BCMA/TNFRSF17 Antibody Blocking Peptide

B cell maturation antigen (BCMA), also known as tumor necrosis factor receptor superfamily member 17 (TNFRSF17), is a type III transmembrane glycoprotein that plays a role in B cell maturation and differentiation into plasma cells and is a therapeutic target for treatment of multiple myeloma (MM) (1,2). BMCA is synthesized as a protein of 184 amino acids (aa) in length with a theoretical molecular weight of 20.2 kDa consisting of an extracellular N-terminus containing 6 cysteine residues, a transmembrane domain, and an intracellular tumor necrosis factor (TRAF) binding domain (1). BCMA is functionally similar to two other TNFR superfamily members, B cell activation factor receptor (BAFF-R) and transmembrane activator and calcium modulator and cyclophilin ligand interactor (TACI) (1,2). BCMA is primarily expressed on plasmablasts, plasma cells, and late-stage B cells (1,2).

BCMA has two agonistic ligands: BAFF and a proliferation-inducing ligand (APRIL) (1,2). APRIL has higher affinity for BCMA than BAFF and the binding is mediated by CD138/syndeclin-1 (2,3). Activation of BCMA promotes the growth and survival of plasma cells, or MM cells in disease, through several signaling pathways such as NFkappaB, MEK/ERK, AKT, JNK, and p38 (1,2). In MM cells the BCMA activation and downstream signaling cascade functions to upregulate antiapoptotic proteins including Bcl-2, Bcl-xL, and Mcl-1 and protect the cells against therapeutic agents like dexamethasone (2,3).

Given its specific expression on plasma cells but not memory B cells, naive B cells, or hematopoietic stem cells, BCMA has garnered much interest as a therapeutic target for the treatment of MM (1-4). Current BCMA-targeted immunotherapy strategies include antibody-drug conjugates (ADC), chimeric antigen receptor (CAR) T cells, bispecific T cell engager (BiTE), and bispecific/trispecific antibodies (1-4). CAR T cell therapy in particular has demonstrated promising clinical results (2,4). Still, more research needs to be done to improve the efficacy and risk of relapse following CAR T cell therapy and may also include targeting additional antigens in combination with BCMA or utilizing pharmacological agents to increase antigen density (4).

References

1. Yu, B., Jiang, T., & Liu, D. (2020). BCMA-targeted immunotherapy for multiple myeloma. Journal of hematology & oncology, 13(1), 125. https://doi.org/10.1186/s13045-020-00962-7

2. Cho, S. F., Anderson, K. C., & Tai, Y. T. (2018). Targeting B Cell Maturation Antigen (BCMA) in Multiple Myeloma: Potential Uses of BCMA-Based Immunotherapy. Frontiers in immunology, 9, 1821. https://doi.org/10.3389/fimmu.2018.01821

3. Dalla Palma, B., Marchica, V., Catarozzo, M. T., Giuliani, N., & Accardi, F. (2020). Monoclonal and Bispecific Anti-BCMA Antibodies in Multiple Myeloma. Journal of clinical medicine, 9(9), 3022. https://doi.org/10.3390/jcm9093022

4. Mikkilineni, L., & Kochenderfer, J. N. (2021). CAR T cell therapies for patients with multiple myeloma. Nature reviews. Clinical oncology, 18(2), 71-84. https://doi.org/10.1038/s41571-020-0427-6

This product is for research use only and is not approved for use in humans or in clinical diagnosis. Peptides and proteins are guaranteed for 3 months from date of receipt.

Array NBP1-76774PEP

• BCMA/TNFRSF17 Antibodies
• BCMA/TNFRSF17 Lysate
• BCMA/TNFRSF17 Proteins
• BCMA/TNFRSF17 ELISAs
• BCMA/TNFRSF17 Proteins and Enzymes