IgG monoclonal antibodies targeting SLAMF7 to promote NK-cell–mediated cytotoxicity and immune activation.
IgG monoclonal antibodies that bind SLAMF7 (CS1) on myeloma and NK cells, activating NK cells and promoting Fcγ receptor–mediated ADCC against SLAMF7+ tumor cells, with additional complement-dependent cytotoxicity and phagocytosis possible.
Anti-SLAMF7 IgG binds SLAMF7 on tumor cells and engages effector cells via Fc to trigger NK cell–mediated ADCC; it can also activate complement (CDC) and promote antibody-dependent cellular phagocytosis (ADCP), leading to target-cell death.
Bispecific antibodies that bind BCMA on myeloma cells and CD3 on T cells to redirect cytotoxic T cells to tumor.
Bispecific antibody that simultaneously binds BCMA on myeloma cells and CD3 on T cells, physically bringing T cells into contact with tumor cells to trigger TCR signaling, immune synapse formation, T‑cell activation and degranulation, resulting in MHC‑independent lysis of BCMA‑expressing myeloma cells.
The bispecific antibody links CD3 on T cells to BCMA on target cells, triggering TCR signaling and immune synapse formation; activated T cells release perforin/granzymes (and other cytotoxic pathways) to lyse BCMA-expressing cells in an MHC-independent manner.
Bispecific antibodies that bind GPRC5D on myeloma cells and CD3 on T cells to redirect cytotoxic T cells to tumor.
Bispecific antibodies simultaneously bind GPRC5D on myeloma cells and CD3 on T cells, forming an immune synapse that activates and redirects cytotoxic T cells to kill GPRC5D-expressing tumor cells via perforin/granzyme release, independent of antigen presentation.
Bispecific antibody bridges CD3+ T cells to GPRC5D+ cells, triggering T-cell cytotoxicity via immune synapse formation and perforin/granzyme-mediated killing.
Engineered autologous T cells expressing a chimeric antigen receptor targeting BCMA on malignant plasma cells.
Autologous T cells are engineered to express a chimeric antigen receptor that recognizes BCMA on malignant plasma cells. CAR engagement activates CD3ζ signaling with costimulatory domains (e.g., 4-1BB or CD28), driving T‑cell proliferation, cytokine release, and perforin/granzyme‑mediated cytotoxic killing of BCMA‑positive myeloma cells.
BCMA-targeted CAR T cells bind BCMA on tumor cells, activate CD3ζ with costimulation, and kill BCMA+ cells via perforin/granzyme-mediated cytolysis (and death-receptor pathways).
Engineered autologous T cells expressing a chimeric antigen receptor targeting GPRC5D on malignant plasma cells.
Autologous T cells are genetically engineered to express a chimeric antigen receptor that binds GPRC5D on malignant plasma cells. Antigen engagement triggers CAR signaling, activating the T cells to proliferate, secrete cytokines, and kill GPRC5D-positive myeloma cells via perforin/granzyme-mediated cytotoxicity.
GPRC5D-directed CAR T cells bind GPRC5D on target cells and kill them via T cell cytotoxic mechanisms (perforin/granzyme release and death-receptor signaling).