Нейрологическая токсичность, не связанная с ИКАНС, после терапии BCMA CAR-T: систематический обзор и метаанализ 4630 Пациенты с множественной миеломой.

Introduction

B-cell maturation antigen (BCMA)–directed chimeric antigen receptor T-cell (CAR-T) therapies for multiple myeloma, including idecabtagene vicleucel (ide-cel) and ciltacabtagene autoleucel (cilta-cel), have transformed the treatment landscape for patients with relapsed or refractory disease, producing deep and durable remissions in patients with heavily pretreated disease. 1 , 2 Despite these therapeutic advances, CAR-T therapies are associated with immune-mediated toxicities that can significantly affect quality of life and mortality. 3 , 4

The most well-characterized toxicities include cytokine release syndrome, an acute systemic inflammatory response due to CAR-T activation, and immune effector cell–associated neurotoxicity syndrome (ICANS), which encompasses a range of neurologic manifestations including altered mental status and encephalopathy. ICANS occurs in ∼10% to 20% of patients receiving commercial BCMA-directed CAR-T products and is supported by standardized grading systems and management guidelines designed to address and mitigate its occurrence. 5 , 6 , 7 In contrast, there is emerging focus on a less frequent and incompletely characterized collection of non-ICANS neurotoxicities (NINTs), that includes Parkinson-like motor and neurocognitive treatment-emergent adverse events (movement and neurocognitive toxicities [MNTs]), cranial nerve palsies, peripheral neuropathies including Guillain-Barré syndrome, among others. 8 , 9 These events, sometimes also referred to as delayed neurotoxicities, typically occur after the resolution of cytokine release syndrome and ICANS, underscoring their distinct clinical course. 9 Although rare, NINTs are often severe, prolonged, and functionally devastating. Inconsistent terminology, variable follow-up, and predefined reporting windows have limited accurate estimation of NINT incidence, with existing literature providing fragmented risk estimates.

To address these gaps, we conducted a systematic review and meta-analysis of clinical trials and real-world studies evaluating US Food and Drug Administration (FDA)–approved and investigational CAR-T therapies in multiple myeloma, with a specific focus on NINTs. Our objectives were to quantify the occurrence of NINTs, characterize its clinical presentation, and evaluate study-level factors associated with increased risk. By synthesizing data across heterogeneous sources, this analysis aims to improve recognition of this rare but serious toxicity.

Methods

Study design and literature search

A systematic search was performed in the PubMed and Embase databases for articles published until 2 October 2025 using predefined combinations of keywords and controlled vocabulary for plasma cell disorders (multiple myeloma, monoclonal gammopathy of undetermined significance, smoldering myeloma, and amyloidosis), CAR-T therapies, and relevant targets (BCMA and G protein–coupled receptor class C group 5 member D [GPRC5D]). For Embase only, the search strategy additionally incorporated terms for neurologic toxicity outcomes (see study protocol in the supplemental Table 1 ). Searches were limited to English-language publications and excluded reviews, meta-analyses, conference abstracts, case reports, small series (<10 patients), and nonoriginal articles. MEDLINE-indexed records were excluded from the Embase search to avoid duplication. After title and abstract screening, full-text articles were independently assessed by 2 investigators (H.v.B. and G.O.) for eligibility according to predefined inclusion criteria, all of which were required to be met:

adult patients with cancer with either multiple myeloma, monoclonal gammopathy of undetermined significance, smoldering multiple myeloma, or amyloid light chain amyloidosis;

use of CAR-T products targeting BCMA or GPRC5D in a clinical trial or real-world setting, including both FDA-approved CAR-T products (ide-cel and cilta-cel) along with any unapproved CAR-T products whose phase 1 and/or 2 results had been fully published;

data available on NINTs;

full-text available in English.

After this initial process of identifying appropriate studies, cohorts were further restricted to BCMA-targeted CAR-T constructs with any non-BCMA target study (ie, GPRC5D) excluded due to low numbers of studies. This study followed the PRISMA (preferred reporting items for systematic reviews and meta-analyses) guidelines for reporting systematic reviews (see study protocol and PRISMA checklist in the supplemental Figure 1 ) and was prospectively registered to the PROSPERO database (study number: CRD42024542037). 10 To mitigate double counting, overlapping cohorts were removed. In some cases, multiple studies on the same patient population were used to extract baseline characteristics and a summative total of NINT cases.

