Type II anti-CD20 monoclonal antibody (brand name Gazyva) used as a priming dose to deplete B cells and mitigate cytokine release syndrome prior to step-up glofitamab.
Glycoengineered humanized type II anti-CD20 IgG1 that binds CD20 on B cells and depletes them via enhanced Fc gamma RIIIa–mediated ADCC/ADCP and direct, caspase-independent cell death (with minimal CDC). In this trial it is used as a priming dose to reduce CD20+ B-cell burden and mitigate cytokine-release risk before glofitamab.
Anti-CD20 IgG1 binds CD20 on B cells and kills them via enhanced Fc gamma RIIIa–mediated ADCC and ADCP, plus direct caspase-independent cell death (with minimal complement-mediated cytotoxicity).
Autologous T cells genetically engineered to express a chimeric antigen receptor targeting carcinoembryonic antigen (CEA/CEACAM5), administered intravenously or intraperitoneally to recognize and kill CEA-positive tumor cells.
Autologous T cells are genetically engineered to express a chimeric antigen receptor that binds carcinoembryonic antigen (CEA/CEACAM5) on tumor cells. CAR engagement triggers CD3ζ (with costimulatory domains) signaling to activate and expand the T cells, resulting in cytokine release and perforin/granzyme-mediated killing of CEA-positive cancer cells.
CAR recognition of CEA activates T cells to kill CEA-expressing cells via perforin/granzyme-mediated cytolysis (and death-receptor apoptosis).
Subcutaneous CD3×CD20 bispecific T‑cell–engaging antibody that redirects patient T cells (via CD3) to CD20‑positive lymphoma cells, inducing perforin/granzyme‑mediated cytotoxicity and cytokine release.
Bispecific CD3×CD20 antibody that binds CD3 on patient T cells and CD20 on B‑cell lymphoma cells, crosslinking them to activate T cells and induce immunologic‑synapse formation, perforin/granzyme‑mediated cytotoxicity, and cytokine release for MHC‑independent killing of CD20‑positive tumor cells.
Bispecific CD3×CD20 engagement redirects patient T cells to CD20+ cells, forming an immunologic synapse and inducing perforin/granzyme-mediated, MHC-independent killing.
Anti‑CD20 IgG1 monoclonal antibody that depletes B cells through antibody‑dependent cellular cytotoxicity (ADCC), complement‑dependent cytotoxicity (CDC), and induction of apoptosis.
Chimeric anti-CD20 IgG1 monoclonal antibody that binds CD20 on B cells and depletes CD20-positive cells via Fc-mediated antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and induction of apoptosis.
Rituximab binds CD20 on B cells and triggers Fc-mediated ADCC by immune effectors, complement-dependent cytotoxicity (CDC), and can directly induce apoptosis of CD20+ cells.
TROP2-targeted antibody-drug conjugate (aka iza-bren; izalontamab brengitecan; BMS-986507) that delivers the topoisomerase I inhibitor brengitecan to TROP2-expressing tumor cells, causing DNA damage and cell death.
TROP2-targeted monoclonal antibody linked to the topoisomerase I inhibitor brengitecan. After binding TROP2 on tumor cells, the ADC is internalized and releases brengitecan, which inhibits topo I, causing DNA damage (replication-associated strand breaks) and tumor cell death, with potential bystander effect in TROP2-expressing tumors.
The TROP2-binding ADC is internalized and releases the topoisomerase I inhibitor brengitecan inside TROP2-expressing cells, causing replication-associated DNA damage and cell death, with potential bystander killing.