Plerixafor (AMD3100)

Catalog No.S8030 Synonyms: JM 3100

Plerixafor (AMD3100) Chemical Structure

Molecular Weight(MW): 502.78

Plerixafor (AMD3100) 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.

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4 Customer Reviews

  • BLI of NSG mice engrafted with BV173, treated with no therapy (control), plerixafor: 1 mg/kg IP daily, ESKM 100 ug twice weekly, and a combination of ESKM and plerixafor. (A) Logarithmic plot of BLI of leukemia growth measured weekly. Error bars are 5-95% confidence intervals. There was a small but not significant difference between ESKM and combination treated group. (B) End of therapy (day 34) BLI.

    Blood 2014 123(21), 3296-304. Plerixafor (AMD3100) purchased from Selleck.

    Chemotaxis (Transwell invasion) assay showing the migration of BMSCs in response to CXCL12 (0–100 ng/ml) and the inhibitory effect of the CXCR4 antagonist AMD3100 (5 mg/ml, 30 min). *P < 0.05, compared with the control group (no treatment); #P < 0.05; n = 4 wells from separate cultures.

    J Clin Invest, 2015, 125(8): 3226-40. Plerixafor (AMD3100) purchased from Selleck.

  • a, ECs were seeded onto collagen gels containing CXCL12 and incubated with vehicle (DMSO) control or AMD3100 (1 μM), rapamycin (100 nM), or PP242 (600 nM) for 24 h after before fixing and imaging. Scale bar = 150 μm. b, The average number of invading cells was calculated by counting five wells per condition.

    Angiogenesis, 2016, 19(3):359-71. Plerixafor (AMD3100) purchased from Selleck.

    (A) Pictures display representative results of the change of invading cells after incubation of human FTC cell line TT2609-C02 with different concentrations of CXCR4 antagonists AMD3100 and WZ811 as well as rh-SDF1α as receptor agonist. Cells were visualized by DAPI staining. (B) Invading cells were counted in five visual fields of at least three different membranes. Differences after treatment are illustrated as fold change to control.

    J Cancer, 2018, 9(6):929-940. Plerixafor (AMD3100) purchased from Selleck.

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Choose Selective CXCR Inhibitors

