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    Cellular and T cell engager Immunotherapy

    Category: Cellular and T cell engager Immunotherapy

    Consolidative Use of BCMA CAR-T Therapy in Relapsed/Refractory Myeloma — A Retrospective Evaluation

    (PA-081) Consolidative Use of BCMA CAR-T Therapy in Relapsed/Refractory Myeloma — A Retrospective Evaluation

    Friday, September 19, 2025
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    Introduction: In initial trials of BCMA-CAR-T cells in heavily (≥4 lines) relapsed/refractory multiple myeloma (RRMM), most patients (pts) were refractory to their most recent regimen at time of apheresis. This approach (ie. waiting until pts are progressing before moving to CAR-T) can lead to difficulty controlling disease during manufacturing, undermining CAR-T clinical use. We hypothesized that using CAR-T cells as a planned consolidation strategy may lead to lower toxicity and improved long-term outcomes.

    Methods: We retrospectively reviewed all RRMM pts treated with commercial BCMA CAR-T cells (ide-cel and cilta-cel) at our institution from 6/2021 to 5/2024 (follow-up through 2/2025). Pts were considered to have CAR-T therapy as consolidation if their pre-apheresis therapy was identical to their bridging therapy, or if consolidation was clearly intended by chart review. Responses were determined by IMWG criteria.  T-cell phenotyping at time of apheresis was performed by flow cytometry.

    Results:

    Among 158 treated patients (median follow-up 22.6 months), 83 received CAR-T as consolidation.  Median prior lines in these pts was 6, with 76% triple-class refractory, 16% with prior BCMA therapy. Carfilzomib-based triplets were the most common pre-/post-apheresis therapy.  At time of apheresis, 10% had PD, 39% SD, 35% PR, and 16% ≥VGPR. 53% received cilta-cel and 47% ide-cel.  Post-CAR-T infusion, 83% achieved ≥VGPR (88% for cilta-cel and 77% ide-cel). Median PFS was not reached for cilta-cel (18-month PFS: 83%) and was 16.5 months for ide-cel. OS at 18 months was 89% in cilta-cel and 82% in ide-cel pts. Grade ≥3 CRS was 3.6%, any grade ICANS 8.4%, and delayed neurotoxicity 6%. We then compared these pts to those who did not receive CAR-T as a consolidative approach (no-consolidation group, 75 pts).  Clinical characteristics were comparable between groups. As expected, the no-consolidation group had poorer disease control at both apheresis and pre-lymphodepletion, and greater disease burden at apheresis. After CAR-T treatment, consolidation group pts had higher: ≥VGPR rates (83% vs 66%, p=0.02), PFS (not reached vs 8 months. p< 0.01), and OS (cilta-cel subgroup only: OS 18 months 88% vs 70%, p=0.02), and lower ICANS (8% vs 19%) and CRS≥G3 (3.6% vs 8%). No differences in delayed neurotoxicity were seen. In multivariate Cox regression, extramedullary disease, high-risk cytogenetics, ide-cel, and absence of consolidation intent were associated with inferior PFS.  Pts in the no-consolidation group who responded to bridging still had inferior PFS compared to the consolidation group.

    Conclusions: Late-line RRMM pts moving to CAR-T cells as consolidation of their current line demonstrated higher CAR-T response rates, longer PFS and OS, and reduced severe toxicity, supporting the use of CAR-T as a consolidation strategy in RRMM. These findings should be confirmed prospectively.  Comparative analyses of apheresis T-cell phenotypes will be presented at the meeting.