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

  • 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.

    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.

  • 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 MXzGeY5kfGmxbjDhd5NigQ>? MVjEbZNxdGGlZX3lcpQhd2ZiW{GyOWleW0SIMXHsdIhiKG[{b32gR3hEWjRiZYjwdoV{e2WmIHnuJGNJV0tzIHPlcIx{NCCLQ{WwQVAvQDFibl2= MV:xO|cyPTF{OB?=
GHOST CXCR4 cell line Mnq2SpVv[3Srb36gZZN{[Xl? MoraTY5pcWKrdH;yfUBkd26lZX70doF1cW:wIH;mJINwdXCxdX7kJIFo[Wmwc4SgTGlXNTFiTFHJJJN1emGrbjDpckBIUE:VVDDDXGNTPCClZXzsJIxqdmVuIFnDOVA:OC57NTDuUS=> M3v4Z|E1Pjl6MUi5
HEK293 cells MXTGeY5kfGmxbjDhd5NigQ>? NGfRXpAzKGSjeYO= MYTBcpRqfmm{YXygZYN1cX[rdImgZYdicW6|dDDUNlAuemW|aYP0ZY51KEiLVkGgUmw1NTNiaX7m[YN1\WRiaX6gTGVMOjl|IHPlcIx{KGG|c3Xzd4VlKGG|IHnubIljcXSrb36gc4Yhfmm{YXygdoVxdGmlYYTpc44h[W[2ZYKgNkBl[Xm|LDDJR|UxRTJwMzDuUS=> Ml3nNVk1PTF|MEW=
PBMC cells MWTGeY5kfGmxbjDhd5NigQ>? M4TtTGVn\mWldHn2[UBkd26lZX70doF1cW:wIH;mJINwdXCxdX7kJIFo[Wmwc4SgTGlXNTFiOEmuOkB{fHKjaX6gbY4hWEKPQzDj[YxteyxiRVO1NF0{Njhibl2= M3Hi[lE1Pjl6MUi5
human MT4 cells MknpSpVv[3Srb36gZZN{[Xl? MnjoOEBl[Xm| NIHmOllCdnSrdnnyZYwh[WO2aY\peJkh[WejaX7zeEBJUVZzIEPCJIlv\mWldHXkJIlvKGi3bXHuJG1VPCClZXzsd{Bie3Onc4Pl[EBieyCrbnjpZol1cW:wIH;mJJZqenW|IILldIxq[2G2aX;uJIFnfGW{IESg[IF6eyCkeTDNWHQh[XO|YYmsJGVEPTB;NDDuUS=> NUfCcYxiOjByNEO2N|g>
human Jurkat cells MnLHSpVv[3Srb36gZZN{[Xl? MWLBcpRi\2:waYP0JIFkfGm4aYT5JIF1KEO[Q2K0JIlvKGi3bXHuJGp2emujdDDj[YxteyCjc4Pld5Nm\CCjczDpcohq[mm2aX;uJI9nKFOGRkGtbY5lfWOnZDDj[YxtKG2rZ4LheIlwdixiSVO1NF0zPy52IH7N Mof0NVkyQDhyN{G=
MT-4 cells MYnGeY5kfGmxbjDhd5NigQ>? MojuSYZn\WO2aY\lJINwdmOnboTyZZRqd25ib3[gZ49ueG:3bnSgZYdicW6|dDDITXYuOSCLSVnCJJN1emGrbjDpckBOXC12IHPlcIx{NCCHQ{WwQVY2KG6P NF:0bnUyPDZ7OEG4PS=>
rat IR983F cells MljOSpVv[3Srb36gZZN{[Xl? NHnOPINFcXOybHHj[Y1mdnRib3[gX|EzPUmfQ2jDUFEzKG[{b32gR3hEWjRiaX6gdoF1KEmUOUizSkBk\WyuczygTWM2OD1zMEigcm0> MnSwNVkxPTN5Nki=
CEM-SS cells NXPwUnBCTnWwY4Tpc44h[XO|YYm= NFT1UpVG\m[nY4TpeoUh[2:wY3XueJJifGmxbjDv[kBkd22yb4Xu[EBi\2GrboP0JGhKXi1zIFzBTUB{fHKjaX6gbY4hS0WPLWPTJINmdGy|LDDFR|UxRTF{NzDuUS=> NETyb5QyPDZ7OEG4PS=>
human HL60 cells MXXGeY5kfGmxbjDhd5NigQ>? MVXEbZNxdGGlZX3lcpQhd2ZiW{GyOWleW0SIMXHsdIhiKG[{b32gR3hEWjRiaX6gbJVu[W5iSFy2NEBk\WyuczygTWM2OD1zNT6yJO69VQ>? MVGxPVE5QDB5MR?=
human MOLT4 cells MWjGeY5kfGmxbjDhd5NigQ>? M2DSdlExODBibl2= MmXUTY5pcWKrdHnvckBw\iCPYXKgNVJIPSCkaX7kbY5oKHSxIFPYR3I1KGW6cILld5Nm\CCrbjDoeY1idiCPT1zUOEBk\WyuczDheEAyODByIH7NJIJ6KE[DQ2OgZY5idHm|aYO= MXuxPVQ2OTNyNR?=
human MT2 cells MV;GeY5kfGmxbjDhd5NigQ>? MlLFNUB2\y:vTB?= MoDmOEBl[Xm| NIHUXJNCdnSrdnnyZYwh[WO2aY\peJkh[WejaX7zeEBJUVZzIEPCJIlv\mWldHXkJIlvKGi3bXHuJG1VOiClZXzsd{Bie3Onc4Pl[EBieyCrbnjpZol1cW:wIH;mJJZqemGuIICyOEBidnSrZ3XuJJBzd2S3Y4Tpc44h[XRiMTD1[{9uVCCjZoTldkA1KGSjeYOgZpkhTUyLU1G= NH3QPXkzOTF4OEOzOi=>
human U87 cells MVnGeY5kfGmxbjDhd5NigQ>? NHnJcVYyODByIH7N M3e3XmFvfGGpb37pd5Qh[WO2aY\peJkh[XRiQ2jDVlQhcW5iaIXtZY4hXTh5IHPlcIx{KGG|c3Xzd4VlKGG|IHnubIljcXSrb36gc4YhW0SIMT3pcoR2[2WmIH3v[JVt[XSrb36gc4Yh[0GPUDDwdo9lfWO2aX;uJIF1KDFyMECgcm0h[nliVGKtSnJGXCCjc4PhfS=> M4fQe|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 individually and in order:
Saline
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
Synonyms JM 3100 8HCl

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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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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID