bone marrow EPCs, and enhancing the activity of fibroblasts and monocytes/macrophages, thereby increasing both angiogenesis and vasculogenesis. Cohorts of mice are administered with PBS, IGF1, PDGF, SCF, or VEGF for five consecutive days and Plerixafor on the 5th day. The number and size of the colonies are highest in IGF1 plus Plerixafor injected mice compared to PDGF, SCF and VEGF treated groups, in combination with Plerixafor.
    Animal modelTwelve-week-old C57BL/6 mice with segmental bone defect
    Formulation & DosageDissolved in PBS; 5 mg/kg; i.p. injection

    J Immunol. 2009 Sep 1;183(5):3204-11; J Invest Dermatol. 2012 Mar;132(3 Pt 1):711-20.

    These protocols are for reference only. InvivoChem does not independently validate these methods.


    Plerixafor 8HCl (AMD3100 8HCl)

    Wound-healing in diabetic mice. J Invest Dermatol. 2012 Mar;132(3 Pt 1):711-20.

    Plerixafor 8HCl (AMD3100 8HCl)

    Mobilization of bone marrow–derived cells. J Invest Dermatol. 2012 Mar;132(3 Pt 1):711-20.

    Plerixafor 8HCl (AMD3100 8HCl)

    Activity and mRNA expression in 3T3 fibroblasts after treatment with AMD3100. J Invest Dermatol. 2012 Mar;132(3 Pt 1):711-20.


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