Autologous, lentiviral-transduced T cells engineered to express CARs targeting both CD19 and CD20 (dual-target CAR T) with CD3ζ and co-stimulatory domains, enabling recognition and elimination of CD19+ and/or CD20+ B-cell malignancies.
Autologous lentiviral-transduced T cells engineered with a dual CAR targeting CD19 and CD20. Binding to CD19/CD20 on B cells triggers CD3zeta signaling with co-stimulatory domains, inducing T-cell activation, expansion, cytokine release, and cytotoxic killing of malignant B cells; dual targeting is intended to mitigate antigen escape and relapse.
YES
DIRECT
CAR T cells recognize CD20 via the CAR, activating CD3zeta/co-stimulatory signaling and inducing T-cell effector functions (perforin/granzymes and Fas–FasL), resulting in lysis/apoptosis of CD20+ cells.
An intravenous bispecific, bivalent T-cell–engaging antibody that binds CD3 on T cells and the MAGE-A4 peptide presented by HLA-A*02:01 on tumor cells to redirect T-cell cytotoxicity.
An intravenous bispecific, bivalent antibody that binds CD3 on T cells and the MAGE-A4 peptide presented by HLA-A*02:01 on tumor cells, cross-linking T cells to cancer cells. This engagement activates TCR/CD3 signaling, induces cytokine release, and redirects cytotoxic T-cell killing of MAGE-A4–expressing tumor cells.
NO
INDIRECT
CDR404 binds CD3 on T cells to activate and tether them to MAGE-A4/HLA-A2–positive tumor cells, leading T-cell–mediated killing of the tumor (perforin/granzyme). CD3+ T cells are effectors, not killed by the drug.
An intravenous bispecific, bivalent T-cell–engaging antibody that binds CD3 on T cells and the MAGE-A4 peptide presented by HLA-A*02:01 on tumor cells to redirect T-cell cytotoxicity.
An intravenous bispecific, bivalent antibody that binds CD3 on T cells and the MAGE-A4 peptide presented by HLA-A*02:01 on tumor cells, cross-linking T cells to cancer cells. This engagement activates TCR/CD3 signaling, induces cytokine release, and redirects cytotoxic T-cell killing of MAGE-A4–expressing tumor cells.
YES
DIRECT
The bispecific T-cell engager binds the MAGE-A4 peptide–HLA-A*02:01 complex on tumor cells and CD3 on T cells, cross-linking and activating T cells to release perforin/granzymes and induce apoptosis of the target-expressing cells.
Izalontamab brengitecan (BMS-986507), a bispecific antibody–drug conjugate targeting EGFR and HER3 that releases a camptothecin/topoisomerase I inhibitor payload to induce DNA damage and tumor cell death.
Bispecific ADC targeting EGFR and HER3; upon receptor binding and internalization, it releases a camptothecin/topoisomerase I–inhibitor payload that induces DNA damage (via Topo I inhibition) leading to tumor cell death, with potential bystander effect.
YES
DIRECT
The bispecific ADC binds EGFR on tumor cells, is internalized, and releases a camptothecin/topoisomerase I–inhibitor payload that induces DNA damage leading to cell death (with potential bystander effect).
Izalontamab brengitecan (BMS-986507), a bispecific antibody–drug conjugate targeting EGFR and HER3 that releases a camptothecin/topoisomerase I inhibitor payload to induce DNA damage and tumor cell death.
Bispecific ADC targeting EGFR and HER3; upon receptor binding and internalization, it releases a camptothecin/topoisomerase I–inhibitor payload that induces DNA damage (via Topo I inhibition) leading to tumor cell death, with potential bystander effect.
YES
DIRECT
The bispecific ADC binds HER3 on tumor cells, is internalized, and releases a camptothecin/topoisomerase I inhibitor payload that induces DNA damage, directly killing HER3-expressing cells (with potential bystander effect).