Autologous anti-CD19 chimeric antigen receptor (CAR) T-cell therapy; genetically engineered T cells administered IV to deplete CD19+ B-cell compartments.
Autologous T cells are engineered ex vivo to express an anti‑CD19 chimeric antigen receptor and, after IV infusion, bind CD19 on B‑lineage cells (naive and memory B cells and plasmablasts). CAR engagement activates the T cells to kill targets via perforin/granzyme and cytokine‑mediated cytotoxicity, depleting CD19+ B cells and reducing autoantibody production and B cell–mediated antigen presentation/co‑stimulation.
YES
DIRECT
Anti-CD19 CAR T cells bind CD19 on B cells and directly kill them via T‑cell cytotoxicity, primarily perforin/granzyme-mediated apoptosis (with cytokine/Fas–FasL contributions).
Bispecific monoclonal antibody immunotherapy targeting PD-L1 and CD47 to restore T-cell activity (via PD-1/PD-L1 checkpoint blockade) and enhance macrophage-mediated phagocytosis (by disrupting CD47–SIRPα signaling).
Bispecific monoclonal antibody that binds PD-L1 (higher affinity) and CD47, blocking PD-1/PD-L1 checkpoint signaling to restore T-cell activity and disrupting CD47–SIRPa interactions to enhance macrophage-mediated phagocytosis of tumor cells; preferential PD-L1 binding aims to concentrate activity on PD-L1/CD47 double-positive tumor cells and reduce on-target hematologic toxicity.
YES
INDIRECT
By blocking PD‑L1, the drug reverses PD‑1/PD‑L1 checkpoint inhibition, enabling cytotoxic T cells to kill PD‑L1–expressing tumor cells; additionally, its CD47 blockade promotes macrophage-mediated phagocytosis of PD‑L1/CD47 double‑positive cells.
An antibody-drug conjugate targeting Trop-2; a humanized anti–Trop-2 IgG linked to SN-38 (active metabolite of irinotecan), a topoisomerase I inhibitor that is released upon internalization to induce DNA damage and apoptosis.
Humanized anti–TROP2 IgG linked to SN-38. Binds TROP2 on tumor cells, is internalized, and releases SN-38 after linker cleavage. SN-38 inhibits topoisomerase I by stabilizing Topo I–DNA complexes, causing DNA strand breaks, impaired replication, and apoptosis; may exert a bystander effect due to membrane-permeable payload.
YES
DIRECT
The ADC binds TROP-2 on target cells, is internalized, and releases SN-38 after linker cleavage; SN-38 inhibits topoisomerase I, causing DNA strand breaks and apoptosis (with possible bystander killing due to payload permeability).
An antibody-drug conjugate targeting Trop-2; a humanized anti–Trop-2 IgG linked to SN-38 (active metabolite of irinotecan), a topoisomerase I inhibitor that is released upon internalization to induce DNA damage and apoptosis.
Humanized anti–TROP2 IgG linked to SN-38. Binds TROP2 on tumor cells, is internalized, and releases SN-38 after linker cleavage. SN-38 inhibits topoisomerase I by stabilizing Topo I–DNA complexes, causing DNA strand breaks, impaired replication, and apoptosis; may exert a bystander effect due to membrane-permeable payload.
NO
INDIRECT
Sacituzumab govitecan targets TROP2 on tumor cells, is internalized, and releases SN-38, which inhibits topoisomerase I to cause DNA damage and apoptosis. Topoisomerase I is the payload’s enzymatic target, not the ADC’s binding target, so Topoisomerase I–expressing cells are not specifically targeted (bystander killing may occur).