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Teclistamab is an active T cell–redirecting bispecific antibody against B-cell maturation antigen for multiple myeloma
Open accessAbstract
B-cell maturation antigen (BCMA), a member of the tumor necrosis factor family of receptors, is predominantly expressed on the surface of terminally differentiated B cells. BCMA is highly expressed on plasmablasts and plasma cells from multiple myeloma (MM) patient samples. We developed a BCMAxCD3 bispecific antibody (teclistamab [JNJ-64007957]) to recruit and activate T cells to kill BCMA-expressing MM cells. Teclistamab induced cytotoxicity of BCMA+ MM cell lines in vitro (H929 cells, 50% effective concentration [EC50] = 0.15 nM; MM.1R cells, EC50 = 0.06 nM; RPMI 8226 cells, EC50 = 0.45 nM) with concomitant T-cell activation (H929 cells, EC50 = 0.21 nM; MM.1R cells, EC50 = 0.1 nM; RPMI 8226 cells, EC50 = 0.28 nM) and cytokine release. This activity was further increased in the presence of a γ-secretase inhibitor (LY-411575). Teclistamab also depleted BCMA+ cells in bone marrow samples from MM patients in an ex vivo assay with an average EC50 value of 1.7 nM. Under more physiological conditions using healthy human whole blood, teclistamab mediated dose-dependent lysis of H929 cells and activation of T cells. Antitumor activity of teclistamab was also observed in 2 BCMA+ MM murine xenograft models inoculated with human T cells (tumor inhibition with H929 model and tumor regression with the RPMI 8226 model) compared with vehicle and antibody controls. The specific and potent activity of teclistamab against BCMA-expressing cells from MM cell lines, patient samples, and MM xenograft models warrant further evaluation of this bispecific antibody for the treatment of MM. Phase 1 clinical trials (monotherapy, #NCT03145181; combination therapy, #NCT04108195) are ongoing for patients with relapsed/refractory MM.
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“This effect occurs regardless of T-cell–receptor specificity or major histocompatibility complex class I molecules on the surface of myeloma cells.18”
From Teclistamab in Relapsed or Refractory Multiple Myeloma (2022) · cites this paper as [18]
In the citing paper
“Teclistamab redirects CD3+ T cells to BCMA+ myeloma cells, resulting in T-cell activation and subsequent lysis and death of BCMA+ cells.18”
From Teclistamab in Relapsed or Refractory Multiple Myeloma (2022) · cites this paper as [18]
Citations
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“Therapeutic approaches such as chimeric antigen receptor T-cell therapies and bispecific T-cell engagers that use T cell–mediated cytotoxicity to target BCMA on plasma cells have shown deep responses in patients with relapsed or refractory disease.(21-25) Another class of T-cell redirecting therapy in development for…”
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B-cell Maturation Antigen Is a Promising Target for Adoptive T-cell Therapy of Multiple Myeloma
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“B-cell maturation antigen (BCMA, CD269, TNFRSF17) is a 20 kDa receptor that is selectively expressed in the B-cell lineage and is also widely expressed on MM cells (in addition to smoldering MM and monoclonal gammopathy of undetermined significance).(14-16) Upon binding to its ligands, a proliferation-inducing ligand…”
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“4 nM, at which point a significant decrease in potency was observed (Figure 4C); these concentrations are higher than that observed in myeloma patients.(34) In contrast, exogenous BAFF had no impact.”
