product name Plerixafor
Description: Plerixafor (also known as AMD3100, JM 3100) 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.
502.78
Formula
C28H54N8
CAS No.
110078-46-1
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: <1 mg/mL
Water: 3 mg/mL (5.96 mM)
Ethanol: 100 mg/mL (198.9 mM)
Solubility (In vivo)
30% Propylene glycol, 5% Tween 80, 65% D5W: 30 mg/mL
Synonyms
JM 3100
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19409524
| 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: For the competition binding studies against CXCR4, a concentration range of Plerixafor was incubated for 3 hours at 4°C in binding buffer (PBS containing 5 mM MgCl2, 1 mM CaCl2, 0.25% BSA, pH 7.4) with 5 × 105 CCRF-CEM cells and 100 pM 125I-SDF-1α (2200 Ci/mmol) in Milipore DuraporeTM filter plates. Unbound 125I-SDF-1α was removed by washing with cold 50 mM HEPES, 0.5 M NaCl pH 7.4. The competition binding assay against BLT1 was performed on membranes from CHO-S cells expressing recombinant BLT1. The membranes were prepared by mechanical cell lysis followed by high speed centrifugation, re-suspended in 50 mm HEPES, 5 mM MgCl2 buffer and flash frozen. The membrane preparation was incubated with Plerixafor for 1 hour at room temperature in an assay mixture containing 50 mM Tris, pH 7.4, 10 mM MgCl2, 10 mM CaCl2, 4 nM LTB4 mixed with 1 nM 3H-LTB4 (195.0 Ci/mmol) and 8 μg membrane. The unbound 3H-LTB4 is separated by filtration on Millipore Type GF-C filter plates. Cell Assay: CXCR4 and SDF-1 were key factors in regulating cancer cell invasion and metastasis, and Plerixafor effectively prevented the binding of SDF-1 to CXCR4, inhibiting cancer metastasis. |
|---|---|
| In Vivo | Cohorts of mice were 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 were highest in mice injected with IGF1 and Plerixafor than those treated with PDGF, SCF or VEGF plus Plerixafor. |
| Animal model | C57BL/6 mice with segmental bone defect |
| Formulation & Dosage | 5 mg/kg; i.p. injection |
| References | J Immunol. 2009 Sep 1;183(5):3204-11; Biochem Pharmacol. 2006 Aug 28;72(5):588-96; Bone. 2012 Apr;50(4):1012-8. |
3-O-(2-Aminoethyl)-25-hydroxyvitamin D3
