Anti‑CD20 monoclonal antibody that depletes B cells via ADCC, complement-dependent cytotoxicity, and induction of apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20-positive malignant and normal B cells via antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and induction of apoptosis.
Rituximab binds CD20 on B cells and its Fc region recruits immune effectors to induce ADCC and complement-dependent cytotoxicity; crosslinking can also trigger apoptosis.
An intravenous MAT-Fab bispecific T-cell–engaging antibody that binds CD3 on T cells and ROR1 on tumor cells to redirect cytotoxic T lymphocytes against ROR1-positive cancers.
EMB-07 is a bispecific antibody that simultaneously binds CD3 on T cells and ROR1 on tumor cells, bringing cytotoxic T lymphocytes into close proximity with ROR1-positive cancer cells to trigger TCR/CD3 activation and perforin/granzyme-mediated tumor cell killing.
EMB-07 links CD3 on T cells to ROR1 on tumor cells, activating CTLs to kill ROR1+ cells via perforin/granzyme-mediated cytotoxicity.
Autologous gene-modified cellular therapy composed of a dual population of CD5-knockout T cells and CD5-knockout anti-CD5 CAR-T cells, engineered to target CD5+ malignant T cells and prevent fratricide; administered as a single IV infusion.
Autologous gene-edited therapy comprising CD5-knockout anti-CD5 CAR-T cells (plus CD5-knockout T cells) that recognize CD5 on malignant T cells. CAR engagement activates T-cell cytotoxicity to kill CD5+ tumor cells, while CD5 knockout prevents fratricide and may relieve inhibitory CD5 signaling to enhance persistence and function.
Anti-CD5 CAR T cells recognize CD5 on target cells, activate, and kill them via perforin/granzyme-mediated cytolysis and Fas-FasL apoptosis.
Intravenous anti-CD20 monoclonal antibody that depletes CD20+ B cells via complement-mediated cytotoxicity, ADCC, and apoptosis.
Chimeric anti‑CD20 monoclonal antibody that binds CD20 on B cells and depletes them via complement-dependent cytotoxicity, antibody‑dependent cellular cytotoxicity, and induction of apoptosis.
Rituximab binds CD20 on B cells and triggers complement-dependent cytotoxicity and Fc-mediated ADCC/ADCP, leading to lysis and apoptosis of CD20+ cells.
Oral BCL-2 inhibitor (BH3 mimetic) that restores mitochondrial apoptosis by inhibiting anti-apoptotic BCL-2.
Selective oral BH3-mimetic that inhibits anti-apoptotic BCL-2, restoring mitochondrial apoptosis by promoting MOMP and caspase activation in BCL-2–dependent tumor cells; spares BCL-XL to reduce thrombocytopenia.
Venetoclax inhibits anti-apoptotic BCL-2, triggering mitochondrial outer membrane permeabilization, cytochrome c release, and caspase activation to induce intrinsic apoptosis in BCL-2-dependent cells.