Biological Activity

Description Plerixafor (AMD3100) 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.
Targets
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 NILvOHdHfW6ldHnvckBie3OjeR?= NGrqSHBFcXOybHHj[Y1mdnRib3[gX|EzPUmfU1TGNYFteGijIH\yc40hS1iFUkSg[ZhxemW|c3XkJIlvKEOKT1uxJINmdGy|LDDJR|UxRTBwOEGgcm0> MXexO|cyPTF{OB?=
GHOST CXCR4 cell line NEnTRnlHfW6ldHnvckBie3OjeR?= MWfJcohq[mm2b4L5JINwdmOnboTyZZRqd25ib3[gZ49ueG:3bnSgZYdicW6|dDDITXYuOSCOQVmgd5Rz[WmwIHnuJGdJV1OWIFPYR3I1KGOnbHygcIlv\SxiSVO1NF0xNjl3IH7N NH;RcmYyPDZ7OEG4PS=>
HEK293 cells NEP0XpFHfW6ldHnvckBie3OjeR?= M3nLN|Ih\GG7cx?= NV:5ZVdVSW62aY\pdoFtKGGldHn2bZR6KGGpYXnud5QhXDJyLYLld4l{fGGwdDDITXYyKE6OND2zJIlv\mWldHXkJIlvKEiHS{K5N{Bk\WyuczDhd5Nme3OnZDDhd{BqdmirYnn0bY9vKG:oII\pdoFtKHKncHzpZ4F1cW:wIHHmeIVzKDJiZHH5d{whUUN3ME2yMlMhdk1? MkjINVk1PTF|MEW=
PBMC cells Ml25SpVv[3Srb36gZZN{[Xl? NIm3XVFG\m[nY4TpeoUh[2:wY3XueJJifGmxbjDv[kBkd22yb4Xu[EBi\2GrboP0JGhKXi1zIEi5MlYhe3S{YXnuJIlvKFCETVOgZ4VtdHNuIFXDOVA:Oy56IH7N MYqxOFY6QDF6OR?=
human MT4 cells MUfGeY5kfGmxbjDhd5NigQ>? MoPxOEBl[Xm| NGGxVXNCdnSrdnnyZYwh[WO2aY\peJkh[WejaX7zeEBJUVZzIEPCJIlv\mWldHXkJIlvKGi3bXHuJG1VPCClZXzsd{Bie3Onc4Pl[EBieyCrbnjpZol1cW:wIH;mJJZqenW|IILldIxq[2G2aX;uJIFnfGW{IESg[IF6eyCkeTDNWHQh[XO|YYmsJGVEPTB;NDDuUS=> M3fEclIxODR|NkO4
human Jurkat cells MXnGeY5kfGmxbjDhd5NigQ>? NUP6NlJKSW62YXfvcol{fCCjY4Tpeol1gSCjdDDDXGNTPCCrbjDoeY1idiCMdYLrZZQh[2WubIOgZZN{\XO|ZXSgZZMhcW6qaXLpeIlwdiCxZjDTSGYyNWmwZIXj[YQh[2WubDDtbYdz[XSrb36sJGlEPTB;MkeuOEBvVQ>? Moi5NVkyQDhyN{G=
MT-4 cells NXPGS5JTTnWwY4Tpc44h[XO|YYm= M2fYemVn\mWldHn2[UBkd26lZX70doF1cW:wIH;mJINwdXCxdX7kJIFo[Wmwc4SgTGlXNTFiSVnJRkB{fHKjaX6gbY4hVVRvNDDj[YxteyxiRVO1NF03PSCwTR?= MUGxOFY6QDF6OR?=
rat IR983F cells NWjQUoZITnWwY4Tpc44h[XO|YYm= Ml;GSIl{eGyjY3Xt[Y51KG:oIGuxNlVKZUO[Q1yxNkBnem:vIFPYR3I1KGmwIILheEBKWjl6M1[gZ4VtdHNuIFnDOVA:OTB6IH7N NFfCbm4yQTB3M{e2PC=>
CEM-SS cells MYLGeY5kfGmxbjDhd5NigQ>? NVvxU4d5TW[oZXP0bZZmKGOxbnPlcpRz[XSrb36gc4Yh[2:vcH;1coQh[WejaX7zeEBJUVZvMTDMRWkhe3S{YXnuJIlvKEOHTT3TV{Bk\WyuczygSWM2OD1zMkegcm0> NITGNXMyPDZ7OEG4PS=>
human HL60 cells M2L5Z2Z2dmO2aX;uJIF{e2G7 M3i0eWRqe3CuYXPlcYVvfCCxZjDbNVI2UV2VRF[xZYxxcGFiZoLvcUBEYEOUNDDpckBpfW2jbjDIUFYxKGOnbHzzMEBKSzVyPUG1MlIh|ryP MYixPVE5QDB5MR?=
human MOLT4 cells NYXnUI5DTnWwY4Tpc44h[XO|YYm= NEPmZVgyODByIH7N M1TBS2lvcGmkaYTpc44hd2ZiTXHiJFEzTzViYnnu[Ilv\yC2bzDDXGNTPCCneIDy[ZN{\WRiaX6gbJVu[W5iTV;MWFQh[2WubIOgZZQhOTByMDDuUUBjgSCIQVPTJIFv[Wy7c3nz Mo\wNVk1PTF|MEW=
human MT2 cells MXXGeY5kfGmxbjDhd5NigQ>? MYexJJVoN22O NXvLSppLPCCmYYnz M4jpZ2FvfGm4aYLhcEBi[3Srdnn0fUBi\2GrboP0JGhKXjFiM1KgbY5n\WO2ZXSgbY4hcHWvYX6gUXQzKGOnbHzzJIF{e2W|c3XkJIF{KGmwaHnibZRqd25ib3[geolz[WxicEK0JIFvfGmpZX6gdJJw\HWldHnvckBifCBzIIXnM41NKGGodHXyJFQh\GG7czDifUBGVEmVQR?= MUmyNVE3QDN|Nh?=
human U87 cells MUnGeY5kfGmxbjDhd5NigQ>? MkTNNVAxOCCwTR?= MnX6RY51[WexbnnzeEBi[3Srdnn0fUBifCCFWFPSOEBqdiCqdX3hckBWQDdiY3XscJMh[XO|ZYPz[YQh[XNiaX7obYJqfGmxbjDv[kBUTEZzLXnu[JVk\WRibX;keYxifGmxbjDv[kBkSU2SIIDyc4R2[3Srb36gZZQhOTByMDDuUUBjgSCWUj3GVmVVKGG|c3H5 NUfpdFd3OTd7NUizOFQ>

... Click to View More Cell Line Experimental Data

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]

Protocol

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

Solubility (25°C)

In vitro Ethanol 100 mg/mL (198.89 mM)
Water 3 mg/mL warmed (5.96 mM)
DMSO Insoluble
In vivo Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
30% propylene glycol, 5% Tween 80, 65% D5W
For best results, use promptly after mixing.
30 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
Formula

C28H54N8

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

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Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT03653247 Not yet recruiting Sickle Cell Disease Bioverativ - a sanofi company|Bioverativ Therapeutics Inc. December 2018 Phase 1|Phase 2
NCT03664830 Recruiting Sickle Cell Disease City of Hope Medical Center September 19 2018 Phase 1
NCT03506802 Recruiting HLA-A*0201 Positive Cells Present|NY-ESO-1 Positive Tumor Cells Present|Recurrent Plasma Cell Myeloma|Refractory Plasma Cell Myeloma Jonsson Comprehensive Cancer Center|National Cancer Institute (NCI) July 10 2018 Phase 1
NCT03547830 Recruiting Chronic Granulomatous Disease Federal Research Institute of Pediatric Hematology Oncology and Immunology May 29 2018 Phase 2
NCT03182426 Recruiting Diabetes Mellitus Type 1 University of Alberta|Alberta Innovates Health Solutions August 15 2017 Phase 1|Phase 2
NCT03240861 Recruiting HLA-A*0201 Positive Cells Present|Locally Advanced Malignant Neoplasm|NY-ESO-1 Positive|Unresectable Malignant Neoplasm Jonsson Comprehensive Cancer Center|California Institute for Regenerative Medicine|National Cancer Institute (NCI) July 26 2017 Phase 1

Tech Support

Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

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Frequently Asked Questions

  • Question 1:

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

  • Answer:

    The biological half-life for this drug is 3-5 hours: https://en.wikipedia.org/wiki/Plerixafor.

CXCR Signaling Pathway Map

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID