Multiple myeloma (MM) is a plasma cell malignancy based in the bone marrow, in which standard treatments have historically included corticosteroids (e.g. dexamethasone and prednisone) and cytotoxic drugs (e.g. melphalan, vincristine, cyclophosphamide, and doxorubicin). However, the treatment paradigm is shifting away from classical chemotherapy to therapies that more directly target the unique plasma cell biology. This may be either through pathways unique to the plasma cell itself or the tumour microenvironment upon which they are dependent. Significant improvements in overall survival and remission duration in multiple myeloma (MM) are largely due to the advent of novel therapeutic agents, including proteasome inhibitors (PIs) and immunomodulatory drugs (IMiDs). Newer agents, including those that affect the epigenome, and antibody-based therapies that directly target the plasma cell are also coming into play. As the therapeutic landscape widens, it will be important to study these agents and their mechanisms of action (MoA).
This paper will focus on the MoA of existing and new agents, in order to promote a better understanding of how they work, and what their implications are in the Canadian clinical setting.