CAR-T or Bispecific Antibodies First? A Practical Sequencing Guide for Relapsed Multiple Myeloma in 2026

CAR-T or Bispecific Antibodies First? A Practical Sequencing Guide for Relapsed Multiple Myeloma in 2026

Both CAR-T cell therapy and bispecific antibodies have transformed the treatment of relapsed/refractory multiple myeloma — but the order in which they're given may determine how well each works. Dr. Sean Maximillian Taasan reviews the latest sequencing evidence, IMWG and European Myeloma Network recommendations, and the clinical factors that should guide treatment selection in 2026.

Introduction: T-cell Redirecting Therapies in Myeloma

The introduction of advanced treatments (including CAR-T therapy and bispecific antibodies) has completely revolutionized the management of relapsed/refractory multiple myeloma since the early 2020s.

Both of these treatments fall under the category of T-cell redirecting therapies (TCRT), and unlike conventional combination regimens that have traditionally been utilized in the relapsed/refractory setting, the sequence in which these treatments are administered may impact the efficacy of subsequent lines of therapy.

Originally, all of these treatments were studied and approved in heavily pretreated (≥4 prior lines of therapy) patients. However, with the publications of CARTITUDE-4 and MajesTEC-3, both cilta-cel and teclistamab (in combination with daratumumab) are now FDA-approved for treatment of myeloma at first relapse. As such, the question of how to sequence these therapies is becoming increasingly important for both myeloma specialists and community oncologists to consider.

A Brief Overview of CAR-T and Bispecific Antibodies

While both CAR-T cell therapy and bispecific antibodies leverage a patient’s immune system to enhance T-cell mediated destruction of myeloma cells, the mechanisms by which they accomplish this have some key differences.

CAR-T therapy utilizes modified versions of a patient’s own T-cells that are engineered to contain a specialized receptor. This receptor combines an extracellular portion that recognizes a specific antigen on myeloma cells (without requiring the assistance of antigen presenting cells) with an intracellular portion that combines CD3 and a co-stimulatory domain (enhancing the activation and expansion of the CAR-T cells). As a result, these cells are highly effective at recognizing and attacking myeloma cells.

Currently, there are two FDA-approved CAR-T products – idecabtagene vicleucel (Abecma) and ciltacabtagene autoleucel (Carvykti). Both products target B-cell maturation antigen (BCMA), a protein widely expressed on plasma cells but also found on other B-lineage cells.

Administration of CAR-T currently requires patients to undergo T-cell collection via apheresis. These cells are then sent for manufacturing, a process that may take anywhere from three to eight weeks on average. Once manufacturing is complete, the CAR-T cells are then sent back to the patient’s treatment center. Patients then receive lymphodepleting chemotherapy with fludarabine and cyclophosphamide a few days prior to CAR-T infusion and this step helps to optimize the cytokine milieu for CAR-T cell expansion in vivo. Following CAR-T infusion, most patients will remain off all myeloma therapy entirely until disease progression; as such, this “one and done” treatment approach is highly appealing to many patients.

Bispecific antibodies also enhance T-cell mediated destruction of myeloma cells, but do so without any modifications to a patient’s T-cells. Instead, these antibodies include two arms – one which binds to CD3 (on T-cells) and another that binds to a myeloma-specific antigen. Three of the currently approved FDA bispecific antibodies for myeloma – teclistamab (Tecvayli), elranatamab (Elrexfio), and linvoseltamab (Lynozyfic) – share the same target (BCMA) as ide-cel and cilta-cel. The fourth FDA bispecific antibody, talquetamab (Talvey), targets G-protein coupled receptor class 5 D (GPRC5D), a protein widely found on plasma cells but also expressed on keratinized epithelial cells. Using their ability to bind to both myeloma cells and T-cells, bispecific antibodies physically bring the two together resulting in enhanced T-cell activation.

Unlike with CAR-T therapy, bispecific antibodies are directly available off-the-shelf (similar to traditional medications); as such, they can be administered far more quickly when compared to CAR-T therapy. However, these treatments require multiple infusions given every 1-2 weeks and in the original landmark trials were continued indefinitely until progression or intolerance.

