Anti-CD20 monoclonal antibody that depletes CD20+ B cells via ADCC, CDC, and apoptosis, decreasing anti-PLA2R autoantibodies.
Anti-CD20 monoclonal antibody that binds CD20 on pre-B and mature B lymphocytes and depletes them via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis, reducing pathogenic autoantibody production (e.g., anti-PLA2R).
Rituximab binds CD20 on B cells and engages immune effectors via its Fc to induce antibody‑dependent cellular cytotoxicity and complement‑dependent cytotoxicity; CD20 crosslinking can also trigger apoptosis.
Type II anti-CD20 monoclonal antibody used to deplete B cells and mitigate cytokine release; mediates ADCC/ADCP and direct cell death.
Glycoengineered type II humanized IgG1 anti‑CD20 monoclonal antibody that binds CD20 on B cells and, via enhanced Fc gamma RIIIa engagement, mediates potent antibody‑dependent cellular cytotoxicity and phagocytosis and induces direct, caspase‑independent cell death, leading to depletion of CD20+ B cells (with minimal complement‑dependent cytotoxicity).
Obinutuzumab binds CD20 on B cells and engages FcγRIIIa on immune effectors to mediate ADCC and phagocytosis, and also induces direct, caspase‑independent cell death (with minimal complement involvement).
Autologous, humanized MAGE-A4-directed T-cell receptor-engineered T-cell therapy. Infused T cells recognize MAGE-A4 peptides presented by HLA-A*02 on tumor cells and mediate TCR signaling, cytokine release, and cytotoxic killing.
Autologous T cells are genetically engineered to express a humanized TCR that recognizes MAGE-A4 peptides presented by HLA-A*02 on tumor cells; engagement triggers TCR signaling, cytokine release, expansion, and perforin/granzyme-mediated cytotoxic killing.
Engineered TCR T cells recognize MAGE-A4 peptide presented by HLA-A*02 and kill target cells via TCR-activated perforin/granzyme-mediated apoptosis (and Fas–FasL).
CD20×CD3 bispecific T-cell–engaging IgG monoclonal antibody that redirects T cells to lyse CD20-positive B cells, inducing T-cell activation and cytokine release.
CD20×CD3 bispecific IgG antibody that binds CD3 on T cells and CD20 on B cells, crosslinking T cells to CD20-positive malignant B cells to activate cytotoxic T-lymphocyte responses and cytokine release, resulting in targeted lysis of the B cells.
CD20×CD3 bispecific antibody crosslinks T cells to CD20+ cells, activating CTLs to kill them via perforin/granzyme-mediated cytolysis and cytokine-driven T-cell cytotoxicity.
Type I anti-CD20 monoclonal antibody that depletes B cells via complement-dependent cytotoxicity and ADCC.
Type I anti‑CD20 chimeric monoclonal antibody that binds CD20 on B cells and depletes them primarily via complement‑dependent cytotoxicity (CDC) and antibody‑dependent cellular cytotoxicity/phagocytosis (ADCC/ADCP), leading to elimination of CD20‑positive B cells.
Rituximab binds CD20 on B cells and induces complement-dependent cytotoxicity and Fc-mediated effector killing (ADCC by NK cells and ADCP by macrophages), leading to lysis/clearance of CD20+ cells.