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Swan, D.; Murphy, P.; Glavey, S.; Quinn, J. Bispecific Antibodies in Multiple Myeloma. Encyclopedia. Available online: https://encyclopedia.pub/entry/42686 (accessed on 11 February 2025).
Swan D, Murphy P, Glavey S, Quinn J. Bispecific Antibodies in Multiple Myeloma. Encyclopedia. Available at: https://encyclopedia.pub/entry/42686. Accessed February 11, 2025.
Swan, Dawn, Philip Murphy, Siobhan Glavey, John Quinn. "Bispecific Antibodies in Multiple Myeloma" Encyclopedia, https://encyclopedia.pub/entry/42686 (accessed February 11, 2025).
Swan, D., Murphy, P., Glavey, S., & Quinn, J. (2023, March 31). Bispecific Antibodies in Multiple Myeloma. In Encyclopedia. https://encyclopedia.pub/entry/42686
Swan, Dawn, et al. "Bispecific Antibodies in Multiple Myeloma." Encyclopedia. Web. 31 March, 2023.
Bispecific Antibodies in Multiple Myeloma
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This entry is adapted from the peer-reviewed paper 10.3390/cancers15061819

Multiple myeloma, a cancer of the bone marrow, is the commonest cancer of adults in the Western World. Therapies have advanced dramatically in recent years, equating to improved survival and quality of life for patients, but those with resistant disease still have less favourable outcomes. Bispecific antibodies represent a new treatment option for patients with myeloma. These antibodies activate the patient’s own T-cells to kill their tumour cells and have shown impressive results in relapsed refractory myeloma.

myeloma tumour T-cell

1. Introduction

Multiple myeloma (MM) is the second most common haematological malignancy of adults in the Western world, with increasing rates reported over recent years [1][2]. MM is characterized by the clonal expansion of neoplastic plasma cells, leading to the production of a paraprotein, anaemia, renal impairment, bone damage, and humoral and cellular immunosuppression [3][4]. Outcomes have improved significantly since the advent of proteosome inhibitors (PIs), immunomodulatory agents (IMiDs), and monoclonal antibodies. The median overall survival (OS) has doubled to approximately 5 years [5]. However, patients with adverse cytogenetics or high-risk disease as determined by the Revised International Staging System (R-ISS) continue to have less durable responses to treatment, and the majority of low-risk patients will eventually develop treatment-resistant disease [6][7][8].
Patients with ultra-high risk disease, so-called ‘double-hit’ myeloma, defined by the presence of biallelic inactivation of TP53 or 1q21 amplification and International Staging System (ISS) stage III disease, typically succumb to their disease within 2 years [9]. Those who are refractory to the 3 classes of novel agents (triple-refractory) have an OS of less than one year, whereas the median OS for penta-refractory patients (refractory to 2 PIs, 2 IMiDs and a monoclonal antibody) is a dismal 5.6 months [10]. Given this unmet need, novel therapies remain a priority in MM.

