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
3 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.
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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*When preparing stock solutions, please always use the batch-specific molecular weight of the product found on the via label and MSDS / COA (available on product pages).
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This equation is commonly abbreviated as: C1V1 = C2V2 ( Input Output )
* When preparing stock solutions always use the batch-specific molecular weight of the product found on the vial label and MSDS / COA (available online).
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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|
Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.
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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.