Chimeric IgG1 anti-CD20 monoclonal antibody that targets B cells and induces cell killing via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and antibody-dependent cellular phagocytosis.
Chimeric IgG1 monoclonal antibody targeting CD20 on B cells; depletes CD20-positive cells via complement-dependent cytotoxicity (CDC), antibody-dependent cellular cytotoxicity (ADCC), and antibody-dependent cellular phagocytosis (ADCP), with possible direct apoptotic signaling.
Rituximab binds CD20 on B cells and induces complement-dependent cytotoxicity and Fc-mediated ADCC/ADCP by immune effectors, with possible direct apoptotic signaling upon CD20 crosslinking.
Autologous CD30-directed chimeric antigen receptor (CAR) T-cell therapy; patient T cells are genetically modified to express a CAR that binds CD30 on malignant lymphocytes, enabling MHC-independent activation and cytotoxic killing with in vivo expansion/persistence.
Autologous T cells genetically modified to express a CD30-specific chimeric antigen receptor. CAR engagement of CD30 on malignant lymphocytes triggers MHC-independent T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing, with in vivo expansion and persistence.
CD30-specific CAR-T cells bind CD30 on target cells, triggering MHC-independent T-cell activation and perforin/granzyme-mediated cytolysis (and Fas/FasL apoptosis).
Bispecific antibody–drug conjugate (aka iza-bren; izalontamab brengitecan; BMS-986507) targeting EGFR and HER3. After binding, it is internalized and releases a camptothecin-class topoisomerase I inhibitor payload (brengitecan) to induce DNA damage; it also blocks EGFR/HER3 signaling.
Bispecific ADC that binds EGFR and HER3 on tumor cells; after receptor-mediated internalization it releases a camptothecin-class topoisomerase I inhibitor payload (brengitecan) to induce DNA damage and cell death, while concurrently inhibiting EGFR/HER3 signaling.
The bispecific ADC binds EGFR on tumor cells, is internalized, and releases a camptothecin-class topoisomerase I inhibitor (brengitecan) that causes DNA damage and cell death; it also inhibits EGFR/HER3 signaling.
Anti-CD38 IgG1 monoclonal antibody that binds CD38 on malignant plasma cells, mediating ADCC, ADCP, and CDC, inducing direct apoptosis, and inhibiting CD38 ectoenzyme activity.
Humanized IgG1 monoclonal antibody targeting CD38 on malignant plasma cells; binding activates Fc-mediated effector functions (ADCC, ADCP, CDC), can induce direct apoptosis, and inhibits CD38 ectoenzyme activity, leading to depletion/lysis of CD38-expressing tumor cells.
Isatuximab binds CD38 on target cells and recruits immune effectors via its Fc to mediate ADCC and ADCP, activates complement for CDC, and can trigger direct apoptosis, leading to lysis of CD38+ cells.
Humanized IgG1 monoclonal antibody targeting HER2 (ERBB2); inhibits downstream signaling and mediates ADCC in HER2‑overexpressing tumors.
Humanized IgG1 monoclonal antibody against HER2 (ERBB2) that binds the extracellular domain, inhibits receptor dimerization and downstream MAPK/PI3K signaling, and mediates antibody‑dependent cell‑mediated cytotoxicity (ADCC) against HER2‑overexpressing tumor cells.
Trastuzumab binds HER2 on target cells and its Fc engages Fcγ receptor–bearing immune cells (e.g., NK cells) to trigger antibody-dependent cell-mediated cytotoxicity, with possible complement activation, leading to lysis of HER2+ cells.