Type II glycoengineered anti-CD20 monoclonal antibody administered IV; depletes B cells via enhanced ADCC, direct cell death, and some complement activation.
Type II glycoengineered anti-CD20 monoclonal antibody that depletes CD20+ B cells via enhanced ADCC/ADCP, direct non-apoptotic cell death, and limited complement-dependent cytotoxicity.
YES
DIRECT
Anti-CD20 mAb depletes CD20+ B cells via enhanced Fc-mediated ADCC/ADCP (NK cells, macrophages), direct non-apoptotic cell death (type II), and some complement-dependent cytotoxicity.
An anti-HER2 antibody–drug conjugate (T-DXd, Enhertu) composed of trastuzumab linked via a cleavable linker to a DXd topoisomerase I inhibitor payload; binds HER2, is internalized, releases DXd to induce DNA damage and cell death with a bystander effect, and the antibody component also inhibits HER2 signaling and mediates ADCC.
Humanized anti‑HER2 mAb (trastuzumab) targets HER2 on tumor cells and is internalized; a cleavable linker releases the DXd payload (a topoisomerase I inhibitor), causing DNA damage, replication arrest, and apoptosis. The membrane‑permeable payload enables a bystander killing effect, and the antibody component also inhibits HER2 signaling and mediates ADCC.
YES
DIRECT
The ADC binds HER2, is internalized, and releases a DXd topoisomerase I inhibitor that causes DNA damage and apoptosis; Fc can also trigger ADCC, with a membrane-permeable payload enabling bystander killing.
An anti-HER2 antibody–drug conjugate (T-DXd, Enhertu) composed of trastuzumab linked via a cleavable linker to a DXd topoisomerase I inhibitor payload; binds HER2, is internalized, releases DXd to induce DNA damage and cell death with a bystander effect, and the antibody component also inhibits HER2 signaling and mediates ADCC.
Humanized anti‑HER2 mAb (trastuzumab) targets HER2 on tumor cells and is internalized; a cleavable linker releases the DXd payload (a topoisomerase I inhibitor), causing DNA damage, replication arrest, and apoptosis. The membrane‑permeable payload enables a bystander killing effect, and the antibody component also inhibits HER2 signaling and mediates ADCC.
NO
INDIRECT
Topoisomerase I is not the antigen targeted by the ADC. The drug binds HER2, is internalized, and releases the DXd payload, which inhibits Topoisomerase I to cause DNA damage and apoptosis (with bystander and ADCC effects). Killing is driven by HER2 targeting, not Top1 expression.
Anti-CLDN18.2 antibody–drug conjugate that binds CLDN18.2 on tumor cells, is internalized, and releases an MMAE payload to disrupt microtubules causing mitotic arrest and apoptosis; may also mediate Fc-dependent ADCC.
Anti-CLDN18.2 antibody–drug conjugate that binds CLDN18.2 on tumor cells, is internalized, and releases an MMAE payload to disrupt microtubules, causing mitotic arrest and apoptosis; may also mediate Fc-dependent ADCC.
YES
DIRECT
Anti-CLDN18.2 ADC binds CLDN18.2, is internalized, and releases MMAE to disrupt microtubules causing mitotic arrest and apoptosis; Fc-mediated ADCC may also contribute.
Anti-CLDN18.2 antibody–drug conjugate that binds CLDN18.2 on tumor cells, is internalized, and releases an MMAE payload to disrupt microtubules causing mitotic arrest and apoptosis; may also mediate Fc-dependent ADCC.
Anti-CLDN18.2 antibody–drug conjugate that binds CLDN18.2 on tumor cells, is internalized, and releases an MMAE payload to disrupt microtubules, causing mitotic arrest and apoptosis; may also mediate Fc-dependent ADCC.
NO
INDIRECT
AZD0901 binds CLDN18.2 (not tubulin), is internalized, and releases MMAE that disrupts tubulin/microtubules to cause mitotic arrest and apoptosis; Fc-mediated ADCC may also contribute.