A bispecific T-cell–engaging antibody that binds BCMA on myeloma plasma cells and CD3 on T cells, redirecting T cells to kill BCMA-positive tumor cells.
Humanized bispecific antibody that binds BCMA on myeloma plasma cells and CD3 on T cells, crosslinking them to form an immune synapse and redirect cytotoxic T-cell activity to kill BCMA-positive tumor cells.
YES
DIRECT
Teclistamab bridges CD3 on T cells to BCMA on target cells, forming an immune synapse and triggering T‑cell–mediated killing via perforin/granzyme-induced apoptosis of BCMA+ cells.
A bispecific T-cell–engaging antibody that binds BCMA on myeloma plasma cells and CD3 on T cells, redirecting T cells to kill BCMA-positive tumor cells.
Humanized bispecific antibody that binds BCMA on myeloma plasma cells and CD3 on T cells, crosslinking them to form an immune synapse and redirect cytotoxic T-cell activity to kill BCMA-positive tumor cells.
NO
INDIRECT
Teclistamab binds CD3 on T cells to activate and redirect them; it does not kill CD3ε+ T cells but uses them to lyse BCMA+ tumor cells via immune synapse and perforin/granzyme-mediated cytotoxicity.
Allogeneic off-the-shelf CAR-γδ T-cell therapy engineered via lentiviral vector to express an anti-CD19 chimeric antigen receptor; administered intravenously to target and kill CD19-positive B-cell malignancies.
Allogeneic, off-the-shelf gamma-delta T cells engineered via lentiviral vector to express an anti-CD19 chimeric antigen receptor. After IV infusion, the CAR binds CD19 on malignant B cells, triggering MHC-independent activation of gamma-delta T-cell cytotoxic mechanisms (e.g., perforin/granzyme release and cytokine-mediated killing) to selectively eliminate CD19-positive cells.
YES
DIRECT
Anti-CD19 CAR-γδ T cells bind CD19 and directly kill target cells via T-cell effector functions (primarily perforin/granzyme-mediated apoptosis; MHC-independent).
Antibody–cytokine fusion (immunocytokine): an anti-CD38 IgG linked to attenuated IFN-alpha2b that binds CD38+ myeloma/immune cells and delivers IFN to activate IFNAR/type I interferon signaling, driving direct antitumor effects and immune activation.
Modakafusp alfa is an anti-CD38 IgG4–IFN-alpha2b immunocytokine that binds CD38+ myeloma and immune cells and locally delivers interferon. The IFN-alpha moiety engages IFNAR to activate type I interferon signaling, inducing antiproliferative/apoptotic programs in CD38+ tumor cells and stimulating innate/adaptive immune responses.
YES
DIRECT
The anti‑CD38 IgG4–IFN‑α2b fusion binds CD38 on target cells and delivers IFN‑α locally; IFN‑α engages IFNAR on the same cell, activating type I interferon signaling that induces antiproliferative/apoptotic programs, killing CD38+ cells (with additional immune stimulation as a secondary effect).
Antibody–cytokine fusion (immunocytokine): an anti-CD38 IgG linked to attenuated IFN-alpha2b that binds CD38+ myeloma/immune cells and delivers IFN to activate IFNAR/type I interferon signaling, driving direct antitumor effects and immune activation.
Modakafusp alfa is an anti-CD38 IgG4–IFN-alpha2b immunocytokine that binds CD38+ myeloma and immune cells and locally delivers interferon. The IFN-alpha moiety engages IFNAR to activate type I interferon signaling, inducing antiproliferative/apoptotic programs in CD38+ tumor cells and stimulating innate/adaptive immune responses.
NO
INDIRECT
The drug targets CD38, not IFNAR1. After binding CD38 on cells, its IFN-alpha payload engages IFNAR1/2 to trigger type I interferon signaling that can cause antiproliferation/apoptosis in those CD38-bound cells; IFNAR1-expressing cells are not directly targeted.