CAR-T cells co-targeting BCMA and CD19 in RRMM: Results from the UKMRA Phase 1 MCARTY trial in relapsed refractory multiple myeloma

Abstract Introduction: BCMA directed CAR-T cell therapy for multiple myeloma (MM) shows promise, but relapses continue to occur despite deep responses. Hypothesizing that increased persistence may prolong responses, we developed a CAR-T cell product double transduced to co-express a highly sensitive, Fab-based BCMA CAR (D8) and a CD19 CAR from obecabatagene autoleucel (also known as CAT19), which is known to drive long-term persistence. Methods: The MCARTY trial (NCT04795882) is a single centre, Phase 1 dose escalation trial uniquely designed with two cohorts to iteratively evaluate D8 CAR-T cells (Cohort 1) and D8/CAT19 CAR-T cells (Cohort 2) in patients with relapsed/refractory MM at a dose of 50 or 150x106 CARs. Inclusion criteria are: progression or stable disease to last treatment, 3 or more previous lines of therapy, exposure to proteasome inhibitors (PI), immunomodulatory drugs (IMID) and CD38 antibodies, ECOG 0/1. Selection was not based on prior BCMA exposure. Notably, dual transduction in Cohort 2 results in 3 populations of CAR-T cells (D8+CAT19-, D8-CAT19+, D8+CAT19+) which can be individually tracked in patients. Results: As of 30th June 2025, 15 patients have been treated, 6 patients with D8 CAR (n=3 at each dose level) and 9 patients with D8/CAT19 CAR-T cells (3 and 6 patients at the lower and higher dose levels respectively). Median age was 50 (range 33-66), previous lines of therapy 4 (range 3-8) and 5 patients (33.3%) had high risk cytogenetics. Doses were well tolerated, CRS was seen in 14 (93%), all Grade 1-2, there was one case of Grade 1 ICANS and no other neurotoxicity. At a median follow up of 21 months, clinical responses ≥PR were seen in 14 patients (ORR 93%). Twelve achieved a CR/sCR (80%, 11/11 evaluable were MRD- to 10-5 by clonoSEQ). Overall median PFS was 18 months (95% CI 5-N/A). Prolonged remissions (>24 months) have been observed in 3 patients from both cohorts so far. Median PFS in Cohort 1(D8) and Cohort 2(D8/CAT/19) were 15 (95% CI 5-N/A) and 18 months (95% CI 2-N/A) respectively. The persistence of CARs was variable between patients and while D8 CAR expansion in the first month (28D AUC) was similar in both cohorts, D8 CARs were detectable up to 3 months (median 2) in Cohort 1 and 5 months (median 3) in Cohort 2. We had hypothesized that the persistence of CAT19 would result in improved survival of D8+CAT19+ cells compared to D8+ cells. In contrast, we observed expansion of both dual and single targeting CARs but persistence of dual D8+CAT19+ CARs was consistently less than that of single transduced CARs. As a possible explanation, by single cell RNA sequencing, an apoptotic signature score (including genes FOS, FASLG, BCL2A1, TNF, calculated by UCell) was increased in D8+CAT19+ compared to single targeting CARs (p<0.01). Further, overnight activation with plate bound CD19 and BCMA of the CAR product caused over-expression of genes mediating INF-a, INF-g, inflammatory responses and NFKB signalling pathways in all populations. However, activation of D8+CAT19- CARs appeared greater in Cohort 2 vs 1 (p<0.01). Together, this data indicates variability in single vs dual targeting CARs with D8+CAT19+ CARs having an increased susceptibility to apoptosis and a suggestion that D8+CAT19+ and D8-CAT19+ may support activation of D8+CAT19- CARs in patients receiving the dual transduced product. Summary: Data from the first 15 patients in the Phase 1 MCARTY trial indicate safety and a high ORR in patients treated with CAR-T cells targeting BCMA alone or dual transduced to target BCMA and CD19. There is a suggestion that a dual targeting strategy can increase BCMA CAR activation and persistence but not through the expected mechanism of being ‘piggy-backed’ on the CD19 CAR-T cells. We have thus modified the manufacturing process to equalize the proportion of single and dual expressing CARs in the D8/CAT transduced product and are introducing a higher dose level to improve persistence and potentially outcomes. We have also initiated the Phase 1 ALARIC study (ISRCTN49320109) of D8 and D8/CAT19 in systemic AL amyloidosis.