2. Overview of Bispecific Antibodies in Myeloma

Bispecific T-cell antibodies (BsAbs) are designed to simultaneously bind to a target moiety on tumour cells and to CD3 on T-cells. This causes direct T-cell activation and subsequent tumour cell killing [11][12]. The earliest BsAbs consisted of fragment antigen-binding (Fab) variable regions connected by a short flexible linker (non IgG-like BsAbs). Such small BsAbs have a short half-life and require continuous intravenous infusion. Newer agents include a fragment crystallizable (Fc) region (IgG-like BsAbs). These larger BsAbs can be administered via intermittent infusion or subcutaneous (S/C) injection [13].
Blinatumumab, the first licensed BsAb, is a CD19-directed non IgG-like construct that was approved for use in acute lymphoblastic leukaemia (ALL) in 2014 [14]. Since then, numerous BsAbs have been developed in a variety of conditions, including MM. Various targets on malignant plasma cells are being investigated, with the majority of work to-date focused on B-cell maturation antigen (BCMA) [15]. BCMA is a member of the tumour necrosis family receptor superfamily, expressed by mature B-cells, plasma cells and MM cells [16][17][18][19]. It has roles in MM cell survival through the upregulation of anti-apoptotic proteins [20][21][22]. Levels of soluble BCMA (sBCMA) increase with disease progression and correlate with adverse outcomes [23][24]. In 2022, two anti-BCMA BsAbs received regulatory approval. Teclistamab was approved by the European Medicines Agency (EMA) and the Food and Drug Administration (FDA) for use in relapsed refractory myeloma (RRMM), and elranatamab also received orphan drug designation by both the EMA and FDA [25][26].
Teclistamab is a humanized IgG Fc anti-BCMA BsAb. Regulatory approval was granted following the publication of results of the phase 1/2 MajesTEC-1 study (NCT03145181) in 165 RRMM patients with triple class-exposed disease. After a median follow-up of 14 months, the overall response rate (ORR) was 63%, and 39% achieved a complete response (CR) or better. The median duration of response (DOR) was 18 months, with a median progression-free survival (PFS) of 11 months. CRS occurred in 72%, immune effector cell-associated neurotoxicity syndrome (ICANS) in 3%, and infections in 76%, of which 45% were grade 3–4 events [27].
Elranatamab is a humanized IgG2A anti-BCMA BsAb. The phase 2 MagnetisMM-3 study (NCT04649359) enrolled and treated 123 RRMM patients. A total of 97% of the trial population were triple-refractory, and 42% were penta-refractory. After a median follow-up of nearly 7 months, the ORR was 61%. Some 51% of patients were still receiving elranatamab at data cut-off, with progressive disease accounting for 33% of those discontinuing therapy. Of 119 patients, CRS occurred in 56% and ICANS in 3%. Infections were reported in 62%, 32% being of grade 3–4 [28]. A summary of the published data for the reported BCMA BsAbs in MM in shown in Table 1.
Table 1. Published clinical trials of BCMA BsAbs in RRMM.
Bispecific Antibody Clinical Trials Identifier Antibody Structure Administration Safety CRS/ICANS Responses Ongoing Studies
Teclistamab MajesTEC-1
NCT03145181		 humanized, IgG Fc Teclistamab 1.5 mg/kg weekly S/C with a 2-step-up priming dose regimen (0.06 mg/kg and 0.3 mg/kg) Anaemia 52%, neutropenia 71%, thrombocytopenia 40%, infections 76% (grade 3–4 45%), neurotoxicity 15% CRS 72% (all but one case grade 1–2), ICANS 3% (all grade 1–2) ORR 63%, 39% CR or better, median DOR 18.4 months Several MagesTEC studies ongoing using teclistamab in RRMM and NDMM in combination therapies
Elranatamab MagnetisMM-3
NCT04649359
Cohort A		 full length, humanized, IgG2a Elranatamab 76 mg weekly S/C on a 28 day cycles with a 2-step-up priming dose regimen (12 mg and 32 mg) Anaemia 56%, neutropenia 53%, thrombocytopenia 27%, infection 62% (grade 3–4 32%), %, peripheral neuropathy 17%, nausea 30%, diarrhoea 45% CRS 56% (all grade 1–2), ICANS 3% (all grade 1–2) ORR 61%, median DOR not reached Several MagnetisMM studies ongoing using elranatamab in RRMM and NDMM in combination therapies
AMG 420 NCT02514239 BiTE Continuous 28 day IV infusion followed by 2 week break. Dose-escalation from 0.2–800 μg/day Infection 33%, polyneuropathy 5%, 12% deranged liver enzymes CRS 38% (94% Grade 1–2) ORR 31% across all doses, 70% for the 400 ug/day cohort Development discontinued by Amgen
AMG 701 NCT03287908 extended half-life, scFvs plus Fc region Weekly IV. Dose-escalation from 5 μg–12 mg Anaemia 43%, neutropenia 23%, thrombocytopenia 20%, diarrhoea 31%, fatigue 25%, infection 17%, elevated pancreatic enzymes 3%. CRS 61% (90% Grade 1–2) ORR 36% for 3–12 mg doses Development discontinued by Amgen
Linvoseltamab (REGN5458) NCT03761108 Fc Fab arms IV weekly, then every 2 weeks. Dose escalation over 9 dose levels. Anaemia 37%, neutropenia 29%, thrombocytopenia 21%, fatigue 34% CRS 48% (all but one case Grade 1–2) ORR 41% for doses <200 mg and 75% ≥200 mg, median DOR not reached Phase 2 study of 200 mg REGN5458 is recruiting
Alnuctamab
(CC-93269)		 NCT03486067 2 arm humanized IgG1 Fc Dose escalation of IV alnuctamab from 0.15–10 mg.
S/C alnuctamab given on D1, 4, 8, 15 and 22 of C1, weekly in C2–3, every other week in C4–6 and every 28 days thereafter. Dose escalation from 10–60 mg		 Anaemia 34%, neutropenia 34% CRS 53% (all grade 1–2), 1 grade 1 ICANS IV alnuctamab ORR 39%, median PFS 13 weeks, median DOR in responding patients 146 weeks.
S/C alnuctamab ORR 51% across all doses, 77% for doses ≥30 mg		 Ongoing recruitment to the phase 1 study
Abbv-383 NCT03933735 IgG4 Fc. 2 heavy chain only anti-BCMA moieties Dose escalation and expansion cohorts (n = 6 in 40 mg cohort, n = 60 in 60 mg cohort) Infections in 50% of 40 mg cohort and 43% of 60 mg cohort, neutropenia in 67%/40%, anaemia in 33%/32%, thrombocytopenia 33%/25% CRS 83% (all grade 1–2) in 40 mg cohort and 72% (2% grade 3–4) in 60 mg cohort ORR 57% across all groups, 83% at 40 mg and 60% at 60 mg. ≥CR 67% at 40 mg and 29% at 60 mg Phase 1b study planned
NCT05650632