Data extraction

For all studies meeting inclusion criteria, 2 independent investigators (H.v.B. and G.O.) extracted variables such as study type (clinical trial vs real-world study), CAR-T product category (ide-cel, cilta-cel, or experimental), sample size, median age, median number of previous lines of therapy, median follow-up time (months), enrollment start dates, and cohort-level proportions for relevant previous exposures (previous autologous stem cell transplantation [ASCT], previous BCMA-directed therapy, and bridging therapy), when reported. The primary end point was the frequency and distribution patterns of NINTs after BCMA CAR-T therapy. In cases in which multiple CAR-T products were used within a single study, the study was separated into distinct cohorts for separate analysis wherever possible.

Statistical analysis

All analyses were performed in R version 2025.05.1 using the meta and metafor packages. Pooled NINTs point estimates were estimated via random-effects meta-analysis of single proportions using a generalized linear mixed model with logit transformation of proportions. 11 The Clopper-Pearson interval was used to compute 95% confidence intervals (95% CI) for within-study proportions. 12 Between-study heterogeneity was assessed using Cochran Q and quantified using I 2 (25%, 50%, and 75% reflect low, moderate, and high between-study heterogeneity, respectively) and τ 2 was estimated using maximum likelihood, as specified. Prespecified subgroup analyses were performed using random-effects meta-analyses. Univariate meta-regressions were performed to examine the association between NINTs point estimates and the following variables: product (cilta-cel vs ide-cel vs experimental vs combined cilta-cel/ide-cel), study type (real-world vs clinical trial), median follow-up, median age, median previous lines, enrollment year, proportion of patients with ICANS, previous bridging proportion, previous ASCT proportion, and previous BCMA-directed therapy exposure proportion. Meta-regressions were performed using random-effects models using the maximum likelihood estimator. 13 Model coefficients and 95% CI were evaluated using the Knapp-Hartung adjustment. 14

Distribution of NINT entities

When NINT subtype information was available, events were categorized as MNT, cranial neuropathy, peripheral neuropathy, and other.

Quality assessment and sensitivity analyses

Funnel plots and Egger regression tests were used to assess small-study effects and reporting bias. The Joanna Briggs Institute appraisal tool was used to further assess bias of each individual article ( supplemental Table 2 ). 15 We performed sensitivity analyses (1) restricted to cilta-cel cohorts only, (2) excluding heterogeneous “other” NINTs, (3) excluding small real-world cohorts (<20 patients) to evaluate the robustness of pooled estimates to small-study contributions in real-world data, (4) of fixed-effects vs random-effects pooled subgroup estimates, and (5) of leave-one-out influence.

Results

Study cohort

A total of 975 articles were identified through the systematic literature search. After removal of duplicates and screening of titles and abstracts, 206 studies were assessed for eligibility, of which 78 met the predefined inclusion criteria ( supplemental Figure 1 ). Seven studies examined GPRC5D-directed products 16 , 17 , 18 , 19 , 20 , 21 , 22 and were removed from subsequent analysis. Four studies were noted to have <10 patients 23 , 24 , 25 , 26 and were removed from analysis. Merging of publications that reported on the same patient population ultimately yielded 50 distinct studies in the meta-analysis spanning 4630 patients ( Table 1 ). Of these studies, 5 studies 7 , 27 , 28 , 29 , 30 reported on multiple CAR-T entities and were further subdivided into distinct cohorts. Of these 55 cohorts, 35 were from clinical trials and 20 from real-world studies. Overall, 9 cohorts assessed cilta-cel, 12 cohorts assessed ide-cel, 30 assessed experimental constructs, and 4 studies assessed both cilta-cel and ide-cel and could not be further separated into subcohorts.

Cilta-cel has the highest NINTs point estimate among all CAR-T products

Across all 4630 patients, the overall NINTs point estimate was 0.81% (95% CI, 0.37-1.77), with a median follow-up of 12.6 months ( supplemental Figure 2 ).

NINTs point estimates differed significantly by product. Cilta-cel was associated with a markedly higher NINTs point estimate compared with ide-cel (4.6% vs 0.5%; P = .001) and compared with experimental constructs (4.6% vs 0.3%; P = .02), whereas NINTs point estimates were similar between ide-cel and experimental constructs (0.5% vs 0.3%; P = .63; Figures 1 and 2 A).

Influence of study features and previous exposures on NINTs point estimates

To assess the influence of study features and previous exposures on NINTs point estimates, we performed subgroup analyses by study type, follow-up, age, previous lines of therapy, enrollment year, previous bridging, previous ASCT, and previous BCMA exposure ( supplemental Figures 3-10 ).

