Plerixafor 8HCl (AMD3100 8HCl)

Catalog No.S3013 Synonyms: JM 3100 8HCl

Plerixafor 8HCl (AMD3100 8HCl) Chemical Structure

Molecular Weight(MW): 794.47

Plerixafor 8HCl (AMD3100 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.

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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 8HCl (AMD3100 8HCl) 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 8HCl (AMD3100 8HCl) purchased from Selleck.

  • Inhibition of SDF-1α signalling in subchondral bone attenuated cartilage degeneration (A) H&E staining of tibia subchondral bone and cartilage from sham, ACLT/PBS, and ACLT/AMD3100 groups. Calibration scale: bar = 100 μm; (B) Safranin O-Fast Green staining of articular cartilage in sagittal sections of tibia from mice treated with PBS or AMD3100 and sacrificed 30 days post ACLT or sham surgery. Calibration scale: bar = 100 μm; (C) MMP13 expression was detected by immunohistochemical staining of cartilage, and representative images are shown. A positive signal was indicated by the brown colour and marked by black arrows, meanwhile a negative control was present. Calibration scale: bar = 50 μm; (D) OARSI scores of sham or ACLT mice treated with PBS or AMD3100.Quantitative analysis of the percentage of MMP13+ chondrocytes in articular cartilage tissue sections in each group, reported as means ± SD. n = 10. * ACLT/PBS different from sham/PBS (p < 0.05), # ACLT/PBS different from ACLT/AMD3100 (p < 0.05).

    Int J Mol Sci, 2016, 17(6): 943.. Plerixafor 8HCl (AMD3100 8HCl) purchased from Selleck.

    CXCR4 is overexpressed in primary osteosarcoma cells and promotes invasion in U2OS cells. (A) We obtained primary cells derived from three patients suffering from osteosarcoma. The splitting of tumor tissues were performed by western blot analysis. The expression of CXCR4 in primary osteosarcoma cells were detected. OS1, OS2, OS3, three primary osteosarcoma cells. (B) Suppression of CXCR4 by plerixafor (CXCR4 inhibitor, 500 ng/ml, 48 h) downregulates the expression of MMP-2 and MMP-9. The downregulation can be reversed by SDF-1 (100 ng/ml, pre-incubate for 2 h). Sinomenine treatment had similar effect to plerixafor. The bands were quantitative analyzed by ImageJ software. *P<0.05, versus control. NS, no significance. #P<0.05 compare with plerixafor treatment. (C) Cells were treated with plerixafor and sinomenine, with or without SDF-1 simultaneously for 24 h. Then cells were harvested for Transwell assay. Representative images are presented. (x200 magnification).

    Int J Oncol, 2016, 48(5):2098-112.. Plerixafor 8HCl (AMD3100 8HCl) purchased from Selleck.

