The Addition of Plerixafor Allows Adequate PBSC Collection in Multiple Myeloma and Lymphoma Patients Poor –mobilizers After Chemotherapy and G-CSF.

Abstract 3233

Poster Board III-170

Peripheral blood stem cell (PBSC) mobilization and subsequent autologous stem cell transplantation (ASCT) is the most effective strategy in many patients with Multiple Myeloma (MM), Hodgkin's Disease (HD) or non-Hodgkin's Lymphoma (NHL). However, a significant proportion of patients are not able to mobilize an adequate number of cells after conventional stem cell mobilization strategies [i.e. chemotherapy and granulocyte colony-stimulating factor (G-CSF) or G-CSF alone], and can not proceed to ASCT.

In the present work, we report, for the first time, of five heavily pre-treated or treatment refractory MM or lymphoma patients (3 males and 2 females, median age 51 years) classified as “poor-mobilizers”, or “no mobilizers” at all, after chemotherapy (DHAP, =2; Cyclophosphamide, =3) and G-CSF mobilization strategy, who received Plerixafor to successfully collect PBSCs. Poor mobilization was defined when the concentration of PB CD34⁺ cells was consistently lower than 10 cells/μL during the recovery phase after chemotherapy and/or the collection of PBSCs was predicted to be inadequate to perform single or double ASCT. The timing for Plerixafor administration was not planned in advance. The rapid biological activity of Plerixafor (i.e. peak time of CD34⁺ cell mobilization occurring 10-12 hours after injection) allowed its administration “on demand”, that is when PBSC mobilization was felt to be inadequate, considering WBCs and CD34⁺ cell kinetics. Plerixafor, at 0.24 mg/Kg, was administered subcutaneously for a maximum of 3 consecutive days, while continuing G-CSF, the evening before the planned leukapheresis.

Overall, the drug proven to be safe and no adverse events were recorded. In all patients we observed a significant fold-increase (mean value= 7.96) in the number of circulating CD34⁺ cells following Plerixafor administration as compared to CD34⁺ cell concentration evaluated daily after chemotherapy and G-CSF. All patients were able to collect the minimum required dose for ASCT (2×10⁶ CD34⁺ cells/Kg) and 4/5 patients collected the target cell dose (4×10⁶ CD34⁺ cells/Kg for single ASCT in NHL and 6×10⁶ CD34⁺ cells/Kg for tandem ASCT in MM). Three of 5 patients have already undergone ASCT with Plerixafor-mobilized PBSCs showing a rapid and durable hematological recovery.

Our results demonstrate that the addition of Plerixafor to G-CSF after chemotherapy is safe and allows the rescue of heavily pre-treated or poor-prognosis NHL and MM patients, who need to perform ASCT as consolidation therapy, but are failing PBSC mobilization.