Intravenous chimeric anti-CD20 monoclonal antibody that targets CD20 on B cells, inducing antibody-dependent cellular cytotoxicity and complement-dependent cytotoxicity, leading to B-cell depletion.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and induces antibody-dependent cellular cytotoxicity and complement-dependent cytotoxicity, leading to depletion of CD20-positive B cells.
Rituximab binds CD20 on B cells and triggers Fc-mediated ADCC/ADCP and complement-dependent cytotoxicity (CDC), leading to lysis and depletion of CD20+ cells.
Actinium-225–conjugated FPI-2053 targeted alpha therapy that binds EGFR/cMET and delivers high-LET alpha radiation causing DNA double-strand breaks and tumor cell kill.
Bispecific anti-EGFR/c-MET humanized antibody (FPI-2053) chelated to DOTA and radiolabeled with actinium-225; targets EGFR/c-MET on tumor cells and delivers high-LET alpha radiation that causes DNA double-strand breaks and tumor cell death, with potential secondary anti-tumor immune activation from antigen release.
A bispecific anti-EGFR/c-MET antibody conjugated to actinium-225 binds c-MET on target cells and delivers high-LET alpha radiation, causing DNA double-strand breaks and apoptotic tumor cell death without immune cell mediation.
Antibody-drug conjugate targeting Nectin-4 that delivers MMAE, a microtubule-disrupting cytotoxin, to kill tumor cells.
Antibody–drug conjugate targeting Nectin-4; upon binding and internalization, a cleavable linker releases MMAE, which inhibits tubulin polymerization, causing G2/M cell-cycle arrest and apoptosis in Nectin-4–expressing tumor cells.
The ADC binds Nectin-4, is internalized, and releases MMAE via linker cleavage; MMAE disrupts microtubules, causing G2/M arrest and apoptosis of Nectin-4–expressing cells.
Off-the-shelf, allogeneic gamma delta T-cell therapy conjugated to an anti-CD20 antibody that redirects gdT cells to CD20+ B cells for targeted cytotoxicity.
Off-the-shelf allogeneic gamma delta T cells are conjugated to rituximab via DNA linkers; rituximab binds CD20 on malignant B cells, redirecting the gdT cells to CD20+ targets to deliver MHC-independent cytotoxicity and IFN-γ secretion, and to stimulate broader anti-tumor immune responses.
Rituximab binds CD20 on B cells and bridges them to allogeneic gamma delta T cells, which form an immune synapse and kill the CD20+ cells via MHC-independent perforin/granzyme-mediated cytotoxicity (with IFN-γ secretion).
Type II anti-CD20 monoclonal antibody that depletes B cells via direct cell death and immune effector mechanisms (e.g., ADCC).
Glycoengineered type II anti-CD20 humanized IgG1 that binds CD20 on B cells and induces depletion via enhanced FcγRIIIa-mediated ADCC and direct, caspase‑independent cell death (with minimal CDC).
Anti-CD20 antibody binds CD20 on B cells, triggering direct caspase-independent cell death and recruiting effector cells via FcγRIIIa to mediate ADCC (with minimal CDC).