Immunomodulators in newly diagnosed multiple myeloma: current and future concepts

ABSTRACT

Introduction: Impressive therapeutic progress is being made in the management of multiple myeloma (MM). his progress is related to the introduction of several new classes of therapeutic agents including proteasome inhibitors, immunomodulatory drugs (IMiDs) and monoclonal antibodies (MoAbs).

Areas covered: In this manuscript, the role of the IMiDs thalidomide and lenalidomide in the management of newly diagnosed MM is discussed. The mode of action of IMiDs and their role in the management of newly diagnosed MM patients is highlighted. In addition, clinical data on how MoAbs such as the anti-CD38 antibody daratumumab can further increase the efficacy of IMiD-based first-line anti-myeloma regimens are provided. A database search in PubMed was carried out.

Expert Opinion: Immunomodulation has become an indispensable part of successful anti-myeloma regimens both at relapse and at diagnosis. The combination of lenalidomide plus dexamethasone with an anti-CD38 MoAb such as daratumumab and a proteasome inhibitor such as bortezomib is currently one of the most potent first-line treatment regimens for MM. A better understanding on how IMiDs synergize with existing and new anti-myeloma treatments can further improve the outcome for patients. Optimal first-line therapy will continue to benefit the long-term outcome of a growing population of young and elderly MM patients.

KEYWORDS:

• Anti-cd38
• immunomodulatory drugs
• lenalidomide
• monoclonal antibody
• multiple myeloma
• thalidomide
• treatment

Article highlights

• Multiple myeloma is one of the malignancies with the highest degree of therapeutic innovation

• The immunomodulatory drugs (IMiDs) thalidomide and lenalidomide have reshaped the treatment paradigm of newly diagnosed myeloma patients

• Anti-CD38 monoclonal antibodies such as daratumumab have synergistic activity with IMiDs such as lenalidomide

• IMiDs have a remarkably complex mode of action

Declaration of interest

M Delforge has received speaker’s honoraria and research grants from Amgen, BMS -Celgene, Janssen, Sanofi & Takeda. 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.

Reviewer disclosures

Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.

Additional information

Funding

This paper was not funded.