Chimeric anti-CD20 monoclonal antibody that depletes B cells via ADCC, CDC, and apoptosis.
Chimeric anti‑CD20 monoclonal antibody that binds CD20 on B cells and depletes them via antibody‑dependent cellular cytotoxicity (ADCC), complement‑dependent cytotoxicity (CDC), and induction of apoptosis.
YES
DIRECT
Rituximab binds CD20 on B cells and induces killing via Fc-mediated ADCC by immune effectors, complement-dependent cytotoxicity, and CD20 cross-linking–induced apoptosis.
A subcutaneous bispecific (CD3xCD20) T-cell–engaging monoclonal antibody (GEN3013; DuoBody-CD3xCD20) that binds CD3 on T cells and CD20 on B cells to form an immune synapse and redirect cytotoxic T-cell killing of malignant B cells.
CD3xCD20 bispecific antibody that binds CD3 on T cells and CD20 on B cells to form an immune synapse, activating T-cell cytotoxicity (perforin/granzyme) and redirecting killing of CD20-positive malignant B cells in an MHC-independent manner.
YES
DIRECT
Bispecific antibody links CD3 on T cells to CD20 on B cells, forming an immune synapse that activates T-cell cytotoxicity (perforin/granzyme) to kill CD20+ cells in an MHC-independent manner.
A subcutaneous bispecific (CD3xCD20) T-cell–engaging monoclonal antibody (GEN3013; DuoBody-CD3xCD20) that binds CD3 on T cells and CD20 on B cells to form an immune synapse and redirect cytotoxic T-cell killing of malignant B cells.
CD3xCD20 bispecific antibody that binds CD3 on T cells and CD20 on B cells to form an immune synapse, activating T-cell cytotoxicity (perforin/granzyme) and redirecting killing of CD20-positive malignant B cells in an MHC-independent manner.
NO
INDIRECT
Epcoritamab engages CD3ε on T cells to activate them and bridge to CD20 on B cells; the activated T cells kill CD20+ B cells via perforin/granzyme. CD3ε+ T cells are not the cytotoxic target.
Rabbit polyclonal antilymphocyte globulin used for in vivo T-cell depletion to reduce graft-versus-host disease risk.
Rabbit polyclonal IgG against multiple human T‑cell surface antigens (e.g., CD2, CD3, CD4, CD8, HLA) that depletes T lymphocytes via complement-dependent cytotoxicity, Fc-mediated ADCC/phagocytosis, and apoptosis, producing in vivo T‑cell immunosuppression to reduce GVHD risk.
YES
DIRECT
Polyclonal rabbit IgG in rATG binds CD7 on T cells; Fc activates complement (CDC) and engages Fcγ receptors for ADCC/phagocytosis, and can trigger apoptosis, depleting CD7+ cells.
Autologous, genetically engineered convertible CAR T-cell therapy expressing an inert NKG2D-based receptor; requires an adaptor (MicAbody) to engage tumor targets and activate T cells.
Autologous T cells engineered with an inert NKG2D-based convertible CAR that requires an adaptor antibody (MA-20/ASP101G MicAbody). The adaptor binds CD20 on tumor cells and presents a ULBP2 ligand to the CAR, triggering T-cell activation and cytotoxicity against CD20-positive B-cell malignancies; without the adaptor, the CAR T cells remain inactive.
YES
DIRECT
The adaptor MicAbody (MA-20/ASP101G) binds CD20 on target cells and engages the NKG2D-based convertible CAR on ASP2802 T cells via a ULBP2 ligand, activating the CAR T cells to kill CD20+ cells via cytotoxic T-cell mechanisms (e.g., perforin/granzyme-mediated lysis).