US-licensed brand of rituximab; chimeric IgG1 anti-CD20 monoclonal antibody that depletes CD20+ B cells via ADCC, CDC, and apoptosis, reducing autoantibody production and B–T cell interactions.
Chimeric IgG1 monoclonal antibody targeting CD20 on pre‑B and mature B lymphocytes; depletes CD20+ B cells primarily via antibody‑dependent cellular cytotoxicity (ADCC), complement‑dependent cytotoxicity (CDC), and apoptosis, thereby reducing autoantibody production and B–T cell interactions (plasma cells largely spared).
YES
DIRECT
Rituximab binds CD20 on B cells and induces killing via Fc-mediated ADCC by NK cells/macrophages, complement-dependent cytotoxicity (CDC), and can trigger apoptosis upon CD20 ligation.
US-licensed brand of rituximab; chimeric IgG1 anti-CD20 monoclonal antibody that depletes CD20+ B cells via ADCC, CDC, and apoptosis, reducing autoantibody production and B–T cell interactions.
Chimeric IgG1 monoclonal antibody targeting CD20 on pre‑B and mature B lymphocytes; depletes CD20+ B cells primarily via antibody‑dependent cellular cytotoxicity (ADCC), complement‑dependent cytotoxicity (CDC), and apoptosis, thereby reducing autoantibody production and B–T cell interactions (plasma cells largely spared).
NO
INDIRECT
Rituximab binds CD20 on B cells; its Fc engages CD16A (FcγRIIIa) on NK cells to trigger ADCC (and complement activation), killing CD20+ targets, not the CD16A+ effector cells.
US-licensed brand of rituximab; chimeric IgG1 anti-CD20 monoclonal antibody that depletes CD20+ B cells via ADCC, CDC, and apoptosis, reducing autoantibody production and B–T cell interactions.
Chimeric IgG1 monoclonal antibody targeting CD20 on pre‑B and mature B lymphocytes; depletes CD20+ B cells primarily via antibody‑dependent cellular cytotoxicity (ADCC), complement‑dependent cytotoxicity (CDC), and apoptosis, thereby reducing autoantibody production and B–T cell interactions (plasma cells largely spared).
NO
INDIRECT
Rituximab binds CD20 on B cells; its Fc engages FcγRIIa (CD32A) on myeloid effectors to trigger ADCC/ADCP and CDC against CD20+ cells. CD32A-expressing cells are not targeted or killed by the drug.
Autologous anti‑CD19 CAR T‑cell therapy with a CD28 co‑stimulatory domain and CD3ζ signaling, engineered to recognize and kill CD19‑positive B cells.
Autologous T cells genetically engineered to express an anti‑CD19 chimeric antigen receptor containing a CD28 co‑stimulatory domain and CD3ζ signaling. Upon binding CD19 on B cells, the CAR activates T‑cell signaling, proliferation, cytokine release, and perforin/granzyme‑mediated cytotoxicity to eliminate CD19‑positive malignant B cells.
YES
DIRECT
Anti‑CD19 CAR T cells recognize CD19 and induce T‑cell cytotoxicity, primarily via perforin/granzyme‑mediated killing (and apoptosis signaling) of CD19+ cells.
US-licensed brand of rituximab; chimeric IgG1 anti-CD20 monoclonal antibody that depletes CD20+ B cells via ADCC, CDC, and apoptosis, reducing autoantibody production and B–T cell interactions.
Chimeric IgG1 monoclonal antibody targeting CD20 on pre‑B and mature B lymphocytes; depletes CD20+ B cells primarily via antibody‑dependent cellular cytotoxicity (ADCC), complement‑dependent cytotoxicity (CDC), and apoptosis, thereby reducing autoantibody production and B–T cell interactions (plasma cells largely spared).
NO
INDIRECT
Rituximab targets CD20, not FcγRIIb (CD32B). Killing occurs when cells express CD20 via ADCC, CDC, and apoptosis; CD32B expression itself does not trigger cytotoxicity (cells are affected only if they also express CD20).