Multiple myeloma (MM) is an inherently incurable plasma cell malignancy characterized by periods of prolonged remissions and inevitable relapses. With a median progression-free survival (PFS) of 3 to 4 months and an overall survival (OS) of less than 12 months, triple-class refractory patients represent a significant unmet need in the treatment landscape of relapsed refractory multiple myeloma (RRMM) [ 1 ]. With its uniform expression and pivotal role in plasma cell proliferation, B-cell maturation antigen (BCMA) represents an ideal therapeutic target for an antibody-drug conjugate (ADC) known as belantamab mafodotin [ 2 , 3 ] Despite the initial accelerated approval as monotherapy for RRMM patients who had failed ≥4 prior lines of therapy (LOT), subsequent randomized confirmatory trial (DREAMM-3) failed to demonstrate statistically significant improvement in outcomes, leading to the withdrawal of belantamab mafodotin from the US market in November 2022 [ 4 , 5 ]. However, data from recent phase III randomized controlled trials (DREAMM-7 and DREAMM-8) [ 6 , 7 ] demonstrated significant improvements in depth and duration of response with belantamab mafodotin combination therapies when compared to standard-of- care treatments for RRMM. With the imminent return of belantamab mafodotin to the U.S. market and expected utilization in clinical practice, we report the real-world safety and efficacy outcomes of standard-of-care belantamab mafodotin for RRMM, with the aim to determine the patterns of its use in a real-world population and highlight the outcomes in high-risk patients who would have been otherwise considered ineligible to receive belantamab mafodotin in a clinical trial.
In this study, we conducted a retrospective chart review of adult patients with RRMM who were treated with belantamab mafodotin monotherapy under the FDA-approved label from October 10, 2019 till September 28, 2023. A total of 81 patients with RRMM were included in the analysis, with baseline patient and disease characteristics highlighted in Table 1 . The median age of the entire patient population was 67 years (range 37–85), with 63% of the patients being male. With a median of 5 (range 2–10) prior lines of therapy, 92, 45, and 15% of the patients were triple-class refractory, penta-class refractory, and BCMA-refractory, respectively. More than half (57%) of the patients had high-risk cytogenetics, 37% had extramedullary disease (EMD), 37% had an Eastern Cooperative Oncology Group (ECOG) performance status (PS) of 2–4, and 67% of the patients would have been considered ineligible for the DREAMM-2 trial. Table 1 Baseline patient and disease characteristics. Characteristic N (%) Male 51/81 (63) Female 30/81 (37) Age median (range) 67 (37–85) Age >70 years 34/81 (42) Race, n (%) Non-Hispanic White 62 (77) Non-Hispanic Black 14 (17) Asian 1 (2) Hispanic 3 (4) Cardiac dysfunction (LVEF <40%), n (%) 11/81 (14) Renal dysfunction (GFR <60 mL/min), n (%) 35/81 (47) Lung dysfunction (COPD or asthma), n (%) 10/81 (12) Baseline cytopenia, grade 3+, n (%) 19/81 (23) IgG subtype, n (%) 44/81 (54) R-ISS stage Stage I, (%) 14/67 (21) Stage II, (%) 22/67 (33) Stage III, (%) 31/67 (46) ECOG PS, n (%) 0–1 51/81 (63) 2–4 30/81 (37) High-risk cytogenetics n (%) Del(17p) 12/81 (15) t(4;14) 14/81 (17) t(14;16) 1/81 (1) gain/amp 1q 33/81(41) EMD, n (%) 30/81(37) Prior LOT, median (range) 5 (2–10) ≥4 LOT, n (%) 65/81 (80) Refractory status n (%) PI 73/81 (91) IMiD 76/81 (94) BCMA 12/81 (15) BsAB 7/12 (58) CAR T 3/12 (25) Trispecific T-cell engager (HPN217) 2/12 (17) Double-refractory 77/81 (95) Triple-refractory 74/81 (91) Penta-refractory 37/81 (46) Prior SCT, n (%) Autologous 55/81 (68) Allogeneic 2/81 (3) Amp amplification, BCMA B-cell maturation antigen, BsAB bispecific antibodies, CAR T chimeric antigen receptor T-cell therapy, COPD chronic obstructive pulmonary disease, ECOG eastern cooperative oncology group, PS performance status, EMD extramedullary disease, Del deletion, GFR glomerular filtration rate, IMiD immunomodulatory drugs, LOT lines of therapy, LVEF left ventricular ejection fraction, PI proteasome inhibitors, R-ISS revised international staging system, SCT stem cell transplant.
