Catalog No.S8030 Synonyms: JM 3100
Molecular Weight(MW): 502.78
Plerixafor (AMD3100) is a chemokine receptor antagonist for CXCR4 and CXCL12-mediated chemotaxis with IC50 of 44 nM and 5.7 nM in cell-free assays, respectively.
Cited by 8 Publications
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 (AMD3100) 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 (AMD3100) purchased from Selleck.
a, ECs were seeded onto collagen gels containing CXCL12 and incubated with vehicle (DMSO) control or AMD3100 (1 μM), rapamycin (100 nM), or PP242 (600 nM) for 24 h after before fixing and imaging. Scale bar = 150 μm. b, The average number of invading cells was calculated by counting five wells per condition.
Angiogenesis, 2016, 19(3):359-71. Plerixafor (AMD3100) purchased from Selleck.
(A) Pictures display representative results of the change of invading cells after incubation of human FTC cell line TT2609-C02 with different concentrations of CXCR4 antagonists AMD3100 and WZ811 as well as rh-SDF1α as receptor agonist. Cells were visualized by DAPI staining. (B) Invading cells were counted in five visual fields of at least three different membranes. Differences after treatment are illustrated as fold change to control.
J Cancer, 2018, 9(6):929-940. Plerixafor (AMD3100) purchased from Selleck.
Purity & Quality Control
Choose Selective CXCR Inhibitors
|Description||Plerixafor (AMD3100) is 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 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. 
|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. |
|In vitro||Ethanol||100 mg/mL (198.89 mM)|
|Water||3 mg/mL warmed (5.96 mM)|
|In vivo||Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
30% propylene glycol, 5% Tween 80, 65% D5W
For best results, use promptly after mixing.
* 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.
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Clinical Trial Information
|NCT Number||Recruitment||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT03653247||Not yet recruiting||Sickle Cell Disease||Bioverativ - a sanofi company|Bioverativ Therapeutics Inc.||December 2018||Phase 1|Phase 2|
|NCT03664830||Recruiting||Sickle Cell Disease||City of Hope Medical Center||September 19 2018||Phase 1|
|NCT03506802||Recruiting||HLA-A*0201 Positive Cells Present|NY-ESO-1 Positive Tumor Cells Present|Recurrent Plasma Cell Myeloma|Refractory Plasma Cell Myeloma||Jonsson Comprehensive Cancer Center|National Cancer Institute (NCI)||July 10 2018||Phase 1|
|NCT03547830||Recruiting||Chronic Granulomatous Disease||Federal Research Institute of Pediatric Hematology Oncology and Immunology||May 29 2018||Phase 2|
|NCT03182426||Recruiting||Diabetes Mellitus Type 1||University of Alberta|Alberta Innovates Health Solutions||August 15 2017||Phase 1|Phase 2|
|NCT03240861||Recruiting||HLA-A*0201 Positive Cells Present|Locally Advanced Malignant Neoplasm|NY-ESO-1 Positive|Unresectable Malignant Neoplasm||Jonsson Comprehensive Cancer Center|California Institute for Regenerative Medicine|National Cancer Institute (NCI)||July 26 2017||Phase 1|
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Frequently Asked Questions
How about the half-life of the product (Cat S8030)?
The biological half-life for this drug is 3-5 hours: https://en.wikipedia.org/wiki/Plerixafor.