An intravenous, glycoengineered type I anti‑CD20 monoclonal antibody immunotherapy that selectively binds CD20 on B cells and depletes them primarily via enhanced antibody‑dependent cellular cytotoxicity, with contributions from complement‑dependent cytotoxicity and apoptosis; targets pre‑B and mature CD20+ B lymphocytes (sparing plasma cells) to reduce antigen presentation, costimulation, and proinflammatory cytokine signaling in multiple sclerosis.
Glycoengineered type I anti‑CD20 monoclonal antibody that binds CD20 on pre‑B and mature B lymphocytes and depletes them primarily via enhanced antibody‑dependent cellular cytotoxicity, with additional complement‑dependent cytotoxicity and apoptosis; spares plasma cells and reduces B‑cell antigen presentation, costimulation, and proinflammatory cytokine signaling.
YES
DIRECT
Ublituximab binds CD20 on B cells and induces killing via Fc-mediated antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis.
Intravenous CD20×CD3 bispecific antibody that redirects T cells to kill CD20-positive B cells.
CD20×CD3 bispecific antibody that binds CD3 on T cells and CD20 on B cells to crosslink them, activating T cells to mediate cytotoxic killing of CD20-positive B-cell malignancies.
NO
INDIRECT
Binds CD3 on T cells to engage and activate them; the activated T cells kill CD20-positive B cells (perforin/granzyme). CD3+ T cells are not targeted for killing.
Fourth-generation dual-target autologous chimeric antigen receptor T cells engineered to recognize CD19 on B cells and BCMA (TNFRSF17) on plasmablasts/plasma cells, inducing cytolytic depletion of autoreactive B-lineage cells to reduce autoantibody production.
Autologous fourth-generation CAR T cells engineered to recognize CD19 and BCMA activate upon antigen binding and mediate cytolytic killing of B cells, plasmablasts, and plasma cells, thereby depleting autoreactive B-lineage populations and reducing autoantibody production.
YES
DIRECT
BCMA-targeted CAR-T cells bind BCMA on plasmablasts/plasma cells, become activated, and kill them via perforin/granzyme-mediated cytolysis and death-receptor pathways (e.g., Fas/FasL).
Anti-HER2 monoclonal antibody that blocks HER2 signaling and mediates antibody-dependent cellular cytotoxicity (ADCC).
Humanized anti-HER2 monoclonal antibody (IgG1) that binds the extracellular domain of HER2 (ERBB2), inhibits HER2-driven signaling (PI3K/AKT/MAPK), promotes receptor internalization/degradation, and induces immune-mediated tumor cell killing via antibody-dependent cellular cytotoxicity (ADCC) in HER2-overexpressing cancers.
YES
DIRECT
Trastuzumab binds HER2 on target cells; its Fc engages Fcγ receptors on NK cells to trigger antibody‑dependent cellular cytotoxicity (ADCC), with some complement activation, leading to lysis/apoptosis of HER2+ cells.
Anti-HER2 monoclonal antibody that prevents HER2/HER3 dimerization and mediates ADCC.
Humanized anti-HER2 monoclonal antibody that binds the HER2 extracellular dimerization domain, preventing HER2/HER3 dimerization and downstream PI3K/AKT/MAPK signaling, leading to growth inhibition/apoptosis; also engages immune effector cells to mediate ADCC.
YES
DIRECT
Pertuzumab binds HER2 and recruits FcγR-bearing immune cells (e.g., NK cells) to mediate ADCC, killing target cells; HER2 dimerization blockade can also promote apoptosis.