Table 1
Baseline patient and disease characteristics.
Amp amplification, BCMA B-cell maturation antigen, BsAB bispecific antibodies, CAR T chimeric antigen receptor T-cell therapy, COPD chronic obstructive pulmonary disease, ECOG eastern cooperative oncology group, PS performance status, EMD extramedullary disease, Del deletion, GFR glomerular filtration rate, IMiD immunomodulatory drugs, LOT lines of therapy, LVEF left ventricular ejection fraction, PI proteasome inhibitors, R-ISS revised international staging system, SCT stem cell transplant.
| Characteristic | N (%) |
| Male | 51/81 (63) |
| Female | 30/81 (37) |
| Age median (range) | 67 (37–85) |
| Age >70 years | 34/81 (42) |
| Race, n (%) | |
| Non-Hispanic White | 62 (77) |
| Non-Hispanic Black | 14 (17) |
| Asian | 1 (2) |
| Hispanic | 3 (4) |
| Cardiac dysfunction (LVEF <40%), n (%) | 11/81 (14) |
| Renal dysfunction (GFR <60 mL/min), n (%) | 35/81 (47) |
| Lung dysfunction (COPD or asthma), n (%) | 10/81 (12) |
| Baseline cytopenia, grade 3+, n (%) | 19/81 (23) |
| IgG subtype, n (%) | 44/81 (54) |
| R-ISS stage | |
| Stage I, (%) | 14/67 (21) |
| Stage II, (%) | 22/67 (33) |
| Stage III, (%) | 31/67 (46) |
| ECOG PS, n (%) | |
| 0–1 | 51/81 (63) |
| 2–4 | 30/81 (37) |
| High-risk cytogenetics n (%) | |
| Del(17p) | 12/81 (15) |
| t(4;14) | 14/81 (17) |
| t(14;16) | 1/81 (1) |
| gain/amp 1q | 33/81(41) |
| EMD, n (%) | 30/81(37) |
| Prior LOT, median (range) | 5 (2–10) |
| ≥4 LOT, n (%) | 65/81 (80) |
| Refractory status n (%) | |
| PI | 73/81 (91) |
| IMiD | 76/81 (94) |
| BCMA | 12/81 (15) |
| BsAB | 7/12 (58) |
| CAR T | 3/12 (25) |
| Trispecific T-cell engager (HPN217) | 2/12 (17) |
| Double-refractory | 77/81 (95) |
| Triple-refractory | 74/81 (91) |
| Penta-refractory | 37/81 (46) |
| Prior SCT, n (%) | |
| Autologous | 55/81 (68) |
| Allogeneic | 2/81 (3) |
With a median follow-up of 11.3 (range 0.3–44.6) months and median number of six cycles (range 1–15) for the entire patient population, best ORR was 40% with 15% of the patients achieving a complete response or better. Partial response, very good partial response, and stable disease were seen in 17, 7, and 23% of the patients, respectively. In comparison, patients with BCMA-refractory disease, penta- refractory disease, and EMD had the best ORR of 17, 24, and 23%, respectively. The median time to first response was 21 days (range 20–42), and the median time to best response was 42 days (range 21–80). Of the 32 patients that responded, the median duration of response was 13 months (range 10.1–26.9). Median PFS was 5 months (range 1–20), and median OS was 12 months (range 3–28) for the entire patient population (Fig. 1A, B ). For patients with high-risk cytogenetics, ECOG 2–4, and EMD at the time of treatment; median PFS was 5 (range 1–12), 3 (range 1–16), and 2 (range 1–5) months, respectively. Similarly, for patients with high-risk cytogenetics, ECOG 2–4, and EMD at the time of treatment; median OS was 9 (range 2–22), 5 (range 2–21), and 5 (range 2–15) months, respectively (Fig. 1C–H ). Using the cox proportional hazard model, the presence of EMD was the only clinical variable associated with inferior PFS (HR = 1.97, 95% CI [1.11, 3.50], p = 0.0205) as well as OS (HR = 3.05, 95% CI [1.71, 5.45], p = 0.0002). At the time of the last follow-up, 58 (72%) patients had experienced disease progression on belantamab mafodotin with most common salvage therapies including alkylating agents (ten patients, 23%), selinexor combinations (eight patients, 19%), and T-cell-directed therapies (seven patients,16%), respectively. Fig. 1 PFS and OS Analysis. A , B Kaplan–Meier curves of median PFS and OS for all patients. C , D Kaplan–Meier curves of PFS and OS for patients with high-risk versus standard risk cytogenetics. E , F Kaplan–Meier curves of PFS and OS for patients with ECOG PS 0–1 versus 2–4. G , H Kaplan–Meier curves of PFS and OS for patients with EMD versus no EMD. PFS progression-free survival, OS overall survival, m median, EMD extramedullary disease, ECOG PS eastern cooperative oncology group performance status, NR not reached.
