Plerixafor (AMD3100) 8HCl

For research use only.

Catalog No.S3013 Synonyms: JM 3100 8HCl

24 publications

Plerixafor (AMD3100) 8HCl Chemical Structure

CAS No. 155148-31-5

Plerixafor (AMD3100, JM 3100) 8HCl is the hydrochloride of Plerixafor, 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 can be used as an anti-HIV agent.

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Selleck's Plerixafor (AMD3100) 8HCl has been cited by 24 publications

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Biological Activity

Description Plerixafor (AMD3100, JM 3100) 8HCl is the hydrochloride of Plerixafor, 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 can be used as an anti-HIV agent.
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 M4rTfmZ2dmO2aX;uJIF{e2G7 NVHRdY1TTGm|cHzhZ4Vu\W62IH;mJHsyOjWLXWPESlFidHCqYTDmdo9uKEO[Q2K0JIV5eHKnc4Pl[EBqdiCFSF;LNUBk\WyuczygTWM2OD1yLkixJI5O MX:xO|cyPTF{OB?=
GHOST CXCR4 cell line MVzGeY5kfGmxbjDhd5NigQ>? M2jnfWlvcGmkaYTvdpkh[2:wY3XueJJifGmxbjDv[kBkd22yb4Xu[EBi\2GrboP0JGhKXi1zIFzBTUB{fHKjaX6gbY4hT0iRU2SgR3hEWjRiY3XscEBtcW6nLDDJR|UxRTBwOUWgcm0> NHz5PFgyPDZ7OEG4PS=>
HEK293 cells MmLoSpVv[3Srb36gZZN{[Xl? NHXveIIzKGSjeYO= NY\UVpBbSW62aY\pdoFtKGGldHn2bZR6KGGpYXnud5QhXDJyLYLld4l{fGGwdDDITXYyKE6OND2zJIlv\mWldHXkJIlvKEiHS{K5N{Bk\WyuczDhd5Nme3OnZDDhd{BqdmirYnn0bY9vKG:oII\pdoFtKHKncHzpZ4F1cW:wIHHmeIVzKDJiZHH5d{whUUN3ME2yMlMhdk1? MlvFNVk1PTF|MEW=
PBMC cells MlXCSpVv[3Srb36gZZN{[Xl? MlLGSYZn\WO2aY\lJINwdmOnboTyZZRqd25ib3[gZ49ueG:3bnSgZYdicW6|dDDITXYuOSB6OT62JJN1emGrbjDpckBRSk2FIHPlcIx{NCCHQ{WwQVMvQCCwTR?= M4PrOVE1Pjl6MUi5
human MT4 cells MmDOSpVv[3Srb36gZZN{[Xl? NEHs[Ys1KGSjeYO= M4\oN2FvfGm4aYLhcEBi[3Srdnn0fUBi\2GrboP0JGhKXjFiM1KgbY5n\WO2ZXSgbY4hcHWvYX6gUXQ1KGOnbHzzJIF{e2W|c3XkJIF{KGmwaHnibZRqd25ib3[geolzfXNicnXwcIlk[XSrb36gZYZ1\XJiNDDkZZl{KGK7IF3UWEBie3OjeTygSWM2OD12IH7N MWKyNFA1OzZ|OB?=
human Jurkat cells M{\w[mZ2dmO2aX;uJIF{e2G7 NYrHcG1vSW62YXfvcol{fCCjY4Tpeol1gSCjdDDDXGNTPCCrbjDoeY1idiCMdYLrZZQh[2WubIOgZZN{\XO|ZXSgZZMhcW6qaXLpeIlwdiCxZjDTSGYyNWmwZIXj[YQh[2WubDDtbYdz[XSrb36sJGlEPTB;MkeuOEBvVQ>? MXSxPVE5QDB5MR?=
MT-4 cells M1fUcmZ2dmO2aX;uJIF{e2G7 NInOTGNG\m[nY4TpeoUh[2:wY3XueJJifGmxbjDv[kBkd22yb4Xu[EBi\2GrboP0JGhKXi1zIFnJTWIhe3S{YXnuJIlvKE2WLUSgZ4VtdHNuIFXDOVA:PjVibl2= NVzT[5MyOTR4OUixPFk>
rat IR983F cells MUDGeY5kfGmxbjDhd5NigQ>? NX;JcpNrTGm|cHzhZ4Vu\W62IH;mJHsyOjWLXVPYR2wyOiCocn;tJGNZS1J2IHnuJJJifCCLUkm4N2Yh[2WubIOsJGlEPTB;MUC4JI5O MVqxPVA2Ozd4OB?=
