Plerixafor (AMD3100)

For research use only.

Catalog No.S8030 Synonyms: JM 3100

48 publications

Plerixafor (AMD3100) Chemical Structure

CAS No. 110078-46-1

Plerixafor (AMD3100, JM 3100) is a chemokine receptor antagonist for CXCR4 and CXCL12-mediated chemotaxis with IC50 of 44 nM and 5.7 nM in cell-free assays, respectively. Plerixafor inhibits human immunodeficiency virus (HIV) replication.

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Selleck's Plerixafor (AMD3100) has been cited by 48 publications

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Biological Activity

Description Plerixafor (AMD3100, JM 3100) is a chemokine receptor antagonist for CXCR4 and CXCL12-mediated chemotaxis with IC50 of 44 nM and 5.7 nM in cell-free assays, respectively. Plerixafor inhibits human immunodeficiency virus (HIV) replication.
CXCL12 [1]
(Cell-free assay)
CXCR4 [1]
(Cell-free assay)
5.7 nM 44 nM
In vitro

Plerixafor inhibits CXCL12-mediated chemotaxis with a potency lightly better than its affinity for CXCR4. [1] 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. [2]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
CHOK1 cells M3rsWGZ2dmO2aX;uJIF{e2G7 Mn;vSIl{eGyjY3Xt[Y51KG:oIGuxNlVKZVOGRkHhcJBp[SCocn;tJGNZS1J2IHX4dJJme3OnZDDpckBEUE:NMTDj[YxteyxiSVO1NF0xNjhzIH7N MXqxO|cyPTF{OB?=
GHOST CXCR4 cell line M2S1XmZ2dmO2aX;uJIF{e2G7 MVHJcohq[mm2b4L5JINwdmOnboTyZZRqd25ib3[gZ49ueG:3bnSgZYdicW6|dDDITXYuOSCOQVmgd5Rz[WmwIHnuJGdJV1OWIFPYR3I1KGOnbHygcIlv\SxiSVO1NF0xNjl3IH7N M2\CT|E1Pjl6MUi5
HEK293 cells M4f0OmZ2dmO2aX;uJIF{e2G7 NXrTXlJJOiCmYYnz M2r4W2FvfGm4aYLhcEBi[3Srdnn0fUBi\2GrboP0JHQzOC2{ZYPpd5RidnRiSFnWNUBPVDRvMzDpcoZm[3SnZDDpckBJTUt{OUOgZ4VtdHNiYYPz[ZN{\WRiYYOgbY5pcWKrdHnvckBw\iC4aYLhcEBz\XCuaXPheIlwdiCjZoTldkAzKGSjeYOsJGlEPTB;Mj6zJI5O NGLRbo0yQTR3MUOwOS=>
PBMC cells MXrGeY5kfGmxbjDhd5NigQ>? NIWyWldG\m[nY4TpeoUh[2:wY3XueJJifGmxbjDv[kBkd22yb4Xu[EBi\2GrboP0JGhKXi1zIEi5MlYhe3S{YXnuJIlvKFCETVOgZ4VtdHNuIFXDOVA:Oy56IH7N NUKyUWdxOTR4OUixPFk>
human MT4 cells MoTrSpVv[3Srb36gZZN{[Xl? NWjvb4dXPCCmYYnz NIfYOYpCdnSrdnnyZYwh[WO2aY\peJkh[WejaX7zeEBJUVZzIEPCJIlv\mWldHXkJIlvKGi3bXHuJG1VPCClZXzsd{Bie3Onc4Pl[EBieyCrbnjpZol1cW:wIH;mJJZqenW|IILldIxq[2G2aX;uJIFnfGW{IESg[IF6eyCkeTDNWHQh[XO|YYmsJGVEPTB;NDDuUS=> M1TGSFIxODR|NkO4
human Jurkat cells NV7rWJZPTnWwY4Tpc44h[XO|YYm= NUTjem95SW62YXfvcol{fCCjY4Tpeol1gSCjdDDDXGNTPCCrbjDoeY1idiCMdYLrZZQh[2WubIOgZZN{\XO|ZXSgZZMhcW6qaXLpeIlwdiCxZjDTSGYyNWmwZIXj[YQh[2WubDDtbYdz[XSrb36sJGlEPTB;MkeuOEBvVQ>? M{f3UFE6OTh6MEex
MT-4 cells NH;FeZlHfW6ldHnvckBie3OjeR?= MmmwSYZn\WO2aY\lJINwdmOnboTyZZRqd25ib3[gZ49ueG:3bnSgZYdicW6|dDDITXYuOSCLSVnCJJN1emGrbjDpckBOXC12IHPlcIx{NCCHQ{WwQVY2KG6P NGfaSnIyPDZ7OEG4PS=>
rat IR983F cells MWrGeY5kfGmxbjDhd5NigQ>? NGK1SolFcXOybHHj[Y1mdnRib3[gX|EzPUmfQ2jDUFEzKG[{b32gR3hEWjRiaX6gdoF1KEmUOUizSkBk\WyuczygTWM2OD1zMEigcm0> M1PLd|E6ODV|N{[4
CEM-SS cells NFHYNoVHfW6ldHnvckBie3OjeR?= MnHhSYZn\WO2aY\lJINwdmOnboTyZZRqd25ib3[gZ49ueG:3bnSgZYdicW6|dDDITXYuOSCOQVmgd5Rz[WmwIHnuJGNGVS2VUzDj[YxteyxiRVO1NF0yOjdibl2= NVH4NJl2OTR4OUixPFk>
human HL60 cells NH\1TVdHfW6ldHnvckBie3OjeR?= M1zUNmRqe3CuYXPlcYVvfCCxZjDbNVI2UV2VRF[xZYxxcGFiZoLvcUBEYEOUNDDpckBpfW2jbjDIUFYxKGOnbHzzMEBKSzVyPUG1MlIh|ryP NVzqR2dzOTlzOEiwO|E>
human MT2 cells M{LMN2Z2dmO2aX;uJIF{e2G7 NGTmZ|EyKHWpL33M NYLDPZQ5PCCmYYnz MojCRY51cX[rcnHsJIFkfGm4aYT5JIFo[Wmwc4SgTGlXOSB|QjDpcoZm[3SnZDDpckBpfW2jbjDNWFIh[2WubIOgZZN{\XO|ZXSgZZMhcW6qaXLpeIlwdiCxZjD2bZJidCCyMkSgZY51cWenbjDwdo9lfWO2aX;uJIF1KDFidXevcWwh[W[2ZYKgOEBl[Xm|IHL5JGVNUVOD Mlr4NlEyPjh|M{[=
human U87 cells NFzrRXVHfW6ldHnvckBie3OjeR?= NV7sVXBmOTByMDDuUS=> NHTnOWhCdnSjZ3;ubZN1KGGldHn2bZR6KGG2IFPYR3I1KGmwIHj1cYFvKFV6NzDj[YxteyCjc4Pld5Nm\CCjczDpcohq[mm2aX;uJI9nKFOGRkGtbY5lfWOnZDDtc4R2dGG2aX;uJI9nKGODTWCgdJJw\HWldHnvckBifCBzMECwJI5OKGK7IGTSMWZTTVRiYYPzZZk> MXyxO|k2QDN2NB?=