Regarding ocular toxicity, any grade keratopathy was seen in 56 (69%) patients, with 24 (30%) patients experiencing grade 3 or worse events. The median time to onset of ocular toxicity was 21 days (range 15–98), and the median time to improvement to grade I or complete resolution was 42 (21–180) days. Twenty-six patients (32%) had a visual decline of <20/50 and 17 patients (21%) had a visual decline of <20/200 on the visual acuity scale. A total of 59, 36, and 53% of the patients had dose delay/interruption, dose reduction, and treatment discontinuation, respectively. Furthermore, 18 (22%) patients had greater than 12 consecutive weeks of treatment delay. For hematologic toxicities, 28 (35%), 16 (20%), 23 (28%), and 25 (31%) patients developed grade 3+ leukopenia, neutropenia, anemia, and thrombocytopenia, respectively. More than one-quarter (27%) of the patients experienced an infection, with 17% of all patients developing a severe infection (grade ≥3). At the time of last follow-up, 60 (74%) patients had died with 68, 13, and 12% of these deaths related to disease progression, infection, and organ failure, respectively.
To our knowledge, this multicenter retrospective study is one of the largest real-world reports comprehensively describing clinical outcomes in RRMM patients treated with standard-of-care belantamab mafodotin. In our analysis, this therapy was associated with notable efficacy in patients with heavily pretreated disease who had progressed through multiple LOT, including prior BCMA-directed therapy. There are some reports of real-world experience with belantamab mafodotin, however, these studies are either limited by the small number of patients [ 8 – 10 ] or exclusion of real-world patients under the strict criteria of compassionate use [ 11 ]. While a large study has reported outcomes of belantamab mafodotin in RRMM [ 12 ], our analysis had higher a proportion of high-risk patients with triple and penta-class refractory disease as well as EMD for a comprehensive subgroup analysis to determine clinical predictors of efficacy. While the toxicities noted were similar to the previously published clinical trials, two-third of the patients in our real-world analysis would have been considered ineligible for the DREAMM-2 trial due to severe baseline cytopenias (24%), renal insufficiency (43%), and ECOG PS 3–4 (5%). Despite these differences, response rates in our study were similar to the DREAMM-2 trial patients (ORR 40% versus (vs) 31%; PFS 5 months vs 2.9 months). More importantly, there was no significant increase in the risk of severe ocular (30 vs 27%), and hematologic toxicities, i.e., thrombocytopenia (31 vs 20%) and anemia (28 vs 20%), despite the presence of severe baseline cytopenias and impaired end organ function [ 13 ]. It is important to highlight that the frailty, cytopenias, and organ dysfunction seen in these patients at the time of relapse are often related to prior therapy and disease progression. These patients reflect a real-world population in need of effective treatments, and the presence of one or more of these clinical trial exclusion criteria should not be conceived as a barrier to receiving effective salvage therapies, especially if these are considered safe with manageable toxicities. Similar to published literature, the most common toxicities associated with belantamab mafodotin included keratopathy and decline in visual acuity, with more than two-third of the patients developing ocular toxicities. Keratopathy resolved in a majority of the patients, with a median time to resolution of 6 weeks, and no patients developed permanent blindness. However, this toxicity did lead to more than half (53%) of the patients discontinuing treatment, likely due to the impact on quality of life, raising the need for less frequent dosing. Presence of EMD was a predictor of both inferior PFS as well as OS on multivariable analysis. EMD is considered a high-risk disease feature for RRMM and has been associated with early progression and overall poor prognosis after BCMA-directed and other traditional plasma cell-directed therapies [ 14 , 15 ]. Tumor-driven inhibition of the immune microenvironment likely contributes to the effector and target disparity, because large tumors seen in EMD require more robust activation of host immune effector cells for deep and durable responses. Consideration should be given to combination therapies, including belantamab with pomalidomide/bortezomib and dexamethasone or administering concurrent radiation therapy to enhance the tumoricidal effect. While our study had a small number of patients with exposure to prior BCMA-directed therapy; all of these patients were refractory to this class of drug, and the majority had received BCMA-directed monoclonal antibody. The poor efficacy seen in this subgroup could be related to loss/ downregulation of target antigen or T-cell exhaustion with the ongoing treatment with monoclonal antibody and T-cell engagers. Whether patients with late relapse after CAR T still may be good candidates for retargeting of BCMA with belantamab mafodotin remains an important clinical investigation.
