Investigational CEACAM5-directed antibody-drug conjugate (also known as SGN-CEACAM5C; SAR445953) with a camptothecin-class topoisomerase I inhibitor payload; binds CEACAM5 on tumor cells, is internalized, and releases payload to induce DNA damage and cell death.
CEACAM5-targeted monoclonal antibody linked to a camptothecin-class topoisomerase I inhibitor; upon binding CEACAM5 on tumor cells, the ADC is internalized and releases the cytotoxic payload to cause TOP1-mediated DNA damage and tumor cell death.
ADC binds CEACAM5 on tumor cells, is internalized, and releases a camptothecin-class TOP1 inhibitor that causes DNA damage leading to tumor cell death.
A minimally blocking anti-CTLA-4 monoclonal antibody (immune checkpoint–targeting biologic) administered intravenously every 3 weeks, designed to bind CTLA-4 while minimally blocking CD80/CD86 interaction to enhance anti-tumor immunity with potentially reduced toxicity.
Human IgG1 monoclonal antibody targeting CTLA-4 that minimally blocks CTLA-4 binding to CD80/CD86 while engaging Fc receptors to deplete intratumoral regulatory T cells and reduce their proliferation, thereby relieving immune suppression and enhancing effector T-cell–mediated antitumor responses with potentially lower toxicity.
IgG1 anti-CTLA-4 binds CTLA-4 on Tregs and engages Fc gamma receptors on NK cells/macrophages to mediate ADCC/ADCP (and possibly complement), depleting CTLA-4–expressing cells.
A T-cell–redirecting bispecific monoclonal antibody that binds CD20 on B cells and CD3 on T cells (2:1 CD20:CD3 format), forming an immune synapse that activates cytotoxic T cells to kill CD20+ malignant B cells.
CD20xCD3 bispecific monoclonal antibody (2:1 CD20:CD3) that binds CD20 on B cells and CD3 on T cells, forming an immune synapse that activates T-cell receptor signaling and redirects cytotoxic T cells to kill CD20-positive malignant B cells.
Bispecific antibody bridges CD20 on B cells and CD3 on T cells, forming an immune synapse that activates T cells to release perforin/granzymes and kill CD20+ cells.
Type I chimeric anti-CD20 monoclonal antibody that depletes CD20+ B cells via antibody-dependent cellular cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC).
Chimeric type I anti‑CD20 monoclonal antibody that binds CD20 on B cells and induces B‑cell depletion primarily via antibody‑dependent cellular cytotoxicity (ADCC) and complement‑dependent cytotoxicity (CDC), leading to lysis/apoptosis of CD20+ cells.
Rituximab binds CD20 on B cells and recruits effector mechanisms—ADCC via Fcγ receptor–bearing cells (e.g., NK cells) and complement-dependent cytotoxicity via C1q activation—resulting in lysis/apoptosis of CD20+ cells.
Also referred to as FDA022-BB05, this is an intravenous HER2-targeted monoclonal antibody–drug conjugate (ADC) that binds HER2 on tumor cells, is internalized, and releases an intracellular cytotoxic payload; it may also contribute to HER2 pathway blockade and Fc-mediated effector functions.
HER2-targeted monoclonal antibody–drug conjugate that binds HER2 on tumor cells, is internalized, and releases an intracellular cytotoxic payload to kill the cells; may also inhibit HER2 signaling and mediate Fc-dependent effector functions (e.g., ADCC).
The HER2-targeted ADC binds HER2, is internalized, and releases an intracellular cytotoxic payload that kills the cell; Fc-mediated ADCC may also contribute.