Autologous BCMA-directed CAR T-cell therapy (CART-ddBCMA) using a D-domain CAR binder; after cyclophosphamide/fludarabine lymphodepletion, infused CAR-T cells recognize BCMA on malignant plasma cells and induce T-cell activation and cytotoxic killing.
Autologous T cells are genetically engineered to express a BCMA-targeting chimeric antigen receptor (D-domain binder). Following cyclophosphamide/fludarabine lymphodepletion, the infused CAR T cells recognize BCMA on malignant plasma cells and trigger CAR-mediated T-cell activation, cytokine release, proliferation, and cytotoxic killing of BCMA-expressing myeloma cells.
BCMA-directed CAR T cells bind BCMA on target cells, activate via CAR signaling, and kill through perforin/granzyme-mediated cytolysis and apoptosis (with cytokine release).
Anti-CD38 monoclonal antibody that depletes CD38-positive clonal plasma cells via ADCC, CDC, apoptosis, and immune modulation.
Human IgG1κ anti-CD38 monoclonal antibody that binds CD38 on clonal plasma cells, triggering Fc-mediated ADCC, ADCP, complement-dependent cytotoxicity, and direct apoptosis; also depletes CD38+ immunosuppressive cells (Tregs, B cells, MDSCs), enhancing antitumor immunity.
Anti-CD38 IgG1 mAb binds CD38 on target cells and triggers Fc-mediated ADCC (NK cells), ADCP (macrophages), complement-dependent cytotoxicity (CDC), and can induce direct apoptosis upon binding/crosslinking.
Anti-CD38 IgG1 monoclonal antibody mediating ADCC, CDC, and ADCP against CD38+ myeloma cells.
Human IgG1κ monoclonal antibody targeting CD38 on myeloma and other hematologic tumor cells; binding triggers immune effector–mediated killing (ADCC, CDC, ADCP) and can directly induce apoptosis, while depleting CD38+ immunosuppressive cells (Tregs, Bregs, MDSCs) to enhance antitumor immunity.
Daratumumab binds CD38 on target cells and, via its Fc region, recruits immune effectors to kill by ADCC (NK cells), CDC (complement), and ADCP (macrophages); crosslinking can also directly induce apoptosis.
CD20×CD3 bispecific T‑cell–engaging antibody that redirects cytotoxic T cells to kill CD20+ B cells.
CD20xCD3 bispecific antibody that binds CD3 on T cells and CD20 on B cells, crosslinks them to form an immune synapse, activating and redirecting cytotoxic T cells to kill CD20-positive B-cell malignancies.
Bispecific antibody links CD3+ T cells to CD20+ cells, forming an immune synapse and activating T cells to kill via perforin/granzyme-mediated cytolysis and apoptosis.
Anti-CD20 monoclonal antibody causing B‑cell depletion via ADCC, CDC, and direct cell death.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes them via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and direct induction of cell death.
Rituximab binds CD20 on B cells and kills them via Fc-mediated ADCC by immune effector cells, complement-dependent cytotoxicity, and direct induction of apoptosis.