ResultExpression of BCMA, TACI, and BAFF-R in multiple myeloma: a mechanism for growth and survival
Novak, A. J., Darce, J. R., Arendt, B. K., Harder, B., Henderson, K., Kindsvogel, W., Gross, J. A., Greipp, P. R., & Jelinek, D. F. (2003) · Blood · doi:10.1182/blood-2003-06-2043 · Cited by 556 · cited 1×
“B-cell maturation antigen (BCMA, CD269, TNFRSF17) is a 20 kDa receptor that is selectively expressed in the B-cell lineage and is also widely expressed on MM cells (in addition to smoldering MM and monoclonal gammopathy of undetermined significance).(14-16) Upon binding to its ligands, a proliferation-inducing ligand…”
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“Within the past decade, the introduction of proteasome inhibitors, immunomodulatory drugs, and monoclonal antibodies has changed the landscape of myeloma management, leading to improved disease control and prolonged survival.(3-12) Despite these therapeutic advances, nearly all patients will eventually relapse”
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Thompson, J. S., Schneider, P., Kalled, S. L., Wang, L., Lefèvre, E. A., Cachero, T. G., Mackay, F., Bixler, S. A., Zafari, M. R., Liu, Z., et al. (2000) · The Journal of Experimental Medicine · doi:10.1084/jem.192.1.129 · Cited by 393 · cited 1×
“Upon binding to its ligands, a proliferation-inducing ligand (APRIL; CD256) and BAFF (CD257), BCMA activates p38/NF-kB and induces upregulation of antiapoptotic proteins to regulate B-cell maturation, proliferation, and survival.(16-20) Increased levels of a soluble form of BCMA (sBCMA), produced through cleavage at t…”
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“Therapeutic approaches such as chimeric antigen receptor T-cell therapies and bispecific T-cell engagers that use T cell–mediated cytotoxicity to target BCMA on plasma cells have shown deep responses in patients with relapsed or refractory disease.(21-25) Another class of T-cell redirecting therapy in development for…”
Backgroundγ-secretase directly sheds the survival receptor BCMA from plasma cells
Laurent, S. A., Hoffmann, F. S., Kuhn, P.-H., Cheng, Q., Chu, Y., Schmidt-Supprian, M., Hauck, S. M., Schuh, E., Krumbholz, M., Rübsamen, H., et al. (2015) · Nature Communications · doi:10.1038/ncomms8333 · Cited by 377
Interaction of the TNF homologues BLyS and APRIL with the TNF receptor homologues BCMA and TACI
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“Upon binding to its ligands, a proliferation-inducing ligand (APRIL; CD256) and BAFF (CD257), BCMA activates p38/NF-kB and induces upregulation of antiapoptotic proteins to regulate B-cell maturation, proliferation, and survival.(16-20) Increased levels of a soluble form of BCMA (sBCMA), produced through cleavage at t…”
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Efficient generation of stable bispecific IgG1 by controlled Fab-arm exchange
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“The DuoBody antibody (JNJ-64007957 or teclistamab) was generated by controlled Fab-arm exchange of a BCMA antibody and a CD3 parental antibody derived from SP34 clone26 following the method developed by Genmab.27 Null arm controls were generated by controlled Fab-arm exchange of mouse anti-human respiratory syncytial…”
MethodTreatment of Multiple Myeloma: ASCO and CCO Joint Clinical Practice Guideline
Mikhael, J. R., Ismaila, N., Cheung, M. C., Costello, C. L., Dhodapkar, M. V., Kumar, S. K., Lacy, M. Q., Lipe, B. C., Little, R. F., Nikonova, A., et al. (2019) · Journal of Clinical Oncology · doi:10.1200/jco.18.02096 · Cited by 344 · cited 1×
“Within the past decade, the introduction of proteasome inhibitors, immunomodulatory drugs, and monoclonal antibodies has changed the landscape of myeloma management, leading to improved disease control and prolonged survival.(3-12) Despite these therapeutic advances, nearly all patients will eventually relapse”
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“Within the past decade, the introduction of proteasome inhibitors, immunomodulatory drugs, and monoclonal antibodies has changed the landscape of myeloma management, leading to improved disease control and prolonged survival.(3-12) Despite these therapeutic advances, nearly all patients will eventually relapse”
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“BCMA is selectively expressed on late-stage B cells and plasma cells, and its expression levels correlate with myeloma tumor burden.(35) Data from a BCMA CAR-T clinical study in patients with MM has shown a high overall response with manageable safety, highlighting the potential for targeting BCMA in the clinical sett…”