... Click to View More Cell Line Experimental Data

Methods Test Index PMID

PubMed: 28521261     

Representative immunofluorescence images of competition-binding affinity assay of three selected compounds compared to AMD3100. CXCR4 receptors on the cell surface are shown in red fluorescent color in this binding affinity assay using biotinylated TN14003 that binds to CXCR4. When our test compounds are preincubated with the cells and block the binding of biotinylated TN14003, the red fluorescent color gets reduced. The effective concentration (EC) of AMD3100 was 1000 nM, while compounds Ie, IIj and Iq showed much better EC of only 1, 1 and 10 nM, respectively.


PubMed: 31186083     

Confocal microscopy analysis of CXCR4 and BA2 in Jurkat cells pretreated with vehicle, AMD3100, or X4-2-6 and stimulated with CXCL12, as indicated. Arrows indicate CXCR4 (red), BA2 (green), or colocalization (orange). Images are representative of three independent experiments. Scale bars, 10 μM. DAPI, 4′,6-diamidino-2-phenylindole, dihydrochloride.

28521261 31186083
In vivo A 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. [3] 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. [4]


Animal Research:[4]
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  • Animal Models: Twelve-week-old C57BL/6 mice with segmental bone defect
  • Dosages: 5 mg/kg
  • Administration: Administered via i.p.
    (Only for Reference)

Solubility (25°C)

In vitro Water 3 mg/mL warmed (5.96 mM)
DMSO Insoluble
Ethanol '''100 mg/mL

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 502.78


CAS No. 110078-46-1
Storage powder
in solvent
Synonyms JM 3100

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Clinical Trial Information

NCT Number Recruitment interventions Conditions Sponsor/Collaborators Start Date Phases
NCT03653247 Recruiting Biological: Plerixafor|Drug: Busulfan|Genetic: BIVV003 Sickle Cell Disease Bioverativ a Sanofi company|Sanofi June 28 2019 Phase 1|Phase 2
NCT03547830 Recruiting Drug: Plerixafor|Drug: Gcsf Chronic Granulomatous Disease Federal Research Institute of Pediatric Hematology Oncology and Immunology April 13 2019 Phase 2
NCT03442673 Recruiting Drug: Vinorelbine|Drug: Gemcitabine|Drug: G-CSF Multiple Myeloma University Hospital Inselspital Berne September 17 2018 Phase 2
NCT02989701 Completed Drug: Plerixafor Sickle Cell Disease Without Crisis Alessandra Biffi|Boston Children''s Hospital January 2017 Phase 1

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Frequently Asked Questions

  • Question 1:

    How about the half-life of the product (Cat S8030)?

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CXCR Signaling Pathway Map

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID