iPSC-derived natural killer cells engineered with a chimeric antigen receptor targeting CD33 to direct NK-mediated cytotoxicity against AML cells.
iPSC-derived natural killer cells engineered to express a chimeric antigen receptor that binds CD33 on AML blasts, triggering antigen-specific NK activation and cytotoxicity (perforin/granzyme release and cytokine-mediated killing) to eliminate CD33-positive leukemia cells.
YES
DIRECT
CAR binding to CD33 activates NK-cell cytotoxicity, leading to immune-synapse formation and perforin/granzyme-mediated apoptosis of CD33+ cells (with possible death-receptor/cytokine-mediated killing).
Autologous T cells engineered ex vivo with a chimeric antigen receptor to recognize a B-cell antigen and eliminate pathogenic B cells to suppress humoral autoimmunity in IgA nephropathy and primary membranous nephropathy; administered at 0.5×10^8 or 1×10^8 cells.
Autologous T cells are engineered ex vivo with a chimeric antigen receptor that recognizes a B‑cell antigen. Upon infusion, the CAR-T cells bind and kill B cells, depleting autoreactive/antibody‑producing clones to suppress humoral autoimmunity and reduce pathogenic immune complexes in IgA nephropathy and primary membranous nephropathy.
YES
DIRECT
CAR-T cells recognize CD19 on B cells and directly kill them via T‑cell cytotoxic pathways (perforin/granzyme release and Fas–FasL–mediated apoptosis).
An anti–Trop-2 antibody–drug conjugate composed of a humanized monoclonal antibody targeting TACSTD2 (Trop-2) linked to a cytotoxic payload; it binds Trop-2 on tumor cells, is internalized, and releases the payload intracellularly to induce tumor cell death.
Humanized anti-Trop-2 monoclonal antibody linked via a cleavable linker to a camptothecin analog; binds TROP-2 (TACSTD2) on tumor cells, is internalized, and releases the topoisomerase I-inhibiting payload intracellularly to block DNA replication, causing cell-cycle arrest and apoptosis in TROP-2–expressing tumors.
NO
INDIRECT
The ADC binds TROP-2 on tumor cells, is internalized, and releases a camptothecin analog that inhibits DNA topoisomerase I, causing DNA damage and apoptosis; topoisomerase I is the intracellular payload target, not the direct cell-surface target.
An antibody-drug conjugate targeting TROP-2 that delivers the cytotoxic payload SN-38 (a topoisomerase I inhibitor) to tumor cells, causing DNA damage and cell death, with potential bystander effect.
Humanized anti-TROP-2 monoclonal antibody linked via a cleavable linker to SN-38 (topoisomerase I inhibitor). After binding TROP-2 on tumor cells, the ADC is internalized and releases SN-38, which stabilizes topoisomerase I-DNA complexes, causing DNA breaks, inhibition of replication, and apoptosis; released payload can also exert a bystander effect.
YES
DIRECT
ADC binds TROP-2, is internalized, linker is cleaved to release SN-38 (topoisomerase I inhibitor), causing DNA damage, replication arrest, and apoptosis; released payload can also cause a bystander effect.
An antibody-drug conjugate targeting TROP-2 that delivers the cytotoxic payload SN-38 (a topoisomerase I inhibitor) to tumor cells, causing DNA damage and cell death, with potential bystander effect.
Humanized anti-TROP-2 monoclonal antibody linked via a cleavable linker to SN-38 (topoisomerase I inhibitor). After binding TROP-2 on tumor cells, the ADC is internalized and releases SN-38, which stabilizes topoisomerase I-DNA complexes, causing DNA breaks, inhibition of replication, and apoptosis; released payload can also exert a bystander effect.
YES
INDIRECT
The ADC does not bind topoisomerase I; it binds TROP-2, is internalized, and releases SN-38, which inhibits DNA topoisomerase I, stabilizing cleavage complexes and causing DNA breaks and apoptosis (with possible bystander effect).