Autologous/allogeneic T cells transduced with a lentiviral vector encoding a CD33-specific CAR; IV infusion with dose escalation; targets CD33+ myeloid blasts in AML and related myeloid malignancies.
Autologous/allogeneic T cells are lentivirally engineered to express a CD33‑specific chimeric antigen receptor. The CAR enables MHC‑independent recognition of CD33 on myeloid blasts, triggering T‑cell activation and expansion, release of perforin/granzymes and inflammatory cytokines, and subsequent cytotoxic clearance of CD33+ AML and related myeloid malignancy cells.
YES
DIRECT
CD33-directed CAR T cells bind CD33 on target cells, activate, and kill them via perforin/granzyme-mediated cytolysis (with cytokine-mediated effects).
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.
YES
DIRECT
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.
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.
NO
INDIRECT
The antibody targets SLAMF7 on tumor cells; its Fc engages CD16A on NK cells to activate ADCC (and possibly CDC/phagocytosis) against SLAMF7+ targets. CD16A-expressing cells are effectors, not killed.
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.
YES
DIRECT
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 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.
NO
INDIRECT
The bispecific binds CD3 on T cells to activate them; the activated T cells then kill BCMA-expressing tumor cells via immune synapse formation and perforin/granzyme-mediated lysis, not CD3+ cells.