Figure 1.

BCMA-targeted immunotherapies. (1) Antibody-drug conjugate (ADC). After identifying BCMA on the cell surface, ADC internalizes into myeloma cells. Through the degradation by lysosomes or endosomes, the payloads are released, resulting in cytotoxicity. (2) Chimeric antigen receptor (CAR) T cell. The second-generation CAR commonly used today is mainly composed of an extracellular recognition domain (the most commonly used is scFv), a spacer, a transmembrane part, and intracellular structures (costimulatory domain such as CD28 or 4-1BB and an activating domain CD3-zeta). The recognition domain binds to BCMA on the myeloma cell surface as signal 1. The costimulatory domain (CD28 or 4-1BB) is then “aroused” to send signal 2, which is beneficial to CAR-T-cell activation and to prevent their disability. Finally, signals 1 and 2 are transmitted to the CD3-zeta domain to induce CAR-T-cells’ final activation. (3) Bispecific T-cell engager (BiTE). BiTEs can target BCMA on MM tumor cells and CD3ε domain of TCR on T cells simultaneously. After causing the binding of T cells to myeloma cells, the cytotoxic T cells can be activated and secrete cytotoxic factors, thus producing the cytolethal effect.