Dr Hans Lee Discusses Infection Risks for Bispecific Therapies for Patients With MM


MD Anderson Cancer Center's Hans Lee, MD, shared considerations for possible infection risk associated with bispecific therapies used to treat relapsed/refractory multiple myeloma (MM) at the European Hematology Association 2023 Congress

Hans Lee, MD, an associate professor and director of multiple myeloma clinical research, Department of Lymphoma/Myeloma, Division of Cancer Medicine, The University of Texas MD Anderson Cancer Center, detailed the possible infection risks for patients with relapsed/refractory multiple myeloma (R/R MM) receiving bispecific therapies at this year's European Hematology Association 2023 Congress in Franfurt, Germany.


What is the current understanding of infection risk in patients with R/R MM receiving bispecific therapies?

So, we know that patients with multiple myeloma at baseline are at increased risk for infection, particularly after successive lines of prior therapy, but we are seeing an increased infection rate than what we typically would probably see in patients receiving bispecific T-cell antibodies in phase 1 and phase 2 trials reported to date. This is represented by an increase in the total number of infections but also the increase in the grade 3 or higher infection rate, as well as the rates of hypogammaglobulinemia, or decreased IgG [immunoglobulin G] levels, that we're seeing in our patients getting bispecific T-cell antibody-based therapy.

Do some bispecific therapies offer reduced risk relative to other types of therapy for R/R MM?

We are getting more data with non-BCMA [B cell maturation antigen] bispecific T-cell antibody-based therapies targeting GPRC5D and FcRH5, and there does seem to be a reduced risk with non-BCMA–targeting bispecific T-cell antibodies compared with those that target BCMA. And this may be in part related to the target itself and that BCMA probably has more biological relevance than GPRC5D and FcRH5. Hence, targeting BCMA through bispecific T-cell antibodies leads to more profound humoral immunodeficiency and subsequent hypogammaglobulinemia and potential infection risk as well.

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