The unmet need for improved multiple myeloma (MM) therapy has stimulated clinical
development of monoclonal antibodies (mAbs) targeting either MM cells or cells of the bone marrow (BM)
microenvironment. In contrast to small-molecule inhibitors, therapeutic mAbs present the potential to
specifically target tumor cells and directly induce an immune response to lyse tumor cells. Unique immuneeffector
mechanisms are only triggered by therapeutic mAbs but not by small molecule targeting agents.
Although therapeutic murine mAbs or chimeric mAbs can cause immunogenicity, the advancement of
genetic recombination for humanizing rodent mAbs has allowed large-scale production and designation of
mAbs with better affinities, efficient selection, decreasing immunogenicity, and improved effector
functions. These advancements of antibody engineering technologies has largely overcome the critical
obstacle of antibody immunogenicity and enabled the development and subsequent Food and Drug
Administration (FDA) approval of therapeutic Abs for cancer and other diseases.
Keywords: Rituximab, tocilizumab, elotuzumab, HuLuc63, daratumumab, anti-HM1.24 mAb,
mapatumumab, milatuzumab, CNTO 328, denosumab, BHQ880, ACE-011, atacicept, bevacizumab.