No significant differences in NINTs point estimates were observed across key study-level characteristics. Specifically, NINTs point estimates did not differ between clinical trial cohorts and real-world studies (0.4% vs 1.4%; P = .17; Figure 2 B), studies with follow-up durations above vs below the median (0.5% vs 0.9%; P = .53; Figure 2 C), or studies with a median age of <65 years compared with at least 65 years (0.6% vs 1.2%; P = .33; Figure 2 D). Similarly, NINTs point estimates were comparable in studies with <5 vs ≥5 median previous lines of therapy (0.9% vs 0.8%; P = .86; Figure 2 E), as well as by enrollment era, with similar rates in studies enrolling patients before January 2021 vs January 2021 or later (0.4% vs 0.8%; P = .49; Figure 2 F).

With respect to previous treatment exposures, studies with bridging therapy use above the cohort median demonstrated numerically higher NINTs point estimates than those below the median (2.3% vs 0.6%), although this difference did not reach statistical significance ( P = .15; Figure 2 G). Likewise, NINTs point estimates were similar between studies with a proportion of patients with previous ASCT below vs above the median (0.7% vs 0.5%; P = .65; Figure 2 H). In contrast, studies with a lower proportion of patients previously exposed to BCMA-directed therapy exhibited higher NINTs point estimates than studies above the cohort median, a difference that approached statistical significance (2.7% vs 0.7%; P = .067; Figure 2 I).

To assess study-level factors associated with NINTs point estimates, we first performed univariate random-effects meta-regression analyses across prespecified covariates. In univariate analyses, only CAR-T product was significantly associated with NINTs point estimates, with ide-cel and experimental products associated with lower NINTs point estimates than cilta-cel ( P = .0007 and P = .007, respectively; supplemental Table 3 ). Next, we conducted a multivariable random-effects meta-regression restricted to covariates with data available in ≥80% of included studies in order to preserve statistical power and limit bias from missing data. In this model, ide-cel and experimental products were associated with lower NINTs point estimates than cilta-cel ( P = .05 and P = .02, respectively), whereas ide-cel/cilta-cel combination studies were associated with higher NINTs than cilta-cel alone ( P = .007; Table 2 ). Furthermore, higher study-level ICANS proportions were associated with lower NINTs point estimates ( P = .02), whereas studies with higher proportions of patients with previous ASCT were more likely to have higher NINTs estimates ( P = .03; Table 2 ).

Distribution of NINT subtypes

To further characterize the spectrum of NINTs after BCMA-directed CAR-T therapy, we performed a detailed analysis of reported NINT phenotypes across included studies. NINT events were categorized into 4 mutually exclusive clinical groups: MNT, cranial neuropathy, peripheral neuropathy, and other non-ICANS neurologic events that were not easily summarized in 1 category ( Figure 3 ). Among 127 NINT events identified across 4630 treated patients, events classified as “other” NINTs represented the largest proportion (48.1%, 64 events), followed by cranial nerve palsies (32.3%, 43 events), MNTs (12%, 16 events), and peripheral neuropathy (7.5%, 10 events) ( Figure 3 A).

Cranial neuropathies represented the most phenotypically consistent NINT subtype and were largely characterized by isolated cranial nerve deficits, most commonly facial nerve palsy, followed by diplopia and other focal cranial neuropathies. These events were frequently reported as delayed-onset neurologic complications occurring weeks to months after CAR-T infusion and were typically distinct from ICANS-associated symptoms. MNTs comprised a clinically distinct subset of NINT events marked by movement disorder or motor-predominant phenotypes. Reported manifestations included parkinsonism or Parkinson-like syndromes, or simply unspecified MNTs. Peripheral neuropathy events were less frequent and included polyneuropathy, Guillain-Barré syndrome, and critical illness–related polyneuropathy. These events were clinically distinct from both cranial nerve palsies and MNTs and were generally described as peripheral nervous system complications rather than central neurotoxicity. The “other” NINTs category encompassed a heterogeneous group of neurologic events that could not be reliably assigned to a single anatomic or mechanistic category. This included delirium or encephalopathy not meeting ICANS criteria, cerebellar toxicity, seizure activity, syncope, and neurologic adverse events lacking sufficient phenotypic detail for classification. As a result, a substantial proportion of NINT events could not be confidently subclassified and were conservatively grouped as “other.”