CEM-SS cells NV\SWlFQTnWwY4Tpc44h[XO|YYm= NFTySnNG\m[nY4TpeoUh[2:wY3XueJJifGmxbjDv[kBkd22yb4Xu[EBi\2GrboP0JGhKXi1zIFzBTUB{fHKjaX6gbY4hS0WPLWPTJINmdGy|LDDFR|UxRTF{NzDuUS=> M2L4elE1Pjl6MUi5
human HL60 cells M1;MNWZ2dmO2aX;uJIF{e2G7 NW\aT4hETGm|cHzhZ4Vu\W62IH;mJHsyOjWLXWPESlFidHCqYTDmdo9uKEO[Q2K0JIlvKGi3bXHuJGhNPjBiY3XscJMtKEmFNUC9NVUvOiEQvF2= MWGxPVE5QDB5MR?=
human MOLT4 cells MX7GeY5kfGmxbjDhd5NigQ>? NXjUN3BWOTByMDDuUS=> MXXJcohq[mm2aX;uJI9nKE2jYjCxNmc2KGKrbnTpcochfG9iQ2jDVlQh\XiycnXzd4VlKGmwIHj1cYFvKE2RTGS0JINmdGy|IHH0JFExODBibl2gZpkhTkGFUzDhcoFtgXOrcx?= NHrjd|MyQTR3MUOwOS=>
human MT2 cells MXrGeY5kfGmxbjDhd5NigQ>? Ml[xNUB2\y:vTB?= NUm1doZzPCCmYYnz Mnf6RY51cX[rcnHsJIFkfGm4aYT5JIFo[Wmwc4SgTGlXOSB|QjDpcoZm[3SnZDDpckBpfW2jbjDNWFIh[2WubIOgZZN{\XO|ZXSgZZMhcW6qaXLpeIlwdiCxZjD2bZJidCCyMkSgZY51cWenbjDwdo9lfWO2aX;uJIF1KDFidXevcWwh[W[2ZYKgOEBl[Xm|IHL5JGVNUVOD MX[yNVE3QDN|Nh?=
human U87 cells NHv4TVdHfW6ldHnvckBie3OjeR?= M1qxdFExODBibl2= MkDKRY51[WexbnnzeEBi[3Srdnn0fUBifCCFWFPSOEBqdiCqdX3hckBWQDdiY3XscJMh[XO|ZYPz[YQh[XNiaX7obYJqfGmxbjDv[kBUTEZzLXnu[JVk\WRibX;keYxifGmxbjDv[kBkSU2SIIDyc4R2[3Srb36gZZQhOTByMDDuUUBjgSCWUj3GVmVVKGG|c3H5 NVTD[|FKOTd7NUizOFQ>

... Click to View More Cell Line Experimental Data

Assay
Methods Test Index PMID
Immunofluorescence
CXCR4; 

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.

β-arrestin2; 

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]

Protocol

Animal Research:[4]
- Collapse
  • 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 100 mg/mL (125.87 mM)
DMSO Insoluble
Ethanol Insoluble
In vivo Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
Saline
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 794.47
Formula

C28H54N8.8HCl

CAS No. 155148-31-5
Storage powder
in solvent
Synonyms JM 3100 8HCl
Smiles C1CNCCNCCCN(CCNC1)CC2=CC=C(C=C2)CN3CCCNCCNCCCNCC3.Cl.Cl.Cl.Cl.Cl.Cl.Cl.Cl

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Clinical Trial Information

NCT Number Recruitment interventions Conditions Sponsor/Collaborators Start Date Phases
NCT04646603 Not yet recruiting Drug: MRG-001|Drug: Placebo COVID-19 MedRegen LLC|Kendall Healthcare Group Ltd. January 5 2021 Phase 1|Phase 2
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

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CXCR Signaling Pathway Map

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID