Investigational antibody–drug conjugate (ADC) in which a tumor-targeting antibody is linked to a cytotoxic payload; binds a tumor cell-surface antigen, is internalized, and releases an intracellular toxin to kill antigen-expressing HER2-negative breast cancer cells. Target antigen and payload not specified.
An investigational antibody-drug conjugate that binds a tumor cell-surface antigen on HER2-negative breast cancer cells; after binding and internalization, a cleavable linker releases a cytotoxic payload inside the cell, inducing tumor cell death and inhibiting proliferation in antigen-expressing cells.
NO
INDIRECT
The target is unspecified (UNKNOWN), and there is no evidence SHR-A1811 binds it. SHR-A1811 is an ADC that kills only antigen-positive cells via binding, internalization, linker cleavage, and intracellular release of a cytotoxic payload (e.g., a topoisomerase I inhibitor), causing DNA damage and apoptosis.
Investigational antibody–drug conjugate (ADC) comprising a tumor-targeting antibody linked to a cytotoxic payload; binds a tumor cell-surface antigen, is internalized, and releases an intracellular toxin to kill antigen-expressing HER2-negative breast cancer cells. Target antigen and payload not specified.
Anti-TROP-2 IgG1 antibody-drug conjugate linked via a cleavable linker to the exatecan-derived topoisomerase I inhibitor SHR9265. After binding TROP-2 on tumor cells and internalization, the payload is released to inhibit topoisomerase I, blocking DNA replication and inducing DNA damage–mediated cell cycle arrest and apoptosis in TROP-2–expressing (e.g., HER2-negative) breast cancer cells.
YES
DIRECT
An anti-TROP-2 antibody-drug conjugate binds TROP-2, is internalized, the cleavable linker is processed, and the exatecan-derived topoisomerase I inhibitor (SHR9265) is released inside the cell, inhibiting topo I and causing DNA damage, replication arrest, and apoptosis of TROP-2-expressing cells.
Investigational antibody–drug conjugate (ADC) comprising a tumor-targeting antibody linked to a cytotoxic payload; binds a tumor cell-surface antigen, is internalized, and releases an intracellular toxin to kill antigen-expressing HER2-negative breast cancer cells. Target antigen and payload not specified.
Anti-TROP-2 IgG1 antibody-drug conjugate linked via a cleavable linker to the exatecan-derived topoisomerase I inhibitor SHR9265. After binding TROP-2 on tumor cells and internalization, the payload is released to inhibit topoisomerase I, blocking DNA replication and inducing DNA damage–mediated cell cycle arrest and apoptosis in TROP-2–expressing (e.g., HER2-negative) breast cancer cells.
NO
INDIRECT
The ADC binds TROP-2 on tumor cells, is internalized, and releases a topoisomerase I–inhibiting payload that causes DNA damage and apoptosis. Topoisomerase I is the intracellular enzymatic target of the payload, not the directly targeted cell-surface antigen.
An afucosylated humanized IgG1 monoclonal antibody targeting BCMA (TNFRSF17) on malignant plasma cells; mediates Fcγ receptor–dependent ADCC and ADCP and may induce apoptosis.
Afucosylated humanized IgG1 antibody that binds BCMA on malignant plasma cells; enhanced Fcγ receptor engagement drives NK cell–mediated ADCC and macrophage-mediated ADCP, and may also induce direct apoptosis of target cells.
YES
DIRECT
Afucosylated anti-BCMA IgG1 opsonizes BCMA+ cells and engages Fcγ receptors on NK cells and macrophages to mediate ADCC and ADCP; may also trigger apoptosis via BCMA ligation.
An anti-BCMA antibody–drug conjugate linking belantamab to the cytotoxic payload MMAF; after BCMA-mediated internalization, MMAF disrupts microtubules causing cell death, and the antibody retains Fc-mediated ADCC/ADCP.
Belantamab mafodotin is an anti-BCMA antibody–drug conjugate that binds BCMA on malignant plasma cells, is internalized, and releases the MMAF payload to inhibit microtubules and induce cell death; the afucosylated IgG1 antibody also engages Fc receptors to promote ADCC and ADCP.
YES
DIRECT
Belantamab mafodotin binds BCMA, is internalized, and releases the MMAF payload to disrupt microtubules and kill the cell; its afucosylated IgG also engages Fc receptors to mediate ADCC/ADCP.