Next, we examined the distribution of NINT subtypes stratified by CAR-T product ( Figure 3 B). Among cilta-cel–associated events, cranial nerve palsies were the most prevalent subtype, accounting for 42% of total events, followed by “other” (30%), MNT (19%), and peripheral neuropathy (9%). In contrast, all NINT events reported in experimental CAR-T constructs were classified as “other” (100%), reflecting heterogeneous and insufficiently specified neurologic phenotypes. Among ide-cel–associated NINTs events, most were similarly categorized as “other” (73%), with smaller proportions attributable to cranial nerve palsies (13%), peripheral neuropathies (13%), and 0 attributable to MNT. Further detail on distribution of NINT subtype and characteristics of “other” NINTs is available in supplemental Table 4 .

Sensitivity analyses

In a sensitivity analysis excluding real-world studies enrolling <20 patients, 52 studies comprising 4594 patients and 123 NINT events were included. The pooled NINTs point estimates remained similar at 0.72% (95% CI, 0.31-1.64) with similar heterogeneity (I 2 = 59.0%) compared with the primary analysis indicating that results were not driven by small real-world studies. In sensitivity analyses comparing fixed- and random-effects models across subgroups, fixed-effects models consistently produced substantially higher NINTs estimates and statistically significant between-group differences that were largely attenuated or absent under random-effects models ( supplemental Tables 5 and 6 ). Given the clear between-study heterogeneity and dominance of small, high-incidence studies, the random-effects estimates were considered more appropriate for all primary and subgroup inferences. The Egger regression test demonstrated significant funnel plot asymmetry ( P < .0001), suggesting potential publication bias vs true heterogeneity between studies ( supplemental Figure 11 ). 91 A leave-one-out sensitivity analysis showed that omission of any single study did not materially change the pooled NINTs estimate (range, ∼0.74%-0.91%), with heterogeneity remaining stable ( supplemental Figure 12 ).

Because cilta-cel had higher NINTs point estimates than other products, we performed a cilta-cel–only subgroup analysis (n = 9) to see whether additional relationships between NINTs and various study-level characteristics could be identified. In subgroup analyses, no findings reached significance, although there was a signal for higher NINTs point estimates in studies with above-median follow-up (above-median follow-up of 11.1% vs below-median follow-up of 0.5%; P = .10; supplemental Figure 13 ).

Because the “other” category of NINTs encompassed heterogeneous neurologic events that were variably defined across studies, we performed a sensitivity analysis excluding “other” NINTs to assess whether this influenced observed associations with study-level characteristics. Exclusion of “other” NINTs did not materially alter the results, and no subgroup analyses demonstrated statistically significant differences in NINTs incidence ( supplemental Figure 14 ).

Discussion

This systematic review and meta-analysis represents, to our knowledge, the first and largest to characterize NINTs after BCMA-directed CAR-T therapies. NINTs are serious side effects but, based on our analysis, remain rare.

We identified cilta-cel as having a higher NINTs point estimate relative to both ide-cel and experimental BCMA CAR-T products currently under development. For patients receiving commercial products, these risks must currently be weighed against the potentially greater efficacy of cilta-cel compared with ide-cel in multiple large retrospective studies, 7 , 29 but it is encouraging that the experimental CAR-T products had a similar point estimate to ide-cel.

We did not find any additional risk factors associated with a higher point estimate of NINTs, including previous ASCT, median lines of therapy, treatment era, and use of bridging therapy. We noted a trend regarding previous BCMA treatment exposure, although this may be confounded by reporting bias because the emergence of alternative BCMA-targeting therapies coincides with heightened awareness of this unique set of toxicities. There is emerging evidence that early and rapid CAR-T expansion as measured by absolute lymphocyte count is associated with a higher point estimate of NINTs, a phenomenon that may be primarily driven by CD4 + CAR-T expansion. 92 , 93 , 94 Similarly, there is a signal that nonresponse to bridging therapy may be an independent predictor of parkinsonism. 95 None of these characteristics could be reliably extracted from our studies. We did not find a substantial difference between the occurrence of NINTs in clinical trials vs real-world studies, pointing to an adequate level of rigor in capturing these rare events in clinical trials, particularly in the phase 3 studies of FDA-approved products.