3. Improving Efficacy

One of the hallmarks of MM is the tumour-permissive microenvironment (TME) [15]. A complex interplay between MM cells, immune cells and bone marrow stromal cells (BMSCs) impairs normal immune function, facilitating MM cell proliferation and survival.
Of concern to BsAb efficacy, effector T-cell function is particularly compromised in MM, with progressive dysfunction observed with disease progression and increasing treatment lines [29]. For example, BM-derived T-cells from MM patients fail to mount a robust cytokine response when exposed to MM cells, compared with T-cells from patients with monoclonal gammopathy of uncertain significance (MGUS) [30]. A number of mechanisms underpin this dysfunction. MM cells induce T-cell anergy by upregulating the expression of checkpoint ligands and receptors such as programmed death-ligand 1 (PD-L1), which binds to programmed death receptor-1 (PD-1), leading to T-cell exhaustion, impaired cytokine production and reduced target cell lysis [31]. PD-L1 expression is increased on MM cells compared with both MGUS cells and healthy donor plasma cells [32][33].
Immunosuppressive Regulatory T-cells (Tregs) are enriched in MM peripheral blood samples. MM cells themselves can induce the formation of Tregs in vitro, [34], promoting immune escape, and perhaps explaining the increasing levels of Tregs present with increasing disease burden. In a murine model, the depletion of Tregs in mice with established MM promoted vigorous T-cell and NK cell-mediated responses, halting disease progression [35]. T-cell function is also impaired by myeloid-derived suppressor cells, present at 5 times the normal level in MM patients [36].
BsAbs rely upon a robust CD8+ cytotoxic T-cell response. Continuous antigen stimulation can lead to T-cell exhaustion, with resultant resistance to therapy anticipated [37]. In patients who respond to BsAb therapy, a selective expansion of clonotypic tumour-reactive CD8+ T-cells is produced, which replaces exhausted BM T-cells. This is not seen in non-responding patients [38]. An analysis of the MajesTEC-1 study of teclistamab in RRMM also showed that patients who failed to respond to treatment had lower peripheral CD8+ T-cell levels, increased levels of Tregs, and enhanced expression of markers associated with T-cell exhaustion in blood and BM samples. Higher levels of exhausted CD8+ T-cells and Tregs pre-treatment were associated with inferior PFS in this research [39].
Given the impairment of T-effector activity seen in MM, combining BsAbs with therapies which augment T-cell function may provide a means to improve efficacy.

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Dawn Swan
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Philip Murphy
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John Quinn
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