A HER2-targeted antibody-drug conjugate consisting of a humanized anti-HER2 IgG1 (trastuzumab) linked to a topoisomerase I inhibitor payload (deruxtecan); binds HER2 (including low expressers), is internalized, releases the payload to inhibit Topo I causing DNA damage and apoptosis, with a membrane-permeable bystander effect; the antibody can also mediate ADCC.
HER2-targeted ADC: trastuzumab binds HER2 on tumor cells (including low expressers), is internalized, and releases the topoisomerase I inhibitor deruxtecan (DXd), causing DNA damage, replication arrest, and apoptosis; the membrane-permeable payload enables bystander killing, and the IgG1 Fc can mediate ADCC.
YES
DIRECT
The ADC binds HER2, is internalized, and releases the topoisomerase I inhibitor deruxtecan, causing DNA damage and apoptosis; the IgG1 Fc can also mediate ADCC, with a membrane-permeable payload enabling bystander killing.
A HER2-targeted antibody-drug conjugate consisting of a humanized anti-HER2 IgG1 (trastuzumab) linked to a topoisomerase I inhibitor payload (deruxtecan); binds HER2 (including low expressers), is internalized, releases the payload to inhibit Topo I causing DNA damage and apoptosis, with a membrane-permeable bystander effect; the antibody can also mediate ADCC.
HER2-targeted ADC: trastuzumab binds HER2 on tumor cells (including low expressers), is internalized, and releases the topoisomerase I inhibitor deruxtecan (DXd), causing DNA damage, replication arrest, and apoptosis; the membrane-permeable payload enables bystander killing, and the IgG1 Fc can mediate ADCC.
NO
INDIRECT
The ADC targets HER2, is internalized, and releases deruxtecan that inhibits Topoisomerase I, causing DNA damage and apoptosis; Topoisomerase I is the payload’s enzymatic target, not the antigen that directs cell killing.
Synthetic long peptide (26 aa) vaccine derived from CMV pp65, formulated in Montanide ISA 51 to induce CMV-specific CD8+ cytotoxic T cells, CD4+ helper T cells, and antibody responses via MHC class I/II; adjuvant enhances dendritic cell activation.
Synthetic long peptide from CMV pp65 formulated in Montanide ISA 51; after injection, peptides are taken up by dendritic cells and presented on MHC class I/II to prime and expand CMV‑specific CD8+ cytotoxic T cells, CD4+ helper T cells, and antibody responses. The Montanide adjuvant provides a depot and enhances dendritic-cell activation, promoting immunity against CMV-expressing tumor cells.
YES
INDIRECT
The vaccine primes CMV pp65–specific CD8+ T cells that recognize pp65 peptides on MHC I of expressing cells and kill them via perforin/granzyme (and Fas–FasL) pathways; the drug itself does not directly kill cells.
Human IgG1k anti-CD38 monoclonal antibody that depletes CD38-expressing myeloma plasma cells via CDC, ADCC, ADCP, and apoptosis, and modulates CD38+ immunosuppressive cells to reduce free light-chain production.
Human IgG1κ anti-CD38 monoclonal antibody that binds CD38 on malignant plasma cells, inducing complement-dependent cytotoxicity (CDC), antibody-dependent cellular cytotoxicity (ADCC), antibody-dependent cellular phagocytosis (ADCP), and apoptosis; also depletes CD38+ immunosuppressive cells, thereby reducing free light-chain production and modulating the tumor microenvironment.
YES
DIRECT
Binds CD38 on target cells and triggers complement-dependent cytotoxicity (CDC), NK cell–mediated ADCC, macrophage ADCP, and direct apoptosis upon crosslinking.
IV bispecific IgG1 monoclonal antibody targeting EGFR and MET; blocks ligand-driven activation, inhibits PI3K/AKT/mTOR and RAS/RAF/MEK/ERK signaling, promotes receptor internalization/degradation, and induces ADCC/ADCP via Fc engagement; studied in EGFR-amplified glioblastoma.
Bispecific IgG1 monoclonal antibody that binds EGFR and MET extracellular domains to block ligand-driven activation, inhibit downstream PI3K/AKT/mTOR and RAS/RAF/MEK/ERK signaling, promote receptor internalization and degradation, and engage Fcγ receptors to induce ADCC/ADCP by NK cells and macrophages.
YES
DIRECT
Amivantamab binds EGFR on target cells and engages FcγR-expressing effector cells (NK cells, macrophages) to induce ADCC and ADCP, killing EGFR+ cells; it also promotes receptor internalization/degradation.