Potential Mechanisms for Decreased Efficacy with Subsequent TCRT

Given the degree of overlap in mechanisms of action for these classes of therapy (including a shared target antigen in BCMA for many of the individual medications), there has been concern that the use of one form of TCRT may impact the subsequent efficacy of future TCRTs. While the data regarding specific sequences of TCRTs is limited overall, there is accumulating evidence that prior exposure to one TCRT has the potential to both directly and indirectly reduce the efficacy of future TCRT. This may occur through several potential mechanisms:

• Antigen loss or mutation: Prior BCMA-directed therapy can promote the selection of clones with mutations in BCMA, leading to alterations in the binding site (causing loss of recognition) or outright deletion of the BCMA gene.
• T-cell exhaustion: Chronic antigen exposure from ongoing stimulation can exhaust T cells, leaving them less capable of the robust expansion needed for effective T-cell activation.
• Clonal selection: Myeloma cells that are intrinsically resistant to T-cell killing may be selectively enriched after exposure to one TCRT.
• Patient fitness: Patients in later lines of therapy are typically sicker overall, and as a result may no longer be eligible for certain treatments based on the comorbidities or functional status.

What Happens When You Use BCMA Bispecific Antibodies Before BCMA CAR-T?

Prospective data for patients receiving BCMA CAR-T after a prior BCMA bispecific antibody is limited overall. In cohort C of CARTITUDE-2 — which enrolled seven heavily pretreated patients (median eight prior lines) who had received prior BCMA bispecifics — the overall response rate was 57% and median PFS was only 5 months (1). Although this population was somewhat more heavily pretreated compared to CARTITUDE-1 and the number of patients evaluated was small, this does raise concern that patients who receive BCMA CAR-T after a prior BCMA bispecific antibody may not receive the same benefit as those who were TCRT naïve at the time of undergoing CAR-T.

This is supported by real world data published in 2025 which evaluated 236 patients receiving cilta cel across 16 US academic institutions (2). Out of the 236 patients, 33 had prior anti-BCMA therapy (8 of which specifically had received bispecific antibodies). Regardless of the type of anti-BCMA therapy, patients with prior TCRT had lower response rates and shorter PFS compared to those who were TCRT-naïve. Interestingly, patients with intervals of >6 months between prior TCRT and when they received cilta cel had significantly higher overall response rates compared to those with intervals <6 months, suggesting that shorter intervals between exposure to BCMA-directed agents are associated with decreased efficacy of the subsequent TCRT.

What About Using GPRC5D Bispecific Antibodies Before BCMA CAR-T?

Compared to BCMA-directed bispecifics, GPRC5D-directed bispecifics may have less of an impact on subsequent BCMA CAR-T therapy. Data from MONUMENTAL-1 show that patients who received talquetamab (GPRC5D-directed) achieved a 78% overall response rate with subsequent BCMA CAR-T therapy (3). This suggests that prior GPRC5D-directed therapy may not significantly impair subsequent BCMA CAR-T.

One important caveat: any bispecific antibody, regardless of target, has the potential to negatively impact T-cell fitness if used in the window immediately before CAR-T apheresis. As a result, all bispecific antibodies should generally be avoided for at least 4 weeks prior to apheresis if possible (4).

What About Using Bispecific Antibodies After BCMA CAR-T?

Current data appear to support the efficacy of bispecific antibodies even after prior BCMA-directed CAR-T therapy. BCMA bispecifics after prior BCMA CAR-T still appear to show meaningful efficacy, albeit with potentially reduced response rates and shorter PFS compared to TCRT-naïve patients (5, 6). Subgroup analysis of MonumenTAL-1 also showed an ORR of 72% and median PFS of 13 months in patients with prior BCMA CAR-T who went on to subsequently receive talquetamab (7).

Real world data also supports the efficacy of both BCMA and GPRC5D bispecifics after prior BCMA CAR-T. In a multicenter retrospective observational study published in 2024, both teclistamab and talquetamab had significantly higher response rates, longer duration of response, and longer median survival compared to salvage therapy with conventional regimens in patients who progressed after prior BCMA CAR-T (8).

Current Recommendations: IMWG and European Myeloma Network

In 2025, the International Myeloma Working Group (IMWG) published formal sequencing recommendations for patients who are appropriate candidates for both CAR-T and bispecific antibodies at the time of disease progression (4). The current recommendation is to consider pursuing CAR-T first, based on two rationales: the potential for longer treatment-free intervals with CAR-T, and stronger data supporting the efficacy of bispecifics used after CAR-T compared to the reverse sequence. Similarly, the European Myeloma Network released similar recommendations in late 2025 with on the basis of high response rates with potential for durable remissions (and improved quality of life) following a single CAR-T infusion (9).

