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Plerixafor, a CXCR4 antagonist for the mobilization of hematopoietic stem cells
Geoffrey L Uy1, Michael P Rettig, Amanda F Cashen
1Washington University School of Medicine, Division of Oncology, 660 S. Euclid Avenue, Campus Box 8007, St. Louis, Missouri 63110, USA. guy@im.wustl.edu
Stem cells harvested from peripheral blood are the most commonly used graft source in hematopoietic stem cell transplantation. While G-CSF is the most frequently used agent for stem cell mobilization, the use of G-CSF alone results in suboptimal stem cell yields in a significant proportion of patients undergoing autologous transplantation. Plerixafor (AMD3100, Genzyme Corporation) is a bicyclam molecule that antagonizes the binding of the chemokine stromal cell-derived factor-1 (SDF-1) to its cognate receptor CXCR4. Plerixafor results in the rapid and reversible mobilization of hematopoietic stem cells into the peripheral circulation and is synergistic when combined with G-CSF. In clinical studies of autologous stem cell transplantation, the combination of plerixafor and G-CSF allows the collection of large numbers of stem cells in fewer apheresis sessions and can salvage those who fail G-CSF mobilization alone.
Stem cells harvested from peripheral blood are the most commonly used graft source in hematopoietic stem cell transplantation. While G-CSF is the most frequently used agent for stem cell mobilization, the use of G-CSF alone results in suboptimal stem cell yields in a significant proportion of patients undergoing autologous transplantation. Plerixafor (AMD3100, Genzyme Corporation) is a bicyclam molecule that antagonizes the binding of the chemokine stromal cell-derived factor-1 (SDF-1) to its cognate receptor CXCR4. Plerixafor results in the rapid and reversible mobilization of hematopoietic stem cells into the peripheral circulation and is synergistic when combined with G-CSF. In clinical studies of autologous stem cell transplantation, the combination of plerixafor and G-CSF allows the collection of large numbers of stem cells in fewer apheresis sessions and can salvage those who fail G-CSF mobilization alone.
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