Bispecific antibody–drug conjugate (aka iza-bren; izalontamab brengitecan; BMS-986507) that binds EGFR and HER3 and delivers a topoisomerase I inhibitor payload (brengitecan) to induce DNA damage and tumor cell death.
Bispecific antibody–drug conjugate that binds EGFR and HER3 on tumor cells, is internalized, and releases a topoisomerase I inhibitor payload (brengitecan) to induce DNA damage and apoptosis in EGFR/HER3-expressing cells.
A bispecific ADC binds EGFR (and HER3) on tumor cells, is internalized, and releases a topoisomerase I inhibitor (brengitecan) that induces DNA damage and apoptosis in the target-expressing cells.
Bispecific antibody–drug conjugate (aka iza-bren; izalontamab brengitecan; BMS-986507) that binds EGFR and HER3 and delivers a topoisomerase I inhibitor payload (brengitecan) to induce DNA damage and tumor cell death.
Bispecific antibody–drug conjugate that binds EGFR and HER3 on tumor cells, is internalized, and releases a topoisomerase I inhibitor payload (brengitecan) to induce DNA damage and apoptosis in EGFR/HER3-expressing cells.
Bispecific ADC binds HER3 (and EGFR), is internalized, and releases a topoisomerase I inhibitor (brengitecan) that causes DNA damage and apoptosis in HER3-expressing cells.
Autologous anti-CD19 CAR T-cell therapy with CD3ζ/CD28 costimulation used to treat relapsed/refractory B-cell lymphomas.
Autologous T cells are genetically engineered to express an anti‑CD19 chimeric antigen receptor with CD28 costimulation and CD3ζ signaling. Upon binding CD19 on malignant B cells, the CAR activates T-cell cytotoxicity, proliferation, and cytokine release, leading to targeted lysis of CD19-positive tumor cells.
Anti-CD19 CAR T cells bind CD19 and, via CD3ζ/CD28 signaling, activate cytotoxic degranulation to kill CD19+ cells through perforin/granzyme–mediated apoptosis.
Autologous anti-CD19 CAR T-cell therapy with CD3ζ/4-1BB costimulation used for B-cell malignancies including DLBCL.
Autologous anti-CD19 CAR T cells incorporating CD3zeta signaling and a 4-1BB costimulatory domain; upon binding CD19 on B cells, they activate, expand, release cytotoxic mediators and cytokines, and kill malignant CD19+ B cells.
Anti-CD19 CAR T cells bind CD19 and, via CD3ζ/4-1BB signaling, activate cytotoxic T-cell functions to kill CD19+ cells through perforin/granzyme release and Fas–FasL–mediated apoptosis.
Autologous anti-CD19 CAR T-cell therapy with CD3ζ/4-1BB costimulation; defined CD4/CD8 composition; used for large B-cell lymphoma.
Autologous T cells engineered to express a CD19-directed chimeric antigen receptor with CD3zeta signaling and 4-1BB costimulation. Upon binding CD19 on malignant B cells, the CAR activates T-cell cytotoxicity, cytokine release, proliferation, and persistence to eliminate CD19-positive tumor cells; product uses a defined CD4/CD8 composition.
Anti-CD19 CAR T cells recognize CD19 on target cells, form an immunologic synapse, and kill via perforin/granzyme cytolysis and death receptor pathways (e.g., Fas–FasL), with supportive cytokine-mediated apoptosis.