Cellular and T cell engager Immunotherapy

Real-world outcomes of teclistamab for the treatment of relapsed/refractory multiple myeloma at UC San Diego Health: A single-institution experience

P-025: Real-world outcomes of teclistamab for the treatment of relapsed/refractory multiple myeloma at UC San Diego Health: A single-institution experience

Friday, September 27, 2024

Farid Ghamsari, MD

Resident Physician
University of California, San Diego
San Diego, California, United States

Introduction: Teclistamab, a bispecific antibody targeting B-cell maturation antigen (BCMA) expressed on plasma cells, received FDA approval for the treatment of relapsed/refractory (R/R) multiple myeloma (MM) in 2022. Here we describe the real-world experience of teclistamab at a single institution.

Methods: We retrospectively reviewed patients with R/R MM who received teclistamab at University of California, San Diego and had at least 6 months of follow up. Baseline characteristics, efficacy outcomes, and safety outcomes were collected. Kaplan-Meier method was used to describe survival.

Results: A total of 25 patients who received teclistamab between 01/01/2023 and 11/15/2023 were included in this analysis. The median age was 67 years old (range 46-86). Median prior lines of therapy was 5 (range 3-11). Twenty-four patients had triple-exposed disease; 23 had penta-exposed disease. Extramedullary plasmacytomas were present in 48% of patients at time of teclistamab initiation; 32% had received prior BCMA therapy (2 belantamab, 6 idecabtagene vicleucel) before teclistamab. Cytogenetics profiles were available for 20 patients; 17 (85%) had high risk cytogenetics (t(4;14), t(14;16), t(14;20), Del17p, Gain1q). 9 had a single high-risk mutation, 7 had two, and 1 had three. Cytokine release syndrome (CRS) occurred in 17 patients (68%), (3 (18%) grade 2, no grade 3-5); 8 (47%) received tocilizumab. Immune effector cell-associated neurotoxicity syndrome (ICANS) incidence occurred in 2 patients (8%), (1 (50%) grade 2, no grade 3-5). Pain crisis occurred in 6 patients (24%), of whom 2 (33%) discontinued treatment after crisis. Infection occurred in 60% of patients. Of 21 discrete infections, 10 (48%) were grade 1-2, 11 (52%) ≥ grade 3; 2 (13%) were grade 5. The overall response rate (ORR) by IMWG criteria was 57%. Median duration of response for the entire cohort was not reached. Median progression-free survival (PFS) was 5.8 months (95% CI 3.2 – not reached (NR)); median overall survival (OS) was NR (95% CI NR–NR). Univariate analyses showed no statistically significant relationship between response and prior BCMA therapy (p = 1), response and presence of extramedullary disease (p = .25), or response and high-risk cytogenetics (p = .06). Upon subgroup analysis of PFS, higher risk cytogenetics were associated with lower PFS (HR = 9.7, 95% CI 2.1 - 45.1; p< .001). PFS did not vary between subgroups with or without prior BCMA therapy (p = 0.79), or with or without extramedullary disease (p=0.38).

Conclusions: Overall, the incidence and grades of CRS, ICANS, and infection in our cohort were similar to those observed in the phase I/II MajesTEC-1 trial. The ORR was also comparable. In contrast, the PFS in this study was lower compared to the MajesTEC-1 study. Considering the association between high risk cytogenetics and poor PFS described, this difference may be in part due to the higher proportion of patients with high-risk cytogenetics in our population vs the trial population.