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Blood
Published
2025-11-03
DOI
https://doi.org/10.1182/blood-2025-4173
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CAR-T cell therapy research
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article

CAR-T cells co-targeting BCMA and CD19 in RRMM: Results from the UKMRA Phase 1 MCARTY trial in relapsed refractory multiple myeloma

Christopher Parrish, Bilyana Popova, B Jarman, Eileen M. Boyle et al.
Blood
CAR-T cell therapy research
article

CAR-T cells co-targeting BCMA and CD19 in RRMM: Results from the UKMRA Phase 1 MCARTY trial in relapsed refractory multiple myeloma

Christopher Parrish, Bilyana Popova, B Jarman, Eileen M. Boyle, Giulia Agliardi, Claire Roddie, Maeve A O'Reilly, Martin Pulé, Yashma Pathak, William Wilson, Evie Lewin, Amatta Mirandari, Victoria J. Spanswick, Lydia Lee, Helen Holmes, Owen Bain, Kwee Yong, Louisa Green, Simon Thomas, Catriona Mactier, Rakesh Popat, John García, Juliana Pinto, Mhairi Vaughan, Aditya Prabu, Eleanor Wooderson, Cristina Realingo, Zainab Kalokoh
article en

Abstract

Abstract Introduction: BCMA directed CAR-T cell therapy for multiple myeloma (MM) shows promise, but relapses continue to occur despite deep responses. Hypothesizing that increased persistence may prolong responses, we developed a CAR-T cell product double transduced to co-express a highly sensitive, Fab-based BCMA CAR (D8) and a CD19 CAR from obecabatagene autoleucel (also known as CAT19), which is known to drive long-term persistence. Methods: The MCARTY trial (NCT04795882) is a single centre, Phase 1 dose escalation trial uniquely designed with two cohorts to iteratively evaluate D8 CAR-T cells (Cohort 1) and D8/CAT19 CAR-T cells (Cohort 2) in patients with relapsed/refractory MM at a dose of 50 or 150x106 CARs. Inclusion criteria are: progression or stable disease to last treatment, 3 or more previous lines of therapy, exposure to proteasome inhibitors (PI), immunomodulatory drugs (IMID) and CD38 antibodies, ECOG 0/1. Selection was not based on prior BCMA exposure. Notably, dual transduction in Cohort 2 results in 3 populations of CAR-T cells (D8+CAT19-, D8-CAT19+, D8+CAT19+) which can be individually tracked in patients. Results: As of 30th June 2025, 15 patients have been treated, 6 patients with D8 CAR (n=3 at each dose level) and 9 patients with D8/CAT19 CAR-T cells (3 and 6 patients at the lower and higher dose levels respectively). Median age was 50 (range 33-66), previous lines of therapy 4 (range 3-8) and 5 patients (33.3%) had high risk cytogenetics. Doses were well tolerated, CRS was seen in 14 (93%), all Grade 1-2, there was one case of Grade 1 ICANS and no other neurotoxicity. At a median follow up of 21 months, clinical responses ≥PR were seen in 14 patients (ORR 93%). Twelve achieved a CR/sCR (80%, 11/11 evaluable were MRD- to 10-5 by clonoSEQ). Overall median PFS was 18 months (95% CI 5-N/A). Prolonged remissions (>24 months) have been observed in 3 patients from both cohorts so far. Median PFS in Cohort 1(D8) and Cohort 2(D8/CAT/19) were 15 (95% CI 5-N/A) and 18 months (95% CI 2-N/A) respectively. The persistence of CARs was variable between patients and while D8 CAR expansion in the first month (28D AUC) was similar in both cohorts, D8 CARs were detectable up to 3 months (median 2) in Cohort 1 and 5 months (median 3) in Cohort 2. We had hypothesized that the persistence of CAT19 would result in improved survival of D8+CAT19+ cells compared to D8+ cells. In contrast, we observed expansion of both dual and single targeting CARs but persistence of dual D8+CAT19+ CARs was consistently less than that of single transduced CARs. As a possible explanation, by single cell RNA sequencing, an apoptotic signature score (including genes FOS, FASLG, BCL2A1, TNF, calculated by UCell) was increased in D8+CAT19+ compared to single targeting CARs (p<0.01). Further, overnight activation with plate bound CD19 and BCMA of the CAR product caused over-expression of genes mediating INF-a, INF-g, inflammatory responses and NFKB signalling pathways in all populations. However, activation of D8+CAT19- CARs appeared greater in Cohort 2 vs 1 (p<0.01). Together, this data indicates variability in single vs dual targeting CARs with D8+CAT19+ CARs having an increased susceptibility to apoptosis and a suggestion that D8+CAT19+ and D8-CAT19+ may support activation of D8+CAT19- CARs in patients receiving the dual transduced product. Summary: Data from the first 15 patients in the Phase 1 MCARTY trial indicate safety and a high ORR in patients treated with CAR-T cells targeting BCMA alone or dual transduced to target BCMA and CD19. There is a suggestion that a dual targeting strategy can increase BCMA CAR activation and persistence but not through the expected mechanism of being ‘piggy-backed’ on the CD19 CAR-T cells. We have thus modified the manufacturing process to equalize the proportion of single and dual expressing CARs in the D8/CAT transduced product and are introducing a higher dose level to improve persistence and potentially outcomes. We have also initiated the Phase 1 ALARIC study (ISRCTN49320109) of D8 and D8/CAT19 in systemic AL amyloidosis.

BloodVol. 146(Supplement 1)
University College London Hospitals NHS Foundation Trust (GB), Leeds Teaching Hospitals NHS Trust (GB), Cancer Research UK (GB), London Cancer (GB), CRUK Lung Cancer Centre of Excellence (GB), Karus Therapeutics (United Kingdom) (GB), University College London (GB)
Openalex Percentile: Top 46%
CAR-T cell therapy research
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