The addition of a CD38 monoclonal antibody to triplet therapy has been shown to improve efficacy in patients with newly diagnosed multiple myeloma (NDMM). Isatuximab is an IgG1 monoclonal antibody targeting CD38, and its combination with lenalidomide, bortezomib and dexamethasone (RVd) is approved for transplant-ineligible patients with NDMM. In the initial analysis of the GMMG-HD7 trial in patients eligible for transplant, 18 weeks of induction with isatuximab plus RVd (Isa-RVd) (without posttransplant consolidation) was associated with an improved rate of minimal residual disease (MRD)-negativity over RVd alone. The aim of the current analysis was to investigate additional prespecified outcomes among GMMG-HD7 participants.

Patients with multiple myeloma often have decreased healthrelated quality of life (HRQoL), and it is important to consider HRQoL alongside clinical benefits when making treatment decisions. Ciltacabtagene autoleucel (ciltacel) is a dual-binding, B-cell maturation antigen-directed chimeric antigen receptor T-cell therapy that is approved for treating lenalidomide-refractory relapsed or refractory multiple myeloma. The aim of this analysis was to understand the effects of cilta-cel on HRQoL and disease-related symptoms.

There is no prospective evidence on whether consolidation and maintenance strategies improve the outcomes of patients with multiple myeloma (MM) following salvage autologous haematopoietic stem-cell transplantation (HSCT). Ixazomib is an oral second-generation proteasome inhibitor that has shown efficacy as a maintenance treatment following first-line autologous HSCT. The aim of this study was to investigate the efficacy of an ixazomib-containing consolidation and maintenance strategy following salvage autologous HSCT in patients with MM.

T-cell redirecting bispecific antibodies can be effective in treating multiple myeloma (MM), and work by simultaneously binding to antigens on MM cells and to CD3 on T cells. Currently approved agents include teclistamab and elranatamab (which target B-cell maturation antigen) and talquetamab (which targets G-protein-coupled receptor, class C, group 5, member D or GPRC5D), while others are in development. However, not all patients respond to this approach and most ultimately relapse because of acquired resistance, the mechanisms of which involve tumour-related features, T-cell characteristics and the immunosuppressive tumour microenvironment. The aim of this article was to review mechanisms of resistance against bispecific antibodies in MM.