Subcutaneous GPRC5D×CD3 bispecific T‑cell–engaging antibody that redirects CD3+ T cells to kill GPRC5D‑positive myeloma cells.
Humanized bispecific antibody that binds CD3 on T cells and GPRC5D on myeloma cells, crosslinking T cells to GPRC5D+ tumor cells to trigger cytotoxic T-cell activation and tumor cell killing.
Bispecific CD3×GPRC5D engagement crosslinks T cells to GPRC5D+ cells, triggering CTL-mediated killing via immunologic synapse, perforin/granzyme release and apoptosis.
Subcutaneous BCMA×CD3 bispecific antibody that induces T‑cell cytotoxicity against BCMA‑positive plasma cells.
Humanized bispecific antibody that binds BCMA on malignant plasma cells and CD3 on T cells, crosslinking them to form an immune synapse and activate T-cell cytotoxicity (perforin/granzyme and cytokine-mediated killing) against BCMA-positive myeloma cells.
Teclistamab bridges CD3 on T cells to BCMA on target cells, forming an immune synapse that triggers T‑cell killing via perforin/granzyme release and cytokine-mediated cytotoxicity of BCMA-expressing cells.
Intravenous anti‑SLAMF7 monoclonal antibody that activates NK cells and mediates ADCC against SLAMF7‑positive myeloma cells.
Humanized anti‑SLAMF7 (CS1) IgG1 monoclonal antibody that binds SLAMF7 on myeloma and NK cells, activates NK cells, and mediates Fc‑dependent antibody‑dependent cellular cytotoxicity (ADCC) to eliminate SLAMF7‑positive myeloma cells.
Elotuzumab binds SLAMF7 on target cells and its Fc engages Fcγ receptors on NK cells, triggering antibody‑dependent cellular cytotoxicity (ADCC) to kill SLAMF7‑positive cells.
Fc-engineered human IgG1 monoclonal antibody (AGEN1181) targeting CTLA-4; blocks CTLA-4 to enhance T-cell priming/expansion and, via its engineered Fc region, may deplete intratumoral regulatory T cells.
Fc-engineered human IgG1 monoclonal antibody targeting CTLA-4; blocks CTLA-4 signaling to enhance T-cell priming and activation, and via enhanced Fc receptor engagement can deplete intratumoral regulatory T cells (e.g., by ADCC), thereby boosting antitumor cytotoxic T-cell responses.
Binds CTLA-4 on T cells (especially intratumoral Tregs) and engages Fcγ receptors on NK cells/macrophages to trigger ADCC/ADCP (and possibly CDC), depleting CTLA-4–expressing cells.
Autologous anti-CD19 chimeric antigen receptor (CAR) T‑cell therapy using a 4‑1BB costimulatory domain; patient T cells are engineered to target CD19+ B cells, inducing T‑cell activation, cytolysis, and cytokine release in relapsed/refractory B‑cell malignancies.
Autologous anti-CD19 chimeric antigen receptor T-cell therapy: patient T cells are transduced to express a CAR with an anti-CD19 scFv linked to CD3zeta and a 4-1BB costimulatory domain; upon binding CD19 on B-cell malignancies, CAR T cells activate, expand, secrete cytotoxic molecules and cytokines, and lyse CD19+ cells, with 4-1BB enhancing activation and persistence.
Anti-CD19 CAR T cells bind CD19 and, via CD3zeta/4-1BB signaling, activate and kill targets through perforin/granzyme-mediated cytolysis (and death-receptor pathways).