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

  • 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.

Purity & Quality Control

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
GHOST CXCR4 cell line NFnX[|JHfW6ldHnvckBie3OjeR?= M1ToXGlvcGmkaYTvdpkh[2:wY3XueJJifGmxbjDv[kBkd22yb4Xu[EBi\2GrboP0JGhKXi1zIFzBTUB{fHKjaX6gbY4hT0iRU2SgR3hEWjRiY3XscEBtcW6nLDDJR|UxRTBwOUWgcm0> M1TLelE1Pjl6MUi5
HEK293 cells M1i1PWZ2dmO2aX;uJIF{e2G7 MXyyJIRigXN? MnTRRY51cX[rcnHsJIFkfGm4aYT5JIFo[Wmwc4SgWFIxNXKnc3nzeIFvfCCKSW[xJG5NPC1|IHnu[oVkfGWmIHnuJGhGUzJ7MzDj[YxteyCjc4Pld5Nm\CCjczDpcohq[mm2aX;uJI9nKH[rcnHsJJJmeGyrY3H0bY9vKGGodHXyJFIh\GG7czygTWM2OD1{LkOgcm0> MkL6NVk1PTF|MEW=
PBMC cells Moe1SpVv[3Srb36gZZN{[Xl? NGfOWW1G\m[nY4TpeoUh[2:wY3XueJJifGmxbjDv[kBkd22yb4Xu[EBi\2GrboP0JGhKXi1zIEi5MlYhe3S{YXnuJIlvKFCETVOgZ4VtdHNuIFXDOVA:Oy56IH7N Ml21NVQ3QThzOEm=
human MT4 cells NH3ZZVdHfW6ldHnvckBie3OjeR?= NEHkV5c1KGSjeYO= MWfBcpRqfmm{YXygZYN1cX[rdImgZYdicW6|dDDITXYyKDOEIHnu[oVkfGWmIHnuJIh2dWGwIF3UOEBk\WyuczDhd5Nme3OnZDDhd{BqdmirYnn0bY9vKG:oII\pdpV{KHKncHzpZ4F1cW:wIHHmeIVzKDRiZHH5d{BjgSCPVGSgZZN{[XluIFXDOVA:PCCwTR?= MXiyNFA1OzZ|OB?=
human Jurkat cells NYrZRoJtTnWwY4Tpc44h[XO|YYm= MlXxRY51[WexbnnzeEBi[3Srdnn0fUBifCCFWFPSOEBqdiCqdX3hckBLfXKtYYSgZ4VtdHNiYYPz[ZN{\WRiYYOgbY5pcWKrdHnvckBw\iCVRF[xMYlv\HWlZXSgZ4VtdCCvaXfyZZRqd25uIFnDOVA:OjdwNDDuUS=> NUTKNI5VOTlzOEiwO|E>
MT-4 cells NVP4UY4zTnWwY4Tpc44h[XO|YYm= M4KxdmVn\mWldHn2[UBkd26lZX70doF1cW:wIH;mJINwdXCxdX7kJIFo[Wmwc4SgTGlXNTFiSVnJRkB{fHKjaX6gbY4hVVRvNDDj[YxteyxiRVO1NF03PSCwTR?= M2K4VFE1Pjl6MUi5
rat IR983F cells NX3lcIprTnWwY4Tpc44h[XO|YYm= MWnEbZNxdGGlZX3lcpQhd2ZiW{GyOWleS1iFTEGyJIZzd21iQ2jDVlQhcW5icnH0JGlTQTh|RjDj[YxteyxiSVO1NF0yODhibl2= NHHhWXAyQTB3M{e2PC=>
CEM-SS cells NVO4WYd1TnWwY4Tpc44h[XO|YYm= NFS1bHhG\m[nY4TpeoUh[2:wY3XueJJifGmxbjDv[kBkd22yb4Xu[EBi\2GrboP0JGhKXi1zIFzBTUB{fHKjaX6gbY4hS0WPLWPTJINmdGy|LDDFR|UxRTF{NzDuUS=> NHq2eVgyPDZ7OEG4PS=>
human HL60 cells NVvTPGY4TnWwY4Tpc44h[XO|YYm= Ml\ESIl{eGyjY3Xt[Y51KG:oIGuxNlVKZVOGRkHhcJBp[SCocn;tJGNZS1J2IHnuJIh2dWGwIFjMOlAh[2WubIOsJGlEPTB;MUWuNkDPxE1? M3HTRVE6OTh6MEex
human MT2 cells NGCwNmZHfW6ldHnvckBie3OjeR?= MnTpNUB2\y:vTB?= NEX1TZc1KGSjeYO= MXfBcpRqfmm{YXygZYN1cX[rdImgZYdicW6|dDDITXYyKDOEIHnu[oVkfGWmIHnuJIh2dWGwIF3UNkBk\WyuczDhd5Nme3OnZDDhd{BqdmirYnn0bY9vKG:oII\pdoFtKHB{NDDhcpRq\2WwIIDyc4R2[3Srb36gZZQhOSC3Zz;tUEBi\nSncjC0JIRigXNiYomgSWxKW0F? M1qwW|IyOTZ6M{O2
human U87 cells MVnGeY5kfGmxbjDhd5NigQ>? NWHIcJhkOTByMDDuUS=> NIftSFdCdnSjZ3;ubZN1KGGldHn2bZR6KGG2IFPYR3I1KGmwIHj1cYFvKFV6NzDj[YxteyCjc4Pld5Nm\CCjczDpcohq[mm2aX;uJI9nKFOGRkGtbY5lfWOnZDDtc4R2dGG2aX;uJI9nKGODTWCgdJJw\HWldHnvckBifCBzMECwJI5OKGK7IGTSMWZTTVRiYYPzZZk> MYSxO|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
NCT01097057 Completed Non-Hodgkin Lymphoma Fred Hutchinson Cancer Research Center|National Cancer Institute (NCI) November 9 2010 Phase 2
NCT02231879 Active not recruiting Myelokathexis|WHIMS|Neutropenia|Warts National Institute of Allergy and Infectious Diseases (NIAID)|National Institutes of Health Clinical Center (CC) September 3 2014 Phase 3
NCT01288573 Completed Ewing''s Sarcoma/Soft Tissue Sarcoma|Neuroblastoma|Brain Tumors Genzyme a Sanofi Company|Sanofi March 3 2014 Phase 1|Phase 2
NCT00322127 Completed Stem Cell Mobilization National Heart Lung and Blood Institute (NHLBI)|National Institutes of Health Clinical Center (CC) May 3 2006 Phase 1
NCT03547830 Recruiting Chronic Granulomatous Disease Federal Research Institute of Pediatric Hematology Oncology and Immunology May 29 2018 Phase 2
NCT00943943 Completed Acute Myelogenous Leukemia|Leukemia M.D. Anderson Cancer Center|Bayer|Genzyme a Sanofi Company|Amgen|National Cancer Institute (NCI)|Georgia Institute of Technology October 29 2010 Phase 1

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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