In ideal circumstances, utilizing CAR-T early and then switching to a bispecific antibody at subsequent relapse has been the recommended approach. However, many of our patients do not have the good fortune of being in ideal circumstances at the time of disease progression. As such, there are several important factors to think about when selecting between these therapies.

Practical Considerations When Choosing Between CAR-T and Bispecific Antibodies

When evaluating a patient who could potentially be treated with either CAR-T or a bispecific antibody, there are several key considerations that may ultimately be the deciding factor for which therapy to pursue.

Logistics and access. Even in 2026, CAR-T is only available at highly specialized treatment centers. Patients in rural areas or who are otherwise unable to access a specialized myeloma center may not be able to receive CAR-T at all. Bispecific antibodies, by contrast, are increasingly being offered in community practices.

That being said, bispecific antibodies have historically been given every 1-2 weeks continuously until disease progression or intolerance. While this may change in the future (due to increased interest in fixed-duration bispecific therapy), the cumulative time spent getting infusions can be a challenge for some patients. In contrast, CAR-T therapy is administered as a single infusion with a potential for far less frequent follow-up visits required in those patients who respond well with minimal complications.

Disease kinetics. For many patients, one of the primary barriers to receiving CAR-T is the length of time required to initiate therapy. This includes both the “brain-to-vein” time (ie, the time required to receive insurance authorization and coordinate all steps necessary prior to apheresis) and the “vein-to-vein” time (ie, the time between apheresis and eventual receipt of the CAR-T product). In one retrospective study performed at the University of Chicago, the median brain-to-vein time ranged from 29 to 39 days and the median vein-to-vein time ranged from 59 to 62 days (depending on the type of insurance) (10).

Patients with rapidly progressive disease often cannot wait several weeks to months before beginning effective therapy. In these scenarios, bispecific antibodies provide an alternative, highly effective option that is available directly off the shelf.

Bridging therapy should be considered in all patients who are planned for CAR-T whose disease activity is expected to cause additional morbidity in the interval time between apheresis and CAR-T infusion. Conventional therapies (such as carfilzomib) are generally utilized when possible, however some patients may have extremely limited options for bridging therapy if they have already progressed through multiple lines of treatment. In these scenarios, it should be noted that talquetamab can be considered as a potential bridging agent between apheresis and CAR-T infusion (11).

Extramedullary disease and plasma cell leukemia. Extramedullary disease (EMD) and plasma cell leukemia (PCL) represent highly aggressive disease states and are associated with poor prognoses. Despite this, CAR-T therapy appears to still be reasonably effective in both extramedullary disease and plasma cell leukemia (2, 12, 13).

Efficacy of bispecific antibodies appears to be far lower in EMD and PCL. Based on various real-world studies, the median PFS with BCMA-directed bispecific antibodies may be as low as 1 month in these settings (13-16). Talquetamab may potentially have somewhat more activity (particularly in PCL) compared to the BCMA-directed bispecifics, but outcomes remain poor overall compared to those without EMD or PCL (15, 17).

Finally, a dual-targeted approach utilizing the combination of teclistamab and talquetamab in patients with EMD was evaluated in the RedirecTT-1 trial (18). High response rates (nearly 80%) were seen and the median PFS was 15.4 months. These results show the potential for improved outcomes with a multi-targeted TCRT approach.

High disease burden (sink effect). While BCMA is normally found on the surface of plasma cells, it can be cleaved by gamma-secretases which results in the release of fragments of soluble BCMA into the blood. In patients with high disease burden, the amount of circulating soluble BCMA increases (19).

Higher concentrations of soluble BCMA correlate with decreased cytolytic activity of bispecific antibodies in vitro, and have also been shown in both univariate and multivariate analyses to be a predictor of poor response to BCMA-directed bispecific antibodies clinically (19, 20). This is thought to be due to binding of the bispecific antibodies to soluble BCMA (rather than to BCMA attached to the surface of myeloma cells), a concept known as the “sink effect”. The cytolytic activity of CAR-T cells does not appear to be affected by the concentration of soluble BCMA, and as such CAR-T may be preferred in patients with a high-disease burden even outside of EMD or PCL.

Toxicity profile and patient fitness. CAR-T carries higher rates of severe CRS and ICANS compared to the bispecific antibodies. For patients with significant comorbidities who cannot tolerate the acute physiologic stress of severe CRS, bispecific antibodies may be a more suitable option.

