An autologous anti-CD20 chimeric antigen receptor T-cell (CAR-T) therapy in which a patient’s T cells are engineered ex vivo to express a CAR that binds CD20 on B cells; CAR activation triggers cytotoxic activity and cytokine release to eliminate CD20-positive malignant B cells, with expected on-target B-cell aplasia.
Autologous T cells are engineered ex vivo to express a chimeric antigen receptor that binds CD20 on B cells; CAR engagement activates T-cell cytotoxicity and cytokine release to eliminate CD20-positive malignant B cells, with expected on-target B-cell aplasia.
YES
DIRECT
Anti-CD20 CAR-T cells bind CD20 on B cells and induce T-cell–mediated killing via perforin/granzyme and death-receptor pathways, leading to apoptosis/lysis.
An antibody–drug conjugate (ADC) consisting of a humanized anti–Trop-2 monoclonal antibody linked to SN-38 (the active metabolite of irinotecan), a topoisomerase I inhibitor. After binding Trop-2 on tumor cells, the ADC is internalized and releases SN-38 to inhibit topoisomerase I, leading to DNA damage and apoptosis. Administered IV at 10 mg/kg on days 1 and 8 of a 21-day cycle.
Humanized anti–Trop-2 monoclonal antibody linked to SN-38 (topoisomerase I inhibitor). After binding Trop-2 on tumor cells, the ADC is internalized and releases SN-38, which stabilizes Topo I–DNA complexes, causing DNA damage, S-phase arrest, and apoptosis; membrane-permeable SN-38 can produce a bystander effect.
YES
DIRECT
ADC binds TROP2 on tumor cells, is internalized, and releases SN-38, a topoisomerase I inhibitor that causes DNA damage (Topo I–DNA complex stabilization), S‑phase arrest, and apoptosis; membrane-permeable SN‑38 can also cause a bystander effect.
An allogeneic, CD19-directed CAR T-cell therapy engineered ex vivo using CRISPR-Cas9; administered as a single IV infusion after lymphodepleting chemotherapy. Donor T cells are modified to express a CD19-specific chimeric antigen receptor that activates cytotoxic pathways (perforin/granzyme release and cytokine-mediated killing) to lyse malignant B cells in relapsed/refractory B-cell malignancies.
Allogeneic donor T cells are CRISPR-Cas9–engineered to express a CD19-specific chimeric antigen receptor and to knock out endogenous TCR, TGFBR2, and Regnase-1. After infusion, CAR binding to CD19 on B cells activates cytotoxic pathways (perforin/granzyme release and cytokine-mediated killing) to eliminate CD19-positive malignant B cells, while edits reduce GVHD risk and enhance potency and persistence.
YES
DIRECT
CD19-directed CAR T cells bind CD19 on target B cells and induce killing via perforin/granzyme-mediated cytolysis and apoptosis (death receptor/cytokine pathways).
Adoptive natural killer (NK) cell therapy intended to eliminate HER2-expressing tumor cells via NK-mediated cytotoxicity; used as a cellular immunotherapy.
Adoptive transfer of ex vivo expanded natural killer (NK) cells designed to recognize and eliminate HER2-expressing tumor cells via NK-mediated cytotoxicity (perforin/granzyme and death-receptor pathways), with lymphodepletion used to enhance NK-cell engraftment and persistence.
YES
DIRECT
HER2-targeted adoptive NK cells recognize HER2+ tumor cells and kill them via NK cytotoxicity, including perforin/granzyme release and death-receptor (e.g., Fas/TRAIL) pathways.
Autologous CAR T-cell gene therapy made by non-viral electroporation of CD3+ T cells to express a mesothelin-specific CAR (alpaca VHH, CD28, CD3ζ) and to secrete anti-PD-1 nanobody and anti-CTLA-4 antibody for local checkpoint blockade in MSLN+ solid tumors.
Autologous T cells are engineered via non-viral electroporation to express a mesothelin-targeted CAR (alpaca VHH binder with CD28 costimulation and CD3ζ signaling) that mediates antigen-specific cytotoxicity against MSLN+ tumor cells. The cells also secrete an anti-PD-1 nanobody and an anti-CTLA-4 antibody to provide local checkpoint blockade within the tumor microenvironment, enhancing T-cell activation, proliferation, and persistence while reducing exhaustion and Treg-mediated suppression.
YES
DIRECT
CAR T cells bind mesothelin on target cells, become activated, and kill them via perforin/granzyme-mediated cytolysis (and death-receptor pathways).