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Addition of plerixafor to G-CSF is useful to achieve efficient collection even in very poor mobilizers: hope for patients with diminished hematopoietic function

Bone Marrow Transplantation volume 52, pages 1049–1050 (2017)Cite this article

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High-dose chemotherapy (HDCT)±irradiation followed by autologous hematopoietic stem cell transplantation (ASCT) is a useful therapeutic component for patients with relapsed non-Hodgkin’s lymphoma (NHL), Hodgkin’s disease (HD) and multiple myeloma (MM).1 Prior to the plerixafor era, 10–30% of these, usually heavily pretreated, patients had a pooled cell harvest below 2.0 × 106 CD34+ cells/kg of body weight.2 These individuals were commonly referred to as ‘poor mobilizers’. The addition of plerixafor, an inhibitor of the interaction between stromal cell-derived factor 1 or CXCL12 and its receptor CXCR4, to G-CSF enhances hematopoietic stem cell (HSC) mobilization.3 Because there is a correlation between pre-apheresis peripheral blood (PB) CD34+ cell counts and collected CD34+ cell numbers, the PB CD34+ cell count is now the recommended biomarker to predict a patient’s capacity to reach the collection target, and to decide on ‘go/no go’ for plerixafor administration and subsequent apheresis; while the cutoff level is often stated as <20 PB CD34+ cells/μL in clinical trials, this threshold may significantly vary across apheresis facilities in routine practice, and be as low as 10/μL.4, 5, 6 Subcutaneous administration of 240 μg/kg plerixafor, 6–11 h prior to the first planned apheresis, that is, in the evening of the day when mobilization is considered insufficient in response to proper administration of G-CSF (+/− chemomobilization) allows over 90% of these so-called poor mobilizers to be adequately collected and proceed to HDCT supported with autologous HSCT.7, 8

In 2015, results of the nationwide post-marketing survey Osmoz on the routine use of plerixafor in daily practice rather than as part of clinical trials confirmed the efficacy of plerixafor, and demonstrated that French practitioners mostly used the product in compliance with the EU marketing authorization recommendations, that is, in adult patients treated for lymphoid malignancies and ‘who mobilize poorly’. The addition of plerixafor in the mobilization regimen resulted in the collection of ⩾2 × 106 CD34+ cells/kg in 92% of these patients, and 75% of these patients reached the collection target,8 defined in the study as more than 90% of the number of collected cells ordered by the prescribing transplant physician. Over 80% of patients with >15 PB CD34+ cells/μL reached the study collection objective, including 62.3% of patients with <5 PB CD34+ cells/μL (Table 1).

Table 1 Percentage of patients reaching the collection objective according to the PB CD34+ cells/μL number
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Authors and Affiliations

  1. Hematology Department, Hôpital Saint Antoine, Assistance Publique des Hôpitaux de Paris (AP-HP), Université Pierre et Marie Curie (UPMC), Paris, France

    M Mohty

  2. INSERM, UMRs 938, Centre de Recherches Saint-Antoine, Paris, France

    M Mohty

  3. Etablissement Français du Sang, Direction Médicale et Scientifique, La Plaine St Denis, France

    P Drillat

  4. Inserm U1219 ‘Population Health’ and Université de Rouen, Rouen, France

    J-M Grouin

  5. Institut Bergonié, Bordeaux, France

    F Bijou

  6. Hematology Department, Centre Hospitalier et Universitaire de Bordeaux, Bordeaux, France

    N Milpied

  7. Institut Paoli-Calmettes, Centre de Lutte Contre le Cancer,

    C Chabannon

  8. Université d’Aix-Marseille, Marseille, France

    C Chabannon

  9. Inserm CBT 1409, Centre d’Investigations Cliniques en Biothérapie, Marseille, France

    C Chabannon

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Correspondence to M Mohty.

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All authors declared that they have received lectures honoraria from Sanofi whose product is discussed in this study.

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Mohty, M., Drillat, P., Grouin, JM. et al. Addition of plerixafor to G-CSF is useful to achieve efficient collection even in very poor mobilizers: hope for patients with diminished hematopoietic function. Bone Marrow Transplant 52, 1049–1050 (2017). https://doi.org/10.1038/bmt.2017.80

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