B7-H3 (CD276)–targeting antibody-drug conjugate that delivers a topoisomerase I inhibitor payload to tumor cells, causing DNA damage and tumor cell death.
Monoclonal antibody targeting B7-H3 (CD276) delivers a topoisomerase I inhibitor via a tumor protease–cleavable linker; upon binding and internalization in B7-H3–expressing tumor cells, the released payload inhibits topoisomerase I, causing DNA damage, replication blockade, cell cycle arrest, and apoptosis.
ADC binds B7-H3 on target cells, is internalized, and releases a topoisomerase I inhibitor via protease-cleavable linker, causing DNA damage, replication blockade, cell cycle arrest, and apoptosis.
Candidate rituximab biosimilar; 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 anti-CD20 monoclonal antibody that binds CD20 on B lymphocytes and depletes them via ADCC, complement-dependent cytotoxicity, and apoptosis, thereby reducing autoantibody production and B–T cell interactions (plasma cells largely spared).
Anti-CD20 IgG1 binds CD20 on B cells and induces killing via Fc-mediated ADCC by effector cells, complement-dependent cytotoxicity (CDC), and apoptosis upon crosslinking.
EU-approved 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 anti-CD20 monoclonal antibody that binds CD20 on pre-B and mature B lymphocytes and depletes them via antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and apoptosis, thereby reducing autoantibody production and B–T cell interactions.
Anti-CD20 IgG1 binds CD20 on B cells and induces Fc-mediated ADCC (NK/macrophages) and complement-dependent lysis; cross-linking can also trigger apoptosis.
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).
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.
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.
Anti‑CD19 CAR T cells recognize CD19 and induce T‑cell cytotoxicity, primarily via perforin/granzyme‑mediated killing (and apoptosis signaling) of CD19+ cells.