Antibody–drug conjugate targeting nectin‑4; the monoclonal antibody delivers the microtubule-disrupting payload MMAE (vedotin) to tumor cells, causing apoptosis.
Monoclonal antibody targets nectin-4 on tumor cells, is internalized, and releases the cytotoxic payload MMAE via a cleavable linker; MMAE binds tubulin, inhibits microtubule polymerization, causes G2/M arrest, and induces apoptosis in nectin-4–expressing cells.
NO
INDIRECT
Enfortumab vedotin targets nectin-4 for internalization; once inside, MMAE binds the vinca site on beta-tubulin to inhibit microtubule polymerization and trigger G2/M arrest and apoptosis. Beta-tubulin expression alone is not sufficient for targeting or killing.
Autologous chimeric antigen receptor (CAR) T-cell therapy engineered to dual-target BCMA and CD19, depleting CD19+ B cells and BCMA+ plasmablasts/long-lived plasma cells to reduce pathogenic autoantibodies and reset humoral immunity in refractory SLE.
Autologous CAR T cells engineered to dual-target CD19 and BCMA, inducing cytolytic depletion of CD19+ B cells and BCMA+ plasmablasts/long‑lived plasma cells to reduce pathogenic autoantibodies and reset humoral immunity in refractory SLE.
YES
DIRECT
CD19-expressing cells are recognized by CD19-directed CAR T cells, triggering T-cell cytotoxicity (perforin/granzyme and Fas-FasL pathways) leading to direct lysis/apoptosis.
Autologous chimeric antigen receptor (CAR) T-cell therapy engineered to dual-target BCMA and CD19, depleting CD19+ B cells and BCMA+ plasmablasts/long-lived plasma cells to reduce pathogenic autoantibodies and reset humoral immunity in refractory SLE.
Autologous CAR T cells engineered to dual-target CD19 and BCMA, inducing cytolytic depletion of CD19+ B cells and BCMA+ plasmablasts/long‑lived plasma cells to reduce pathogenic autoantibodies and reset humoral immunity in refractory SLE.
YES
DIRECT
BCMA-targeted CAR T cells recognize BCMA on cells and kill them via T-cell cytotoxic mechanisms (perforin/granzyme-mediated apoptosis and Fas–FasL).
Autologous T cells engineered to express a chimeric antigen receptor targeting CD19, administered as a single IV infusion after lymphodepletion to deplete CD19+ B-lineage cells and modulate humoral autoimmunity.
Autologous T cells engineered to express a CD19-specific chimeric antigen receptor recognize and bind CD19 on B-lineage cells, triggering T-cell activation, proliferation, and cytotoxic killing (perforin/granzyme). This results in deep depletion of CD19+ B cells (including naive, memory, and plasmablasts), reducing autoantibody production and B cell–mediated immune activation after lymphodepletion and a single IV infusion.
YES
DIRECT
CD19-specific CAR-T cells bind CD19 on target cells and kill them via T-cell cytotoxicity (perforin/granzyme-mediated apoptosis, with possible Fas/FasL signaling).
Therapeutic monoclonal antibody targeting CCR8 on tumor-infiltrating regulatory T cells, engineered for enhanced ADCC to selectively deplete CCR8+ Tregs and reduce intratumoral immunosuppression.
HC006 is a monoclonal antibody that binds CCR8 on tumor-infiltrating regulatory T cells and is Fc-engineered for enhanced ADCC, recruiting FcγR-expressing effector cells (e.g., NK cells) to selectively deplete CCR8+ Tregs in the tumor microenvironment, thereby reducing intratumoral immunosuppression and promoting antitumor immunity.
YES
DIRECT
Anti-CCR8 mAb binds CCR8 on Tregs; its Fc engages FcγR on NK cells (and other effectors) to trigger ADCC (and ADCP), leading to depletion of CCR8+ cells.