Defucosylated humanized anti-CCR4 monoclonal antibody (Poteligeo) that binds CCR4 on malignant T cells and Tregs, blocks chemokine signaling/trafficking, and enhances Fc-mediated ADCC to deplete CCR4+ cells.
Defucosylated humanized anti-CCR4 monoclonal antibody (mogamulizumab/Poteligeo) that binds CCR4 on malignant T cells and Tregs, blocks CCR4 chemokine signaling and trafficking, and enhances Fc-mediated ADCC to deplete CCR4-positive cells.
YES
DIRECT
Mogamulizumab binds CCR4 on target cells and, via its defucosylated Fc, strongly engages Fcγ receptors on NK cells to trigger ADCC (and phagocytes for ADCP), depleting CCR4+ cells.
Fc-competent anti-TIGIT monoclonal antibody (GSK4428859A/EOS-448) that blocks TIGIT interactions with CD155/CD112 to enhance T- and NK-cell activity and may deplete TIGIT-high Tregs via ADCC.
Fc-competent anti-TIGIT IgG1 monoclonal antibody that blocks TIGIT interactions with CD155/CD112, restoring CD226 co-stimulation to activate T and NK cells; its Fc domain can mediate ADCC to deplete TIGIT-high regulatory T cells, enhancing anti-tumor immunity.
YES
DIRECT
IgG1 Fc engages Fcγ receptors to mediate ADCC/ADCP against TIGIT-high cells (e.g., Tregs) bound by the antibody, leading to their depletion.
CD30-directed antibody–drug conjugate; internalized into Hodgkin/Reed-Sternberg cells to release MMAE (a microtubule inhibitor), inducing apoptosis and potentially mediating ADCC.
CD30-directed antibody–drug conjugate that binds CD30 on tumor cells, is internalized, and releases the microtubule inhibitor MMAE via proteolytic cleavage of a valine–citrulline linker, causing tubulin depolymerization, G2/M arrest, and apoptosis; may also mediate ADCC.
NO
INDIRECT
Brentuximab vedotin selectively binds CD30, is internalized, and releases MMAE that binds the beta-tubulin vinca site to disrupt microtubules, causing G2/M arrest and apoptosis in CD30-positive cells (ADCC may also contribute). Beta-tubulin expression alone is not directly targeted.
Autologous, genetically engineered T cells modified to express a BCMA-targeted chimeric antigen receptor; upon BCMA engagement, induces MHC-independent T-cell activation (CD3ζ with co-stimulation), expansion, cytokine release, and perforin/granzyme-mediated lysis of multiple myeloma cells.
Autologous T cells engineered to express a BCMA-targeted chimeric antigen receptor; upon BCMA binding, the CAR delivers CD3-zeta and co-stimulatory signals to drive MHC-independent T-cell activation, expansion, and cytokine release, resulting in perforin/granzyme-mediated lysis of BCMA-positive multiple myeloma cells.
YES
DIRECT
BCMA-targeted CAR-T cells bind BCMA on tumor cells, become activated via CD3ζ/co-stimulation, and kill targets by perforin/granzyme-mediated lysis (MHC-independent).
HER2-targeted antibody-drug conjugate that binds HER2 and delivers a cytotoxic payload to kill HER2-expressing tumor cells (with potential bystander effect).
HER2‑targeted trastuzumab‑based ADC that binds HER2, is internalized, and releases a cleavable camptothecin (topoisomerase I–inhibiting) payload, causing DNA damage and apoptosis in HER2‑expressing tumor cells with potential bystander effect.
YES
DIRECT
The trastuzumab-based ADC binds HER2, is internalized, and releases a camptothecin (topoisomerase I inhibitor) payload that causes DNA damage and apoptosis in HER2-expressing cells (with potential bystander effect).