product name Plerixafor 8HCl
Description: Plerixafor 8HCl (also known as AMD3100 8HCl, 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 is a bicyclam with hematopoietic stem cell-mobilizing activity. Plerixafor blocks the binding of stromal cell-derived factor (SDF-1alpha) to the cellular receptor CXCR4, resulting in hematopoietic stem cell (HSC) release from bone marrow and HSC movement into the peripheral circulation.
References: J Immunol. 2009 Sep 1;183(5):3204-11; J Invest Dermatol. 2012 Mar;132(3 Pt 1):711-20.
794.47
Formula
C28H54N8.8HCl
CAS No.
155148-31-5
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: <1 mg/mL
Water: 100 mg/mL (125.9 mM)
Ethanol: <1 mg/mL
Solubility (In vivo)
Saline: 30 mg/mL
Synonyms
JM 3100 8HCl
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19409477
| In Vitro |
In vitro activity: Plerixafor inhibits CXCL12-mediated chemotaxis with a potency lightly better than its affinity for CXCR4. 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. Kinase Assay: Cell Assay: Plerixafor 8HCl showed to inhibit I-SDF-1 ligand binding to CCRF–CEM T-lymphoblastoid cells which express CXCR4. Plerixafor 8HCl has shown to block CXCR4 activation, SDF-1 mediated calcium flux and SDF-1 mediated chemotaxis with IC50 values of 27.3, 572 and 51 nM, respectively. |
|---|---|
| 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. 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. |
| Animal model | Twelve-week-old C57BL/6 mice with segmental bone defect |
| Formulation & Dosage | Dissolved in PBS; 5 mg/kg; i.p. injection |
| References | J Immunol. 2009 Sep 1;183(5):3204-11; J Invest Dermatol. 2012 Mar;132(3 Pt 1):711-20. |
