Autologous genetically engineered T cells expressing a chimeric antigen receptor targeting CD19 to deplete CD19-positive B-lineage cells and reset autoreactive B-cell pools in autoimmune disease.
Autologous T cells are engineered to express a chimeric antigen receptor targeting CD19, enabling MHC-independent recognition and cytotoxic killing of CD19-positive B-lineage cells (naive and memory B cells, plasmablasts). Through T-cell activation and effector mechanisms (perforin/granzyme and cytokines), the therapy depletes B cells, reduces autoantibody production, and helps reset autoreactive B-cell pools in autoimmune disease.
YES
DIRECT
CAR-T cells recognize CD19 via the CAR and kill target cells through T-cell effector mechanisms (perforin/granzyme-mediated cytolysis and apoptosis, ± death-receptor pathways).
Anti-CD123 antibody-drug conjugate (ADC) that binds IL-3Rα (CD123) on leukemic blasts and delivers an internalized DNA-alkylating cytotoxic payload.
Humanized anti‑CD123 (IL‑3Rα) IgG1 antibody–drug conjugate that binds CD123 on leukemic cells, is internalized, and via a cleavable linker releases an indolino‑benzodiazepine dimer DNA‑alkylating payload. The payload alkylates DNA (via an imine moiety), causing S‑phase arrest and apoptosis in CD123‑overexpressing cells.
YES
DIRECT
The anti-CD123 ADC binds IL3RA on target cells, is internalized, and releases a DNA-alkylating indolino-benzodiazepine payload via a cleavable linker, leading to DNA damage, S-phase arrest, and apoptosis of CD123-expressing cells.
Anti-CD123 antibody-drug conjugate (ADC) that binds IL-3Rα (CD123) on leukemic blasts and delivers an internalized DNA-alkylating cytotoxic payload.
Humanized anti‑CD123 (IL‑3Rα) IgG1 antibody–drug conjugate that binds CD123 on leukemic cells, is internalized, and via a cleavable linker releases an indolino‑benzodiazepine dimer DNA‑alkylating payload. The payload alkylates DNA (via an imine moiety), causing S‑phase arrest and apoptosis in CD123‑overexpressing cells.
NO
INDIRECT
Pivekimab sunirine targets CD123 on the cell surface; after internalization it releases a DNA‑alkylating payload that damages genomic DNA, causing S‑phase arrest and apoptosis in CD123‑overexpressing cells. DNA itself is not the targeted antigen.
Autologous, genetically engineered T cells expressing a chimeric antigen receptor targeting MUC16 to recognize and kill MUC16-positive tumor cells.
Autologous T cells engineered to express a chimeric antigen receptor that binds MUC16 on tumor cells; CAR signaling activates the T cells to proliferate, release cytotoxic mediators, and lyse MUC16-positive cancer cells.
YES
DIRECT
Anti-MUC16 CAR T cells recognize MUC16 on target cells, activate, and directly lyse them via T-cell cytotoxic pathways (perforin/granzyme release and Fas-FasL-mediated apoptosis).
Autologous, gene-modified CAR T-cell therapy that dual-targets CD19 and CD20 to induce antigen-dependent T-cell activation, proliferation, cytokine release, and cytotoxic elimination of malignant B cells; administered as a single-dose infusion after lymphodepletion.
Autologous T cells genetically engineered to express chimeric antigen receptors that co-target CD19 and CD20; antigen engagement activates CAR signaling leading to T-cell activation, proliferation, cytokine release, and cytotoxic elimination of malignant B cells (on-target B-cell aplasia).
YES
DIRECT
CAR T cells recognize CD19 and are activated via CAR signaling, then kill target cells through perforin/granzyme-mediated cytolysis (and Fas–FasL apoptosis), causing on-target B-cell aplasia.