BackgroundSanchez, E., Li, M., Kitto, A., Li, J. S. Y., Wang, C. S., Kirk, D. T., Yellin, O., Nichols, C. M., Dreyer, M. P., Ahles, C. P., et al. (2012) · British Journal of Haematology · doi:10.1111/j.1365-2141.2012.09241.x · Cited by 280 · cited 2×
“Upon binding to its ligands, a proliferation-inducing ligand (APRIL; CD256) and BAFF (CD257), BCMA activates p38/NF-kB and induces upregulation of antiapoptotic proteins to regulate B-cell maturation, proliferation, and survival.(16-20) Increased levels of a soluble form of BCMA (sBCMA), produced through cleavage at t…”
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Hipp, S., Tai, Y., Blanset, D. L., Deegen, P., Wahl, J., Thomas, O. S., Rattel, B., Adam, P. J., Anderson, K. C., & Friedrich, M. (2016) · Leukemia · doi:10.1038/leu.2016.388 · Cited by 234
Pillarisetti, K., Edavettal, S., Mendonça, M., Li, Y., Tornetta, M., Babich, A., Majewski, N., Husovsky, M., Reeves, D., Walsh, E., et al. (2020) · Blood · doi:10.1182/blood.2019003342 · Cited by 174 · cited 2×
“Cytokine measurement Production of interferon-g, IL-1b, IL-2, IL-4, IL-6, IL-8, IL-10, IL12p70, IL-13, and tumor necrosis factor (TNF)-a was assayed by using the Meso Scale Discovery human pro-inflammatory panel 1 kit as per the instructions.(30)”
MethodSelf-citationVafa, O., Gilliland, G. L., Brezski, R. J., Strake, B., Wilkinson, T., Lacy, E. R., Scallon, B. J., Teplyakov, A., Malia, T., & Strohl, W. R. (2013) · Methods · doi:10.1016/j.ymeth.2013.06.035 · Cited by 158 · cited 2×
“223 10(5) cells/mL in complete medium containing 2 mg/mL of Fc block.(29) Assay was established by using 90 mL (23 10(4)) of target cells and 90 mL (13 10(5)) of freshly thawed normal donor pan-T cells along with 20 mL of 103 concentration of antibody dilutions, and they were incubated at 37°C with 5% carbon dioxide f…”
MethodMadduri, D., Usmani, S. Z., Jagannath, S., Singh, I., Zudaire, E., Yeh, T., Allred, A. J., Banerjee, A., Goldberg, J. D., Schecter, J. M., et al. (2019) · Blood · doi:10.1182/blood-2019-121731 · Cited by 108
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“gov #NCT03145181 and #NCT04108195).(38) Acknowledgments The authors thank Brendan Weiss, Blake J.”
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“Within the past decade, the introduction of proteasome inhibitors, immunomodulatory drugs, and monoclonal antibodies has changed the landscape of myeloma management, leading to improved disease control and prolonged survival.(3-12) Despite these therapeutic advances, nearly all patients will eventually relapse”
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“Null arm controls were generated by controlled Fab-arm exchange of mouse anti-human respiratory syncytial virus neutralizing antibody (Null) with anti-CD3 antibody (NullxCD3) or anti-BCMA antibody (BCMAxNull).(28) Flow cytometry analysis of BCMA expression Human BM mononuclear cells (BM MNCs; ProteoGenex) and MM cell…”
MethodRossi, M., Altomare, E., Botta, C., Cantafio, M. E. G., Gaspari, M., Taverna, D., Sarvide, S., Caracciolo, D., Critelli, P., Conforti, F. S., et al. (2019) · Blood · doi:10.1182/blood-2019-122429 · Cited by 1
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Metadata
- Authors
- Pillarisetti, K., Powers, G., Luistro, L., Babich, A., Baldwin, E., Li, Y., Zhang, X., Mendonça, M., Majewski, N., Nanjunda, R., Chin, D., Packman, K., Elsayed, Y., Attar, R., & Gaudet, F.
- Affiliations
- Oncology and
- Janssen Research & Development (United States) (US)
- IBM (United States) (US)
- Legend Biotech (United States) (US)
- Century Therapeutics (United States) (US)
- Venue
- Blood Advances
- Publisher
- American Society of Hematology
- Published
- 2020-09-21
- Volume
- 4
- Issue
- 18
- Pages
- 4538-4549
- ISSN
- 2473-9529 (ISSN-L)
- 2473-9537
- PMC
- PMC7509877
- OpenAlex
- W3087111554
- Cited by
- 144
- References
- 40
- Citations by year
- 2026: 23 · 2025: 21 · 2024: 31 · 2023: 27 · 2022: 19 · 2021: 20 · 2020: 1
- FWCI
- 10.58
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by-nc-nd
- Locations
- Blood Advances (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Hematology › Multiple Myeloma Research and Treatments
- Life Sciences › Immunology and Microbiology › Immunology › Monoclonal and Polyclonal Antibodies Research
- Health Sciences › Medicine › Oncology › CAR-T cell therapy research
- Keywords
- teclistamab, BCMA, multiple myeloma, bispecific antibodies, T cell redirection, T cell activation, gamma-secretase inhibitors, tumor cell lysis, xenograft models, relapsed/refractory multiple myeloma
- MeSH terms
- Animals, Humans, Lymphocyte Activation, Multiple Myeloma, T-Lymphocytes, Antibodies, Bispecific, Mice, B-Cell Maturation Antigen
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