In summary, belantamab mafodotin appeared safe and relatively effective in this real-world heavily pretreated RRMM population, where the majority of patients did not meet the eligibility criteria for the DREAMM-2 trial and had high-risk disease features. Ocular toxicities remained a major therapeutic challenge, highlighting the need for future investigations to optimize dosing and frequency of administration for better tolerability.
Publisher’s note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
Author contributions
RD collected and analysed data and prepared the manuscript. YY provided the statistical analysis. PM contributed to the data collection and reviewed the final manuscript. KB contributed to the data collection and reviewed the final manuscript. CS contributed to the data collection and reviewed the final manuscript. EC contributed to the data collection and reviewed the final manuscript. HS contributed to the data collection and reviewed the final manuscript. JAD contributed to the data collection and reviewed the final manuscript. KMG contributed to the data collection and reviewed the final manuscript. OA contributed to the data collection and reviewed the final manuscript. AR contributed to the data collection and reviewed the final manuscript. BP contributed to the data collection and reviewed the final manuscript. NA contributed to the data collection and reviewed the final manuscript. AA contributed to the data collection and reviewed the final manuscript. HH conceived and designed the study, collected and analysed data, and prepared and finalized the manuscript.
Data availability
The data that support the findings of this study are available from the corresponding author upon reasonable request.
Conflict of interest
Authors RD, KB, YY, EC, HS, KG, OA, AR, BP, and A-OA have no conflicts of interest to disclose. HH disclosed Janssen, Amgen, Honoraria, and Karyopharm as conflicts of interest. PM disclosed Celegene and Pfizer as conflict of interests. CS has disclosed Pfizer, Janssen, Bristol Meyer Squibb, Seagen, and Poseida as conflict of interests. JD has disclosed Janssen Biotech as a conflict of interest. NA has disclosed BMS, Kite/Gilead, and Legend Biotech as conflicts of interest.
Consent to participate
All methods were performed in accordance with the relevant guidelines and regulations. As this is a multicenter consortium study, the study was reviewed and approved by the institutional review boards (incorporating the ethics committee) at each site. As this is a multicenter consortium study utilizing retrospective data, the study was reviewed and approved by the institutional review boards (incorporating ethics committee) at each site, and the need for obtaining informed consent from the participants was waived.
Ethical approval
This multicenter study was a collaborative effort by US Myeloma Innovations Research Collaborative (USMIRC) and was approved by respective institutions’ Institutional Review Board.
