Izalontamab brengitecan (BMS-986507), a bispecific EGFR/HER3-targeted antibody–drug conjugate that is internalized upon binding and releases a topoisomerase I inhibitor payload (brengitecan) to induce DNA damage and tumor cell death.
Bispecific EGFR/HER3-targeted antibody–drug conjugate that binds EGFR- and HER3-expressing tumor cells, is internalized, and releases a topoisomerase I inhibitor payload (brengitecan) to induce DNA damage and tumor cell death.
The EGFR/HER3-targeted ADC binds HER3 on tumor cells, is internalized, and releases a topoisomerase I inhibitor (brengitecan) that causes DNA damage leading to cell death.
B7-H6–targeted, CD3-redirecting bispecific T-cell–engaging monoclonal antibody that binds B7-H6 on tumor cells and CD3 on T cells to activate cytotoxic T-cell killing.
IgG-like bispecific antibody that binds B7-H6 on tumor cells and CD3 on T cells, cross-linking T cells to B7-H6–expressing cancer cells to activate and redirect cytotoxic T-lymphocyte killing (perforin/granzyme-mediated lysis) of tumor cells with minimal normal tissue expression.
Bispecific antibody binds B7-H6 on tumor cells and CD3 on T cells, cross-linking and activating CTLs to kill target cells via perforin/granzyme-mediated lysis.
Patient-derived CD4/CD8 T cells are collected, lentivirally transduced ex vivo to express a CD19-specific chimeric antigen receptor, expanded, and infused. CAR engagement of CD19 activates T-cell cytotoxicity, producing deep depletion of CD19+ B cells and their precursors to curb autoreactive B-cell activity and autoantibody production.
Autologous T cells are lentivirally engineered to express a CD19-specific chimeric antigen receptor; upon binding CD19 on B cells, CAR signaling activates T-cell cytotoxicity and cytokine release, leading to deep depletion of CD19+ B cells and their precursors, thereby suppressing autoreactive B-cell activity and autoantibody production.
CAR-engineered T cells bind CD19 on target cells and trigger cytotoxic T-cell killing via perforin/granzyme release (and Fas–FasL apoptosis), depleting CD19+ cells.
Autologous gamma delta T cells engineered to express a third-generation chimeric antigen receptor targeting glypican-3 (GPC3) with co-stimulatory domains to enhance activation and tumor cell lysis.
Autologous gamma delta T cells are genetically engineered to express a third‑generation chimeric antigen receptor targeting glypican‑3 (GPC3). Upon binding GPC3 on tumor cells, the CAR delivers activation and co‑stimulatory signals (e.g., CD28/4‑1BB), driving gamma delta T‑cell activation, cytokine release, proliferation, and MHC‑independent cytotoxic killing of GPC3‑positive tumor cells.
CAR-engineered gamma-delta T cells bind GPC3 on target cells, receive CD3z/CD28/4-1BB signaling, and kill GPC3+ cells via MHC-independent cytotoxicity (perforin/granzyme and Fas/FasL-mediated apoptosis).
Autologous, non–genetically engineered, ex vivo–expanded polyclonal multi–tumor-associated antigen (multiTAA)–specific T-cell therapy that recognizes multiple shared TAAs on pancreatic adenocarcinoma via native, MHC-restricted TCRs to mediate cytotoxic killing and cytokine-driven immune activation.
Autologous, ex vivo-expanded polyclonal CD4+/CD8+ T cells with native, MHC-restricted TCRs specific for multiple shared tumor-associated antigens on pancreatic adenocarcinoma. After infusion, these T cells recognize antigen-MHC complexes on tumor cells and mediate cytotoxic killing (perforin/granzyme) and cytokine-driven immune activation; multi-antigen targeting reduces antigen-loss escape and may improve durability.
Autologous T cells recognize survivin-derived peptides presented on MHC via native TCRs and directly kill target cells through perforin/granzyme-mediated cytotoxicity (with supportive cytokine effects).