ABSTRACT
Introduction: Monoclonal antibodies (MoAbs), non-chemotherapeutic agents targeting the antigens present on chronic lymphocytic leukemia (CLL) lymphocytes, are being implemented increasingly more often as treatment options.
Areas covered: This article reviews the similarities and differences in the structure, mechanism of action, efficacy and safety profile of commercially-available MoAbs and prevents new agents potentially useful for CLL treatment. Publications in English before June 2016 were surveyed on the MEDLINE database for articles. Proceedings of the American Society of Hematology held during the last five years were also included.
Expert opinion: MoAbs, especially those targeting CD20, are highly effective biological options for first-line and salvage treatment of CLL, particularly in chemoimmunotherapy, and possibly also as maintenance therapy. Treatment with MoAbs is associated with reduced risk of such adverse events as cytopenias, infections and secondary neoplasias and is generally well tolerated. Depending on antibody type, the most common adverse events are usually transient and limited to grade 1 and 2 infusion-related reactions. In addition to commercially available MoAbs, several other antibodies exist which are targeted against different antigens studied in the clinical trials.
Article highlights
Anti-CD20 monoclonal antibodies (rituximab, ofatumumab and obinuztuzumab) belong to the available biologically active treatment options useful in the untreated and relapsed/refractory CLL patients.
The drugs are usually well tolerated with infusion-related reactions being the most frequently observed adverse events, especially after the first infusion.
The frequency of infusion-related reactions is higher after obinutuzimab as compared to rituximab and ofatumumab administration.
Hematological toxicity all grades is generally transient.
Non-hematological toxicity included immunosuppressive or immunomodulatory effects such increased frequency of infections including HBV reactivation
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Declaration of interest
D Wolowiec received consulting fees, travel grants and/or honoraria from: Janssen-Cilag, Roche, Novartis, Gilead, Teva, Amgen, Mundipharma, AbbVie, Sanofi-Genzyme and Sanofi Aventis. T Robak received consulting fees from F. Hoffmann–La Roche, Gilead, and Janssen and performed contracted research for F. Hoffmann–La Roche, GlaxoSmithKline, Janssen, Celgene, Mor-phoSys AG, Emergent BioSolutions, Pharmacyclics, Gilead, and Seattle Genetics. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.