References
1. Gandhi UH Cornell RF Lakshman A Gahvari ZJ McGehee E Jagosky M Outcomes of patients with multiple myeloma refractory to CD38-targeted monoclonal antibody therapy Leukemia 2019 33 2266 75 10.1038/s41375-019-0435-7 30858549 PMC6820050 Gandhi UH, Cornell RF, Lakshman A, Gahvari ZJ, McGehee E, Jagosky M, et al. Outcomes of patients with multiple myeloma refractory to CD38-targeted monoclonal antibody therapy. Leukemia. 2019;33:2266–75. 30858549 10.1038/s41375-019-0435-7 PMC6820050
2. Trudel S Lendvai N Popat R Voorhees PM Reeves B Libby EN Antibody–drug conjugate, GSK2857916, in relapsed/refractory multiple myeloma: an update on safety and efficacy from dose expansion phase I study Blood Cancer J 2019 9 37 10.1038/s41408-019-0196-6 30894515 PMC6426965 Trudel S, Lendvai N, Popat R, Voorhees PM, Reeves B, Libby EN, et al. Antibody–drug conjugate, GSK2857916, in relapsed/refractory multiple myeloma: an update on safety and efficacy from dose expansion phase I study. Blood Cancer J. 2019;9:37. 30894515 10.1038/s41408-019-0196-6 PMC6426965
3. Ketchum EB Clarke A Clemmons AB Belantamab mafodotin-blmf: a novel antibody-drug conjugate for treatment of patients with relapsed/refractory multiple myeloma J Adv Pract Oncol 2022 13 77 85 10.6004/jadpro.2022.13.1.7 35173991 PMC8805802 Ketchum EB, Clarke A, Clemmons AB. Belantamab mafodotin-blmf: a novel antibody-drug conjugate for treatment of patients with relapsed/refractory multiple myeloma. J Adv Pract Oncol. 2022;13:77–85. 35173991 10.6004/jadpro.2022.13.1.7 PMC8805802
4. Trudel S Lendvai N Popat R Voorhees PM Reeves B Libby EN Targeting B-cell maturation antigen with GSK2857916 antibody-drug conjugate in relapsed or refractory multiple myeloma (BMA117159): a dose escalation and expansion phase 1 trial Lancet Oncol 2018 19 1641 53 10.1016/S1470-2045(18)30576-X 30442502 PMC6328058 Trudel S, Lendvai N, Popat R, Voorhees PM, Reeves B, Libby EN, et al. Targeting B-cell maturation antigen with GSK2857916 antibody-drug conjugate in relapsed or refractory multiple myeloma (BMA117159): a dose escalation and expansion phase 1 trial. Lancet Oncol. 2018;19:1641–53. 30442502 10.1016/S1470-2045(18)30576-X PMC6328058
5. Lonial S Lee HC Badros A Trudel S Nooka AK Chari A Belantamab mafodotin for relapsed or refractory multiple myeloma (DREAMM-2): a two-arm, randomised, open-label, phase 2 study Lancet Oncol 2020 21 207 21 10.1016/S1470-2045(19)30788-0 31859245 Lonial S, Lee HC, Badros A, Trudel S, Nooka AK, Chari A, et al. Belantamab mafodotin for relapsed or refractory multiple myeloma (DREAMM-2): a two-arm, randomised, open-label, phase 2 study. Lancet Oncol. 2020;21:207–21. 31859245 10.1016/S1470-2045(19)30788-0
6. Hungria V Robak P Hus M Zherebtsova V Ward C Ho PJ Belantamab mafodotin, bortezomib, and dexamethasone for multiple myeloma N Engl J Med 2024 391 393 407 10.1056/NEJMoa2405090 38828933 Hungria V, Robak P, Hus M, Zherebtsova V, Ward C, Ho PJ, et al. Belantamab mafodotin, bortezomib, and dexamethasone for multiple myeloma. N Engl J Med. 2024;391:393–407. 38828933 10.1056/NEJMoa2405090
7. Dimopoulos MA Beksac M Pour L Delimpasi S Vorobyev V Quach H Belantamab mafodotin, pomalidomide, and dexamethasone in multiple myeloma N Engl J Med 2024 391 408 21 10.1056/NEJMoa2403407 38828951 Dimopoulos MA, Beksac M, Pour L, Delimpasi S, Vorobyev V, Quach H, et al. Belantamab mafodotin, pomalidomide, and dexamethasone in multiple myeloma. N Engl J Med. 2024;391:408–21. 38828951 10.1056/NEJMoa2403407
8. Ntanasis-Stathopoulos I Malandrakis P Fotiou D Migkou M Theodorakakou F Roussou M Real-world effectiveness and safety of belantamab mafodotin monotherapy in triple-class refractory multiple myeloma Int J Mol Sci 2023 24 11829 10.3390/ijms241411829 37511588 PMC10380484 Ntanasis-Stathopoulos I, Malandrakis P, Fotiou D, Migkou M, Theodorakakou F, Roussou M, et al. Real-world effectiveness and safety of belantamab mafodotin monotherapy in triple-class refractory multiple myeloma. Int J Mol Sci. 2023;24:11829. 37511588 10.3390/ijms241411829 PMC10380484
