Profile and Management of Toxicity of Selinexor and Belantamab Mafodotin for the Treatment of Triple Class Refractory Multiple Myeloma

Abstract

Treatment options are limited for multiple myeloma patients who have developed four/five drug-refractory disease. Selinexor (Sel) and belantamab mafodotin (belamaf) were recently approved by the US FDA for treatment of RRMM. The toxicity profile of these drugs is a concern since these agents are used in patients who have already undergone multiple lines of treatment. In this review, we discuss the toxicity profile and strategies for the management of toxicities of Sel and belamaf for the treatment of RRMM. We conducted a comprehensive literature search on PubMed, Embase, Cochrane, and Clinicaltrials.gov using the terms “selinexor”, “belantamab”, “belamaf”, and “multiple myeloma” without applying any limitations based on the date of the study, language, or country of origin. The most common hematological toxicity associated with these two drugs is thrombocytopenia. Cytopenias, constitutional symptoms, gastrointestinal effects, and hyponatremia are the major toxicities of Sel. Keratopathy and anemia are the major toxicities of belamaf. Treatment modifications and dose interruption are usually needed when side effects are more than grade II. As these are newer drugs with limited data, continuous surveillance and monitoring are warranted during the treatment course with early mitigation strategies.

Keywords:

• hematological malignancy
• treatment
• safety
• ocular toxicity
• relapsed and refractory multiple myeloma

Acknowledgments

Authors thank Ms. Marsha Halajian and Laeth George, MD for providing English language editing services and proofreading.

Disclosure

F. Anwer reports personal fees from Bristol Myers Squibb as a speaker and fee from Janssen pharmaceutical as an advisory board member, this fee was not related to the submitted work. Without receiving direct funding, served as the local principal investigator for Allogene Therapeutics, Celgene, GlaxoSmithKline, and Bristol Myers Squibb; has a consulting or advisory role for Seattle Genetics, Incyte Corporation Speakers’ Bureau, Company: Incyte Corporation; receives travel and accommodations expenses from Seattle Genetics, Incyte; receives honoraria from Incyte, Company: Seattle Genetics; and received research funding from Seattle Genetics, Company: Celgene, Acetylon Pharmaceuticals, Millennium, Astellas Pharma and AbbVie; and reports no other potential conflicts of interest for this work. The other authors report no conflicts of interest for this work.