Universal (allogeneic) chimeric antigen receptor T cells engineered to target BCMA (TNFRSF17) to ablate BCMA-expressing plasmablasts and long‑lived plasma cells, aiming to reduce autoantibody production in lupus nephritis.
Allogeneic T cells engineered with a chimeric antigen receptor targeting BCMA (TNFRSF17) recognize and kill BCMA-expressing plasmablasts and long-lived plasma cells via CAR-mediated cytotoxicity, depleting antibody-secreting cells and reducing pathogenic autoantibody production in lupus nephritis.
YES
DIRECT
BCMA-targeted CAR T cells recognize BCMA on plasmablasts/plasma cells and directly kill them via T-cell cytotoxicity (perforin/granzyme release and death-receptor–mediated apoptosis).
Universal (allogeneic) chimeric antigen receptor T cells targeting CD19 to deplete naïve, memory, and activated B cells, aiming to suppress humoral immunity in lupus nephritis.
Allogeneic gene-modified T cells expressing a CD19-directed chimeric antigen receptor bind CD19 on B-lineage cells and trigger cytotoxic killing (perforin/granzyme), depleting naive, memory, and activated B cells to suppress humoral immunity and reduce autoantibody production in lupus nephritis.
YES
DIRECT
CD19 CAR-T cells bind CD19 on B cells and directly induce cytolysis via perforin/granzyme release (and death-receptor signaling), killing CD19+ cells.
An antibody-drug conjugate targeting integrin beta-6 (ITGB6) that is internalized into tumor cells and releases the microtubule inhibitor monomethyl auristatin E (MMAE), leading to microtubule disruption and tumor cell death.
Monoclonal antibody targets integrin beta-6 (ITGB6) on tumor cells, is internalized, and releases the cytotoxic payload monomethyl auristatin E (MMAE). Released MMAE inhibits tubulin polymerization, disrupting microtubules, inducing mitotic arrest, and causing tumor cell death.
YES
DIRECT
ADC binds ITGB6 on tumor cells, is internalized, and releases MMAE that inhibits tubulin polymerization, causing mitotic arrest and cell death.
An antibody-drug conjugate targeting integrin beta-6 (ITGB6) that is internalized into tumor cells and releases the microtubule inhibitor monomethyl auristatin E (MMAE), leading to microtubule disruption and tumor cell death.
Monoclonal antibody targets integrin beta-6 (ITGB6) on tumor cells, is internalized, and releases the cytotoxic payload monomethyl auristatin E (MMAE). Released MMAE inhibits tubulin polymerization, disrupting microtubules, inducing mitotic arrest, and causing tumor cell death.
NO
INDIRECT
The ADC binds ITGB6 on tumor cells, is internalized, and releases MMAE; MMAE then binds the beta‑tubulin vinca site to block microtubule polymerization and cause mitotic arrest and cell death. Killing depends on ITGB6 targeting, not on beta‑tubulin expression per se.
An investigational anti-HER2 (ERBB2) antibody–drug conjugate administered intravenously every 21 days (1–8 mg/kg). The monoclonal antibody targets HER2 on tumor cells, is internalized, and releases a cytotoxic payload to induce tumor cell death; payload not disclosed.
Monoclonal antibody binds HER2 (ERBB2) on tumor cells, is internalized, and releases a linked cytotoxic payload intracellularly to kill the cancer cell; payload type not disclosed.
YES
DIRECT
An anti-HER2 antibody–drug conjugate binds HER2, is internalized, and releases an intracellular cytotoxic payload that kills the target cell.