Our study comes with several limitations. Reporting and publication bias may have led to underestimation in our point estimate, particularly in earlier studies, studies using experimental constructs, and those with inadequate follow-up periods to capture NINTs, which can emerge weeks or even months after infusion. Although we excluded double-counted patient populations when we encountered them, we cannot completely rule out some overlap between real-world studies and clinical trial patients. Consistent with a recent FDA Adverse Event Reporting System analysis, 96 cranial nerve palsies represented the most common discrete NINT, followed by MNTs and peripheral neuropathies. In our study, there was a large number of NINTs that were either not specified or did not fit into either of the 3 previous categories. This speaks to the innate heterogeneity of a toxicity defined by the absence of the clinical characteristics associated with ICANS. Although some studies have found an association with any-grade ICANS and NINTs, 46 the likely overlap between these 2 diagnoses represents a potential confounder. Furthermore, many of the studies that looked at experimental, non–FDA-approved constructs may not have reported NINTs with the rigor required for a reliable point estimate from a meta-analysis.

The underlying mechanism of NINTs is poorly understood. In 1 patient on the CARTITUDE-1 study, BCMA was identified as present in the basal ganglia, 97 pointing toward a potential mechanism for MNTs such as parkinsonism from cilta-cel. Despite this compelling finding, MNTs seem to be most prevalent in cilta-cel compared with ide-cel, suggesting that this phenomenon may not be solely a class effect. 98 The mechanisms underlying cranial nerve palsies and peripheral neuropathies are even less clear, although inflammation appears to play a role. 8 , 99 Although there were no significant associations in our analysis, we did note a trend toward increased NINTs in patients who had received previous BCMA-targeted therapies. The mechanisms behind this potential relationship are unclear and invite further investigations into the importance of antigen density and the role of previous sensitization to the emergence of NINTs during subsequent lines of therapy.

An additional concern is the absence of effective, standardized management approaches to NINTs, which are characterized by their resistance to general immunosuppressive regimens. 9 , 100 These poor outcomes likely reflect an incomplete understanding of NINT pathophysiology, as well as the absence of standardized definitions, grading criteria, and surveillance strategies. 4 , 98 As a result, recognition and reporting of these events remain inconsistent across studies.

Despite these difficulties, there is reason for hope that these toxicities can be either mitigated or managed. There are multiple anti-BCMA CAR constructs that seem to have a lower NINTs point estimate than cilta-cel. Anitocabtagene autoleucel was given to 117 patients in the phase 2 iMMagine-1 trial with no incidents of parkinsonism, cranial nerve palsy, or Guillain-Barré syndrome reported. 101 Continued advancements in bispecific antibody and antibody-drug conjugates targeting BCMA may also provide a path toward safer therapies. 102 , 103 , 104

In conclusion, this systematic review and meta-analysis highlights an important but rare set of neurotoxicities associated with BCMA-directed CAR-T therapy in plasma cell dyscrasias. As professional societies and governing bodies continue to study NINTs, more work must be done in characterizing and grading these phenomena to develop the most effective prevention and treatment strategies.

Conflict-of-interest disclosure: R.S. declares speaker honoraria from Incyte, Sanofi, and Merck Sharp and Dohme (MSD). K.R. declares research funding from Kite/Gilead; consultancy for Kite/Gilead, Bristol Myers Squibb (BMS)/Celgene, and CSL Behring; travel support from Kite/Gilead and Pierre Fabre; and reports honoraria from Kite/Gilead, Novartis, BMS/Celgene, and MSD. S.Y. declares a consultant role with BMS, Ipsen, and Kite Pharma; and has served on an advisory board for AbbVie, ADC Therapeutics, BMS, Genmab, Ipsen, Kite Pharma, and Pfizer. The remaining authors declare no competing financial interests.

Acknowledgments

H.v.B. acknowledges support from the American Society of Hematology Research Training Award for Fellows and support from the Lymphoma Research Foundation. K.R. acknowledges grant support from the Bruno and Helene Jöster Foundation and the “CAR-T Control” translational group within the Bavarian Center for Cancer Research (BZKF-#TLG-22). The authors from the Ludwig Maximilian University acknowledge structural support from the Munich partner site of the German Cancer Consortium and Bavarian Cancer Research Center.

Authorship

Contribution: H.v.B., T.T., S.Y., and K.R. designed the research; H.v.B. and G.O. obtained data and wrote the manuscript; N.E. analyzed data and wrote the manuscript; M.A. and R.S. were involved in data interpretation and in review and editing of the manuscript; and all authors contributed to writing, editing, and research of the manuscript.

Footnotes

H.v.B. and G.O. are joint first authors.

K.R. and S.Y. contributed equally as senior authors to this study.

The data used in this study were extracted from the primary sources cited in this article. Original data are available from the corresponding author, Samuel Yamshon ( samuel.yamshon@nyulangone.org ), on request.

The full-text version of this article contains a data supplement.

Supplementary Material

Supplemental Figures and Tables

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