9. Alegre A Benzo G Alonso R Martínez-López J Jimenez-Ubieto A Cuéllar C Real-world outcomes of belantamab mafodotin for relapsed/refractory multiple myeloma (RRMM): preliminary results of a Spanish expanded access program (EAP) Oncol Ther. 2023 11 83 96 10.1007/s40487-022-00212-5 36509945 PMC9744371 Alegre A, Benzo G, Alonso R, Martínez-López J, Jimenez-Ubieto A, Cuéllar C, et al. Real-world outcomes of belantamab mafodotin for relapsed/refractory multiple myeloma (RRMM): preliminary results of a Spanish expanded access program (EAP). Oncol Ther. 2023;11:83–96. 36509945 10.1007/s40487-022-00212-5 PMC9744371
10. Vaxman I Abeykoon J Dispenzieri A Kumar SK Buadi F Lacy MQ “Real-life” data of the efficacy and safety of belantamab mafodotin in relapsed multiple myeloma-the Mayo Clinic experience Blood Cancer J 2021 11 196 10.1038/s41408-021-00592-3 34876555 PMC8651684 Vaxman I, Abeykoon J, Dispenzieri A, Kumar SK, Buadi F, Lacy MQ, et al. “Real-life” data of the efficacy and safety of belantamab mafodotin in relapsed multiple myeloma-the Mayo Clinic experience. Blood Cancer J. 2021;11:196. 34876555 10.1038/s41408-021-00592-3 PMC8651684
11. Shragai T Magen H Lavi N Gatt M Trestman S Zektser M Real-world experience with belantamab mafodotin therapy for relapsed/refractory multiple myeloma: a multicentre retrospective study Br J Haematol 2023 200 45 53 10.1111/bjh.18479 36205375 PMC10091809 Shragai T, Magen H, Lavi N, Gatt M, Trestman S, Zektser M, et al. Real-world experience with belantamab mafodotin therapy for relapsed/refractory multiple myeloma: a multicentre retrospective study. Br J Haematol. 2023;200:45–53. 36205375 10.1111/bjh.18479 PMC10091809
12. Talbot A Bobin A Tabone L Lambert J Boccaccio C Deal C Real-world study of the efficacy and safety of belantamab mafodotin (GSK2857916) in relapsed or refractory multiple myeloma based on data from the nominative ATU in France: the IFM 2020-04 study Haematologica 2023 108 2774 82 10.3324/haematol.2022.281772 37078253 PMC10543185 Talbot A, Bobin A, Tabone L, Lambert J, Boccaccio C, Deal C, et al. Real-world study of the efficacy and safety of belantamab mafodotin (GSK2857916) in relapsed or refractory multiple myeloma based on data from the nominative ATU in France: the IFM 2020-04 study. Haematologica. 2023;108:2774–82. 37078253 10.3324/haematol.2022.281772 PMC10543185
13. Nooka AK Cohen AD Lee HC Badros A Suvannasankha A Callander N Single-agent belantamab mafodotin in patients with relapsed/refractory multiple myeloma: final analysis of the DREAMM-2 trial Cancer 2023 129 3746 60 10.1002/cncr.34987 37622738 PMC11055177 Nooka AK, Cohen AD, Lee HC, Badros A, Suvannasankha A, Callander N, et al. Single-agent belantamab mafodotin in patients with relapsed/refractory multiple myeloma: final analysis of the DREAMM-2 trial. Cancer. 2023;129:3746–60. 37622738 10.1002/cncr.34987 PMC11055177
14. Rees MJ Mammadzadeh A Bolarinwa A Elhaj ME Bohra A Bansal R Clinical features associated with poor response and early relapse following BCMA-directed therapies in multiple myeloma Blood Cancer J 2024 14 122. 10.1038/s41408-024-01081-z 39043638 PMC11266661 Rees MJ, Mammadzadeh A, Bolarinwa A, Elhaj ME, Bohra A, Bansal R, et al. Clinical features associated with poor response and early relapse following BCMA-directed therapies in multiple myeloma. Blood Cancer J. 2024;14:122. 39043638 10.1038/s41408-024-01081-z PMC11266661
15. Hashmi H Hansen DK Peres LC Puglianini OC Freeman C De Avila G Factors associated with refractoriness or early progression after idecabtagene vicleucel in patients with relapsed/ refractory multiple myeloma: US Myeloma Immunotherapy Consortium real world experience Haematologica 2024 109 1514 24 37855036 10.3324/haematol.2023.283888 PMC11063864 Hashmi H, Hansen DK, Peres LC, Puglianini OC, Freeman C, De Avila G, et al. Factors associated with refractoriness or early progression after idecabtagene vicleucel in patients with relapsed/ refractory multiple myeloma: US Myeloma Immunotherapy Consortium real world experience. Haematologica. 2024;109:1514–24. 37855036 10.3324/haematol.2023.283888 PMC11063864