Anti-CD38 IgG1 monoclonal antibody that kills CD38-positive plasma cells via ADCC, CDC, ADCP, and direct apoptosis.
Humanized IgG1 monoclonal antibody targeting CD38 on plasma cells; induces cell death via antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), antibody-dependent cellular phagocytosis (ADCP), and direct apoptosis of CD38-expressing tumor cells.
YES
DIRECT
Isatuximab binds CD38 on target cells and kills them via Fc-mediated ADCC (NK cells), complement-dependent cytotoxicity (CDC), antibody-dependent cellular phagocytosis (ADCP), and can also induce direct apoptosis.
An intravenous antibody–drug conjugate (ABBV-400) consisting of a humanized anti–c-Met monoclonal antibody linked via a cleavable linker to a topoisomerase I–inhibitor payload; targets MET on tumor cells, is internalized, and releases the topo-I inhibitor to induce DNA damage and cell death with potential bystander effect.
Humanized anti–c-Met monoclonal antibody linked via a cleavable linker to a topoisomerase I inhibitor. After binding MET on tumor cells, the ADC is internalized and the linker is cleaved to release the topo‑I inhibitor, causing DNA damage and cell death, with potential bystander killing of adjacent tumor cells.
YES
DIRECT
The anti-MET ADC binds MET on target cells, is internalized, and its cleavable linker releases a topoisomerase I inhibitor that causes DNA damage and cell death (with potential bystander killing).
An intravenous antibody–drug conjugate (ABBV-400) consisting of a humanized anti–c-Met monoclonal antibody linked via a cleavable linker to a topoisomerase I–inhibitor payload; targets MET on tumor cells, is internalized, and releases the topo-I inhibitor to induce DNA damage and cell death with potential bystander effect.
Humanized anti–c-Met monoclonal antibody linked via a cleavable linker to a topoisomerase I inhibitor. After binding MET on tumor cells, the ADC is internalized and the linker is cleaved to release the topo‑I inhibitor, causing DNA damage and cell death, with potential bystander killing of adjacent tumor cells.
NO
INDIRECT
Cells are killed when the ADC binds MET, is internalized, and releases a topoisomerase I–inhibitor payload that poisons TOP1 to cause DNA damage and cell death; killing is determined by MET targeting (with possible bystander effect), not by TOP1 expression itself.
An antibody–drug conjugate (Trodelvy): a humanized anti–TROP‑2 monoclonal antibody linked to SN‑38 (active metabolite of irinotecan), a topoisomerase I inhibitor. After binding TROP‑2 on tumor cells, it is internalized and releases SN‑38 to induce DNA damage and apoptosis with a bystander effect.
Humanized anti–TROP-2 monoclonal antibody linked to SN-38 (topoisomerase I inhibitor). After binding TROP-2 on tumor cells, the ADC is internalized and cleaved to release SN-38, which stabilizes topo I–DNA complexes, causing DNA breaks, inhibition of DNA replication, and apoptosis, with a bystander killing effect.
YES
INDIRECT
After binding TROP-2 and internalization, the ADC releases SN-38, which inhibits DNA topoisomerase I, trapping TOP1-DNA complexes and causing DNA damage and apoptosis; payload can also diffuse for bystander killing.
Anti-CD20 monoclonal antibody that depletes CD20+ B cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20+ cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and induction of apoptosis.
YES
DIRECT
Binds CD20 on B cells and induces killing via antibody-dependent cellular cytotoxicity (Fc-engaged NK/myeloid cells), complement-dependent cytotoxicity, and direct apoptosis signaling.