Anti-CD20 chimeric monoclonal antibody that depletes B cells via ADCC, CDC, and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B lymphocytes and depletes them via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and induction of apoptosis.
YES
DIRECT
Rituximab binds CD20 on B cells and kills via Fc-mediated ADCC, complement-dependent cytotoxicity, and direct apoptosis signaling.
Autologous chimeric antigen receptor T-cell therapy engineered to target CD33 and CD123 on AML cells, inducing T-cell activation and cytotoxic killing with in vivo expansion/persistence.
Autologous T cells are genetically engineered to express chimeric antigen receptors that bind CD33 and CD123 on AML cells. Antigen engagement triggers T‑cell activation, cytokine release, proliferation, and perforin/granzyme‑mediated cytotoxic killing, with in vivo expansion and persistence enabling ongoing clearance of CD33/CD123‑positive leukemic cells.
YES
DIRECT
CD33-specific CAR T cells bind CD33 on target cells, triggering T-cell activation and perforin/granzyme-mediated killing (with possible death receptor pathways), leading to apoptosis of CD33+ cells.
Autologous chimeric antigen receptor T-cell therapy engineered to target CD33 and CD123 on AML cells, inducing T-cell activation and cytotoxic killing with in vivo expansion/persistence.
Autologous T cells are genetically engineered to express chimeric antigen receptors that bind CD33 and CD123 on AML cells. Antigen engagement triggers T‑cell activation, cytokine release, proliferation, and perforin/granzyme‑mediated cytotoxic killing, with in vivo expansion and persistence enabling ongoing clearance of CD33/CD123‑positive leukemic cells.
YES
DIRECT
CAR T cells bind CD123 on target cells and kill them via perforin/granzyme-mediated cytotoxicity (and death-receptor apoptosis).
TROP2-targeting antibody–drug conjugate that delivers a cleavable topoisomerase I inhibitor payload; binding to TROP2 leads to internalization and payload release, causing DNA damage/replication stress and tumor cell death (potential bystander effect).
Humanized anti‑TROP2 IgG1 ADC linked via a cleavable linker to the topoisomerase I inhibitor tirumotecan. Binding to TROP2 on tumor cells triggers internalization and linker cleavage, releasing the payload to inhibit topoisomerase I, inducing DNA damage/replication stress and apoptosis, with a potential bystander effect on neighboring cells.
YES
DIRECT
An anti-TROP2 antibody–drug conjugate binds TROP2 on tumor cells, is internalized, and releases a cleavable topoisomerase I inhibitor (tirumotecan) intracellularly, causing DNA damage/replication stress and apoptosis, with potential bystander killing of neighboring cells.
Anti-HER2 antibody–drug conjugate linking a monoclonal antibody to MMAE via an enzyme-specific linker; binds HER2, is internalized, and releases MMAE to inhibit microtubules and induce tumor cell death.
Anti-HER2 monoclonal antibody linked to MMAE via a cleavable linker; binds HER2 on tumor cells, is internalized, and releases MMAE intracellularly to inhibit microtubule polymerization, causing G2/M arrest and apoptosis in HER2-expressing cells.
NO
INDIRECT
DP303c targets HER2 for internalization and releases MMAE intracellularly; MMAE binds beta-tubulin (vinca site) to inhibit microtubule polymerization, causing G2/M arrest and apoptosis in HER2-positive cells. Tubulin expression alone is not sufficient for killing.