In addition, delayed side effects related to both inflammation (immune effector cell-associated hemophagocytic lymphohistiocytosis-like syndrome, immune effector cell-associated enterocolitis) and neurotoxicity (cranial nerve palsies, atypical Guillain-Barre syndrome, Parkinsonism) can be seen with CAR-T but are not typically associated with the currently available bispecific antibodies. And although rare, there is also an increased risk of secondary malignancies with CAR-T therapy including the potential for cancers (such as T-cell lymphomas) that directly result from malignant behavior of the CAR-T cells themselves.

Finally, the side effect profile for the specific antigen being targeted should also be considered. BCMA therapies are known for increased risk of infections, and grade 3 or higher infections appear to actually be higher with BCMA-directed bispecific antibodies compared to BCMA-directed CAR-T in at least one study (21). While the risk of infection is not as pronounced with GPRC5D-directed therapies, expression of GPRC5D on epithelial cells can lead to dysgeusia, anorexia, severe unintentional weight loss, rash, and nail changes that can often be the limiting factor for continued treatment (22).

Maximizing the Interval Between BCMA-directed Therapies

Although prospective data evaluating patients comparing specific sequences of TCRT remains limited, real-world data does provide important insights into factors that may impact the efficacy of these therapies. As more data emerges, it appears that shorter lengths of time between TCRT modalities targeting the same antigen may be associated with decreased efficacy. This has been shown in patients who received a BCMA bispecific antibody followed by ide-cel as well as patients who received a BCMA bispecific antibody followed by cilta-cel (2, 23). In addition, a similar pattern has been seen with patients who previously received a BCMA-directed CAR-T product and then subsequently went on to receive teclistamab (24). The optimal minimum length of time between exposure to BCMA-directed TCRT is not known, but the European Myeloma Network guidelines suggest aiming for at least 6 months if possible (9). For patients that are progressing within that timeframe, alternative therapies that utilize different modes of action (or target different antigens, such as GPRC5D) should be considered.

Cilta-cel or teclistamab + daratumumab should be considered standards of care after one to three lines of therapy in 2026

One of the key questions in 2026 is whether to utilize cilta-cel or teclistmab + daratumumab at the time of first relapse, as both of options are now FDA approved for patients with one to three prior lines of treatment following the publications of CARTITUDE-4 and MajesTEC-3, respectively (25-27). However, there is no formal guidance as to which specific option is preferred. It is worthwhile to note that the previously mentioned IMWG and European Myeloma Network guidelines were made prior to the publication of MajesTEC-3 at a time when bispecific antibodies were limited to later lines of therapy (where the potential for longer treatment-free intervals and overall improved efficacy appears to be stronger in favor of CAR-T).

Currently, there are no direct randomized comparisons between these two options in the early relapse setting. Caution should also be used when interpreting the results of these trials against one another, particularly as there were differences in the study populations between these two trials – for instance, CARTITUDE-4 featured more patients with high-risk cytogenetics (59% vs 36%) and about a quarter of patients in CARTITUDE-4 were anti-CD38 refractory (while none were in MajesTEC-3).

That being said, both options were highly effective with substantially longer PFS and OS compared to conventional combination regimens. As such, both of these options should be considered standards of care for patients who progress after one to three prior lines of treatment in 2026.

When choosing between these two options, specialists should carefully consider the factors mentioned previously (rate of disease progression, presence of EMD/PCL, overall disease burden, logistics, and comorbidities). In some cases there may be a clear factor (ex: presence of extramedullary disease) that would favor one option over the other; in many other cases it may be patient preference (due to logistics and side effect profiles) that helps guide treatment selection.

For some patients, both treatment options are equally appropriate and, in these scenarios, either choice should be considered acceptable. Teclistamab + daratumumab is highly appealing due to its more favorable side effect profile and the increasing ability to administer bispecific antibodies in community centers. The potential impact on subsequent TCRT may be partially mitigated with longer intervals between BCMA bispecific antibodies and BCMA CAR-T – this could potentially be achieved using alternative regimens (such as conventional combinations or talquetamab) as the next line of therapy.

Looking Forward: A Rapidly Evolving Landscape

Treatment of myeloma is rapidly evolving, and many of the points discussed here may no longer apply within the next few years. Bispecific antibodies and CAR-T continue to be evaluated in earlier lines of therapy, including as consolidation therapy in the frontline setting. Depending on the results of these studies, patients may already have been exposed to TCRT by the time of first relapse in the near future.