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Biological Activity

Description Plerixafor 8HCl (AMD3100 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.
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 MULGeY5kfGmxbjDhd5NigQ>? NUnsTGFITGm|cHzhZ4Vu\W62IH;mJHsyOjWLXWPESlFidHCqYTDmdo9uKEO[Q2K0JIV5eHKnc4Pl[EBqdiCFSF;LNUBk\WyuczygTWM2OD1yLkixJI5O MnTONVc4OTVzMki=
GHOST CXCR4 cell line NF;1e|hHfW6ldHnvckBie3OjeR?= MmLUTY5pcWKrdH;yfUBkd26lZX70doF1cW:wIH;mJINwdXCxdX7kJIFo[Wmwc4SgTGlXNTFiTFHJJJN1emGrbjDpckBIUE:VVDDDXGNTPCClZXzsJIxqdmVuIFnDOVA:OC57NTDuUS=> M{W2W|E1Pjl6MUi5
HEK293 cells M3T6TGZ2dmO2aX;uJIF{e2G7 MYWyJIRigXN? Ml3xRY51cX[rcnHsJIFkfGm4aYT5JIFo[Wmwc4SgWFIxNXKnc3nzeIFvfCCKSW[xJG5NPC1|IHnu[oVkfGWmIHnuJGhGUzJ7MzDj[YxteyCjc4Pld5Nm\CCjczDpcohq[mm2aX;uJI9nKH[rcnHsJJJmeGyrY3H0bY9vKGGodHXyJFIh\GG7czygTWM2OD1{LkOgcm0> M2nWd|E6PDVzM{C1
PBMC cells MmTFSpVv[3Srb36gZZN{[Xl? M1TBeWVn\mWldHn2[UBkd26lZX70doF1cW:wIH;mJINwdXCxdX7kJIFo[Wmwc4SgTGlXNTFiOEmuOkB{fHKjaX6gbY4hWEKPQzDj[YxteyxiRVO1NF0{Njhibl2= MoqyNVQ3QThzOEm=
human MT4 cells NUPyWnpnTnWwY4Tpc44h[XO|YYm= NVK4VWZEPCCmYYnz MlraRY51cX[rcnHsJIFkfGm4aYT5JIFo[Wmwc4SgTGlXOSB|QjDpcoZm[3SnZDDpckBpfW2jbjDNWFQh[2WubIOgZZN{\XO|ZXSgZZMhcW6qaXLpeIlwdiCxZjD2bZJ2eyC{ZYDsbYNifGmxbjDh[pRmeiB2IHThfZMh[nliTWTUJIF{e2G7LDDFR|UxRTRibl2= Mne1NlAxPDN4M{i=
human Jurkat cells MnrLSpVv[3Srb36gZZN{[Xl? MlzlRY51[WexbnnzeEBi[3Srdnn0fUBifCCFWFPSOEBqdiCqdX3hckBLfXKtYYSgZ4VtdHNiYYPz[ZN{\WRiYYOgbY5pcWKrdHnvckBw\iCVRF[xMYlv\HWlZXSgZ4VtdCCvaXfyZZRqd25uIFnDOVA:OjdwNDDuUS=> MkG4NVkyQDhyN{G=
MT-4 cells NHLBNGtHfW6ldHnvckBie3OjeR?= NHf0dW9G\m[nY4TpeoUh[2:wY3XueJJifGmxbjDv[kBkd22yb4Xu[EBi\2GrboP0JGhKXi1zIFnJTWIhe3S{YXnuJIlvKE2WLUSgZ4VtdHNuIFXDOVA:PjVibl2= NXH2NmVlOTR4OUixPFk>
rat IR983F cells MYnGeY5kfGmxbjDhd5NigQ>? M4jkfWRqe3CuYXPlcYVvfCCxZjDbNVI2UV2FWFPMNVIh\nKxbTDDXGNTPCCrbjDyZZQhUVJ7OEPGJINmdGy|LDDJR|UxRTFyODDuUS=> NUjqTZpzOTlyNUO3Olg>
CEM-SS cells NWHkV497TnWwY4Tpc44h[XO|YYm= MULF[oZm[3SrdnWgZ49v[2WwdILheIlwdiCxZjDjc41xd3WwZDDh[4FqdnO2IFjJWk0yKEyDSTDzeJJicW5iaX6gR2VONVOVIHPlcIx{NCCHQ{WwQVEzPyCwTR?= MXKxOFY6QDF6OR?=
human HL60 cells M3zEWWZ2dmO2aX;uJIF{e2G7 MlHZSIl{eGyjY3Xt[Y51KG:oIGuxNlVKZVOGRkHhcJBp[SCocn;tJGNZS1J2IHnuJIh2dWGwIFjMOlAh[2WubIOsJGlEPTB;MUWuNkDPxE1? NFnWSpcyQTF6OEC3NS=>
human MOLT4 cells NWXZeGVYTnWwY4Tpc44h[XO|YYm= MofTNVAxOCCwTR?= NE[2S2VKdmirYnn0bY9vKG:oIF3hZkAyOkd3IHLpcoRqdmdidH:gR3hEWjRiZYjwdoV{e2WmIHnuJIh2dWGwIF3PUHQ1KGOnbHzzJIF1KDFyMECgcm0h[nliRlHDV{BidmGueYPpdy=> NVXpZ3o2OTl2NUGzNFU>
human MT2 cells MoX1SpVv[3Srb36gZZN{[Xl? MnTWNUB2\y:vTB?= MmK5OEBl[Xm| NEm5W4RCdnSrdnnyZYwh[WO2aY\peJkh[WejaX7zeEBJUVZzIEPCJIlv\mWldHXkJIlvKGi3bXHuJG1VOiClZXzsd{Bie3Onc4Pl[EBieyCrbnjpZol1cW:wIH;mJJZqemGuIICyOEBidnSrZ3XuJJBzd2S3Y4Tpc44h[XRiMTD1[{9uVCCjZoTldkA1KGSjeYOgZpkhTUyLU1G= M2\xfVIyOTZ6M{O2
human U87 cells NFvLc4JHfW6ldHnvckBie3OjeR?= NFfGR3UyODByIH7N NIiwVnFCdnSjZ3;ubZN1KGGldHn2bZR6KGG2IFPYR3I1KGmwIHj1cYFvKFV6NzDj[YxteyCjc4Pld5Nm\CCjczDpcohq[mm2aX;uJI9nKFOGRkGtbY5lfWOnZDDtc4R2dGG2aX;uJI9nKGODTWCgdJJw\HWldHnvckBifCBzMECwJI5OKGK7IGTSMWZTTVRiYYPzZZk> M3;0N|E4QTV6M{S0

... 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 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

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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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CXCR Signaling Pathway Map

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID