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.
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.
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).
Chimeric anti-CD20 monoclonal antibody that mediates antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and direct apoptosis of CD20-positive B cells.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and mediates depletion via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and induction of apoptosis of CD20-positive cells.
Rituximab binds CD20 on B cells and triggers killing via Fc-mediated ADCC (NK cells/macrophages) and complement-dependent cytotoxicity, and can also induce apoptosis of CD20+ cells.
A full-length bispecific monoclonal antibody (Lunsumio; RO7030816) that binds CD20 on B cells and CD3 on T cells to redirect autologous T-cell cytotoxicity against malignant B cells in indolent B-cell lymphomas.
Humanized full-length bispecific monoclonal antibody that simultaneously binds CD20 on B cells and CD3 on T cells, physically linking T cells to CD20+ malignant B cells. This T-cell engagement triggers TCR-mediated activation, immune synapse formation, cytokine release, and perforin/granzyme-dependent cytotoxicity, leading to apoptosis of CD20-expressing lymphoma cells.
Mosunetuzumab bridges CD3 on T cells and CD20 on B cells, activating T cells to form an immune synapse and kill CD20+ cells via perforin/granzyme-mediated apoptosis.
Glycoengineered type II anti‑CD20 IgG1 monoclonal antibody that induces direct B‑cell death and enhances immune effector functions (ADCC/ADCP, some CDC) against CD20‑positive B cells.
Glycoengineered humanized type II anti‑CD20 IgG1 monoclonal antibody that binds CD20 on B cells and depletes them via enhanced FcγRIIIa-mediated ADCC/ADCP and direct (caspase‑independent) cell death, with some complement‑dependent cytotoxicity.
Binds CD20 on B cells, causing direct caspase-independent cell death and recruiting Fc gamma RIIIa–bearing effector cells for ADCC/ADCP; also some complement-dependent cytotoxicity.