The use of bispecific antibodies as time-limited therapy is also becoming an increasing area of interest, as this may mitigate side effects and reduce the impact on subsequent TCRT. While there is no randomized data yet to support a specific duration of therapy, future trials are likely to include either fixed-duration (or MRD response-adapted duration) treatment protocols.

Many of the current limitations of TCRT have informed the ongoing development of new therapies being studied at this time. Dual-antigen targeted TCRT (such as trispecific antibodies that target both BCMA and GPRC5D) may further enhance the already impressive efficacy of these treatments. Newer agents may potentially reduce the risk for the more severe side effects that are seen currently with both bispecific antibodies and CAR-T. Off-the-shelf CAR-T products are also being developed and would allow for more rapid initiation of therapy in patients who are actively progressing.

Given the increasing complexity in treatment sequencing and the rapid rate at which new data becomes available, early referrals to a specialized myeloma center that offers both CAR-T and bispecific therapies should be prioritized. As access to bispecific antibodies expands to more community centers, many patients will ideally be able to continue to receive their treatment primarily through their local oncologist and simultaneously follow with a myeloma specialist who can help direct their care and facilitate timely initiation of any therapies (such as CAR-T) that are not offered locally.

Clinical Implications and Practice Takeaways

• The sequence that T-cell redirecting therapies (such as bispecific antibodies and CAR-T treatments) are given may impact the efficacy of whichever treatment is given second.
• Early referrals to specialized centers capable of both CAR-T and bispecific antibodies should be emphasized, given the potential for treatment sequencing to impact future outcomes
• Prior BCMA-directed bispecific therapy is associated with decreased efficacy of subsequent BCMA CAR-T. This effect appears to be more pronounced with shorter intervals between giving a BCMA bispecific and proceeding to BCMA CAR-T. An interval of at least six months between prior BCMA therapy and CAR-T infusion is recommended.
• GPRC5D bispecific antibodies before BCMA CAR-T appear to better preserve subsequent CAR-T efficacy, however data is limited overall.
• Both BCMA and GPRC5D directed bispecific antibodies have activity in patients who previously received BCMA CAR-T.
• For patients who are appropriate candidates for both CAR-T and bispecific antibodies, IMWG and European Myeloma Network guidelines recommend CAR-T first, based on longer treatment-free intervals and better post-CAR-T bispecific data to support the efficacy of bispecific antibodies after CAR-Tdata. However, these recommendations were made prior to the publication of MajesTEC-3 and may be more applicable to patients with 4 or more prior lines of therapy.
• All bispecific antibodies should be avoided in the weeks immediately prior to CAR-T apheresis due to potential impairment of T-cell fitness.
• For patients who have actively progressing disease that would cause morbidity if left untreated, bridging therapy (following apheresis) should be considered while awaiting CAR-T manufacturing to be completed. Conventional regimens are often preferred, but talquetamab is a reasonable option in patients who are refractory (or have contraindications) to all available conventional regimens.
• Extramedullary disease and plasma cell leukemia are associated with poor prognoses. Bispecific antibodies (particularly BCMA-directed bispecifics) appear to have very limited efficacy in these settings, and CAR-T should be utilized if possible.
• Disease kinetics, disease burden, comorbidities, and patient preference should all be considered when choosing between a bispecific antibody and CAR-T as next line of therapy.

For Patients: What This Means for Your Care

Treatment of multiple myeloma has dramatically evolved over the last few years. Increasingly effective therapies are being introduced, and many of these treatments can provide a good response in patients whose myeloma has already progressed through several lines of treatment. These advanced treatments are now being introduced into earlier lines of treatment as they have been shown to be even more beneficial in these settings. The order that treatments are given may potentially impact how effective they are, and as a result it is important to be evaluated by a myeloma specialist who is familiar with both CAR-T cell and bispecific antibody therapies who can help determine the optimal treatment sequence for you.

About the Author

Sean Maximillian Taasan, MD, is an Assistant Professor of Internal Medicine at UT Southwestern Medical Center in Dallas, Texas, where he specializes in the treatment of multiple myeloma, Waldenström macroglobulinemia, and amyloidosis. He earned his medical degree at the University of Florida College of Medicine and completed his residency in internal medicine at Duke University Medical Center. He then completed his hematology and oncology fellowship at UT Southwestern, where he served as Chief Fellow. Dr. Taasan joined the UT Southwestern faculty in 2025 and leads the Program for Specialty Professional Education and Community Training (ProSPECT) at the Harold C. Simmons Comprehensive Cancer Center.

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