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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3 Customer Reviews

  • 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.

    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.

  • 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.

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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.
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 MVrGeY5kfGmxbjDhd5NigQ>? MWXEbZNxdGGlZX3lcpQhd2ZiW{GyOWleW0SIMXHsdIhiKG[{b32gR3hEWjRiZYjwdoV{e2WmIHnuJGNJV0tzIHPlcIx{NCCLQ{WwQVAvQDFibl2= M1HvclE4PzF3MUK4
GHOST CXCR4 cell line M1fEXGZ2dmO2aX;uJIF{e2G7 NHv3PI9KdmirYnn0c5J6KGOxbnPlcpRz[XSrb36gc4Yh[2:vcH;1coQh[WejaX7zeEBJUVZvMTDMRWkhe3S{YXnuJIlvKEeKT2PUJGNZS1J2IHPlcIwhdGmwZTygTWM2OD1yLkm1JI5O MWexOFY6QDF6OR?=
HEK293 cells NHfpU5BHfW6ldHnvckBie3OjeR?= NXywdVBHOiCmYYnz MmrVRY51cX[rcnHsJIFkfGm4aYT5JIFo[Wmwc4SgWFIxNXKnc3nzeIFvfCCKSW[xJG5NPC1|IHnu[oVkfGWmIHnuJGhGUzJ7MzDj[YxteyCjc4Pld5Nm\CCjczDpcohq[mm2aX;uJI9nKH[rcnHsJJJmeGyrY3H0bY9vKGGodHXyJFIh\GG7czygTWM2OD1{LkOgcm0> MnizNVk1PTF|MEW=
PBMC cells MWfGeY5kfGmxbjDhd5NigQ>? M2m4cmVn\mWldHn2[UBkd26lZX70doF1cW:wIH;mJINwdXCxdX7kJIFo[Wmwc4SgTGlXNTFiOEmuOkB{fHKjaX6gbY4hWEKPQzDj[YxteyxiRVO1NF0{Njhibl2= MUSxOFY6QDF6OR?=
human MT4 cells NUjUVmVsTnWwY4Tpc44h[XO|YYm= MlPuOEBl[Xm| MXfBcpRqfmm{YXygZYN1cX[rdImgZYdicW6|dDDITXYyKDOEIHnu[oVkfGWmIHnuJIh2dWGwIF3UOEBk\WyuczDhd5Nme3OnZDDhd{BqdmirYnn0bY9vKG:oII\pdpV{KHKncHzpZ4F1cW:wIHHmeIVzKDRiZHH5d{BjgSCPVGSgZZN{[XluIFXDOVA:PCCwTR?= MlTrNlAxPDN4M{i=
human Jurkat cells NICzd5dHfW6ldHnvckBie3OjeR?= MXnBcpRi\2:waYP0JIFkfGm4aYT5JIF1KEO[Q2K0JIlvKGi3bXHuJGp2emujdDDj[YxteyCjc4Pld5Nm\CCjczDpcohq[mm2aX;uJI9nKFOGRkGtbY5lfWOnZDDj[YxtKG2rZ4LheIlwdixiSVO1NF0zPy52IH7N M3zJXlE6OTh6MEex
MT-4 cells M1PZRmZ2dmO2aX;uJIF{e2G7 NUDRU5lWTW[oZXP0bZZmKGOxbnPlcpRz[XSrb36gc4Yh[2:vcH;1coQh[WejaX7zeEBJUVZvMTDJTWlDKHO2cnHpckBqdiCPVD20JINmdGy|LDDFR|UxRTZ3IH7N NWrhcHNKOTR4OUixPFk>
CEM-SS cells MU\GeY5kfGmxbjDhd5NigQ>? NGXteY1G\m[nY4TpeoUh[2:wY3XueJJifGmxbjDv[kBkd22yb4Xu[EBi\2GrboP0JGhKXi1zIFzBTUB{fHKjaX6gbY4hS0WPLWPTJINmdGy|LDDFR|UxRTF{NzDuUS=> M3HNcFE1Pjl6MUi5
human HL60 cells MmfpSpVv[3Srb36gZZN{[Xl? NFjzNJRFcXOybHHj[Y1mdnRib3[gX|EzPUmfU1TGNYFteGijIH\yc40hS1iFUkSgbY4hcHWvYX6gTGw3OCClZXzsd{whUUN3ME2xOU4zKM7:TR?= MmmzNVkyQDhyN{G=
human MOLT4 cells M3;aTWZ2dmO2aX;uJIF{e2G7 MmHxNVAxOCCwTR?= NImxXmxKdmirYnn0bY9vKG:oIF3hZkAyOkd3IHLpcoRqdmdidH:gR3hEWjRiZYjwdoV{e2WmIHnuJIh2dWGwIF3PUHQ1KGOnbHzzJIF1KDFyMECgcm0h[nliRlHDV{BidmGueYPpdy=> MoLLNVk1PTF|MEW=
human MT2 cells NWmzZYJbTnWwY4Tpc44h[XO|YYm= M{XwOlEhfWdxbVy= M4P3UlQh\GG7cx?= NVvkUlIxSW62aY\pdoFtKGGldHn2bZR6KGGpYXnud5QhUEmYMTCzRkBqdm[nY4Tl[EBqdiCqdX3hckBOXDJiY3XscJMh[XO|ZYPz[YQh[XNiaX7obYJqfGmxbjDv[kB3cXKjbDDwNlQh[W62aXflckBxem:mdXP0bY9vKGG2IEGgeYcwdUxiYX\0[ZIhPCCmYYnzJIJ6KEWOSWPB NYn4S3hPOjFzNkizN|Y>
human U87 cells NF3WdWVHfW6ldHnvckBie3OjeR?= MU[xNFAxKG6P MmjzRY51[WexbnnzeEBi[3Srdnn0fUBifCCFWFPSOEBqdiCqdX3hckBWQDdiY3XscJMh[XO|ZYPz[YQh[XNiaX7obYJqfGmxbjDv[kBUTEZzLXnu[JVk\WRibX;keYxifGmxbjDv[kBkSU2SIIDyc4R2[3Srb36gZZQhOTByMDDuUUBjgSCWUj3GVmVVKGG|c3H5 MXWxO|k2QDN2NB?=

... 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]


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


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
NCT01026987 Completed Stem Cell Transplant Patients Washington University School of Medicine April 29, 2010 Phase 1
NCT02231879 Recruiting Myelokathexis|WHIMS|Neutropenia|Warts National Institute of Allergy and Infectious Diseases (NIAID)|National Institutes of Health Clinical Center (CC) August 27, 2014 Phase 3
NCT01547806 Active, not recruiting Plasma Cell Myeloma|Multiple Myeloma National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC) February 22, 2012 Phase 2
NCT01331018 Recruiting Fanconi Anemia Fred Hutchinson Cancer Research Center|National Cancer Institute (NCI)|National Heart, Lung, and Blood Institute (NHLBI) February 22, 2012 Phase 1
NCT02989701 Recruiting Sickle Cell Disease Without Crisis Alessandra Biffi|Boston Children’s Hospital January 2017 Phase 1
NCT02790957 Recruiting Diabetes|Wounds|Critical Limb Ischemia Gian Paolo Fadini|University Hospital Padova|University of Padova June 2016 Phase 2

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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:

CXCR Signaling Pathway Map

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID