Anti-CLDN18.2 antibody-drug conjugate that binds claudin 18.2 on tumor cells, is internalized, and delivers a cytotoxic payload to kill CLDN18.2-expressing cells.
Anti-CLDN18.2 monoclonal antibody linked to MMAE; binds CLDN18.2 on tumor cells, is internalized, and releases MMAE to inhibit tubulin polymerization, causing G2/M arrest and apoptosis in CLDN18.2-expressing cells.
NO
INDIRECT
EO-3021 targets CLDN18.2 for uptake; after internalization it releases MMAE, which binds beta-tubulin to inhibit microtubule polymerization, causing G2/M arrest and apoptosis in CLDN18.2-positive cells.
Donor-derived anti-CD33 chimeric antigen receptor (CAR) T-cell therapy using lentiviral-transduced allogeneic T cells from the patient’s original HLA-matched alloHCT donor; targets CD33 on AML cells to induce T-cell activation and cytolytic killing of CD33-positive leukemia and myeloid cells.
Allogeneic donor-derived T cells are lentivirally engineered to express a CD33-specific chimeric antigen receptor; upon binding CD33 on AML and other myeloid cells, CAR signaling (CD3ζ/costimulation) activates the T cells to proliferate, release cytokines, and mediate cytolytic killing of CD33-positive cells.
YES
DIRECT
CD33-specific CAR T cells bind CD33 on target cells, become activated via CAR (CD3ζ/costim) signaling, and kill CD33+ cells via perforin/granzyme-mediated cytolysis (and related T-cell effector mechanisms).
Anti-CD20 monoclonal antibody that depletes B cells via complement-dependent cytotoxicity and antibody-dependent cellular cytotoxicity.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20-positive cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and phagocytosis, with potential direct induction of apoptosis.
YES
DIRECT
Rituximab binds CD20 on B cells and triggers complement-dependent cytotoxicity (classical pathway lysis) and Fc-mediated antibody-dependent cellular cytotoxicity/phagocytosis by NK cells and macrophages; it may also induce apoptosis.
Investigational next-generation HER2-targeted antibody–drug conjugate that binds HER2, is internalized, and releases a cytotoxic payload to kill HER2-expressing tumor cells.
Humanized anti-HER2 monoclonal antibody linked via an enzyme-cleavable linker to a topoisomerase I inhibitor payload. After binding HER2 and internalization, the payload is released to inhibit DNA topoisomerase I, blocking DNA replication and inducing cell-cycle arrest and apoptosis in HER2-expressing tumor cells.
YES
DIRECT
ADC binds HER2 on tumor cells, is internalized, and releases a topoisomerase I inhibitor that blocks DNA replication, causing cell-cycle arrest and apoptosis of HER2-expressing cells.
Engineered Toxin Body biologic protein that binds CTLA-4 and delivers a toxin-based kill signal to selectively deplete CTLA-4–expressing cells (e.g., regulatory T cells) within tumors to dismantle the immunosuppressive tumor microenvironment.
Engineered toxin body with biparatopic VHHs that bind CTLA-4 on tumor-infiltrating cells (primarily Tregs), internalize, and release the Shiga-like toxin A subunit, which depurinates 28S rRNA to block protein synthesis and induce apoptosis, selectively depleting CTLA-4+ immunosuppressive cells and enhancing anti-tumor T-cell responses.
YES
DIRECT
Biparatopic VHHs bind CTLA-4 on target cells, internalize, and release Shiga-like toxin A that depurinates 28S rRNA, blocks protein synthesis, and induces apoptosis of CTLA-4+ cells.