Microbial-derived peptide therapeutic cancer vaccine composed of HLA-A2–restricted OncoMimic peptides that prime and expand tumor-specific CD8+ T cells via dendritic-cell presentation to elicit cytotoxic antitumor immunity.
Microbiome-derived HLA-A2–restricted OncoMimic peptides are taken up by dendritic cells and presented on MHC class I to prime and expand tumor-specific CD8+ T cells. The induced CTLs recognize tumor-associated antigen–mimicking epitopes on cancer cells, generating memory and cytotoxic antitumor immunity that targets TAA-expressing tumor cells (e.g., in colorectal cancer).
YES
INDIRECT
Vaccine peptides are presented by dendritic cells on HLA-A2 to prime CD8+ T cells; the induced CTLs then recognize corresponding TAA epitopes on tumor cells and kill them via perforin/granzyme-mediated cytotoxicity.
Humanized anti-EGFR IgG1 monoclonal antibody that blocks EGFR signaling and can mediate ADCC.
Humanized IgG1 monoclonal antibody against EGFR that binds the receptor’s extracellular domain, blocking ligand binding, receptor activation/dimerization, and downstream MAPK/PI3K signaling to inhibit tumor cell proliferation and survival; its Fc region can engage immune effector cells to mediate ADCC. May enhance radiosensitivity.
YES
DIRECT
IgG1 anti‑EGFR antibody binds EGFR on tumor cells and its Fc engages Fcγ receptors on immune effectors (e.g., NK cells) to trigger ADCC, killing EGFR+ cells; EGFR blockade mainly inhibits proliferation.
Anti-CD20 monoclonal antibody mediating complement-dependent cytotoxicity and antibody-dependent cellular cytotoxicity; used for CD20+ tumors.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and induces B-cell depletion primarily via complement-dependent cytotoxicity (CDC) and antibody-dependent cellular cytotoxicity/phagocytosis (ADCC/ADCP), with potential direct apoptotic signaling; used to target CD20-positive tumors.
YES
DIRECT
Rituximab binds CD20 on B cells and kills via complement-dependent cytotoxicity (MAC-mediated lysis) and Fcγ receptor–mediated ADCC/ADCP by NK cells and macrophages; it may also trigger direct apoptotic signaling.
An anti-HER2 antibody–drug conjugate that binds HER2 on tumor cells and delivers a cytotoxic payload.
Trastuzumab-based anti-HER2 antibody-drug conjugate linked via a cleavable linker to a camptothecin-derived topoisomerase I inhibitor (rezetecan). After HER2 binding and internalization, linker cleavage releases the payload, which stabilizes Topo I-DNA complexes, causing DNA strand breaks, replication arrest, and apoptosis in HER2-expressing tumor cells.
YES
DIRECT
The ADC binds HER2 on target cells, is internalized, and upon linker cleavage releases a camptothecin-derived topoisomerase I inhibitor that traps Topo I–DNA complexes, causing DNA breaks, replication arrest, and apoptosis in HER2-expressing cells.
An anti-HER2 antibody–drug conjugate that binds HER2 on tumor cells and delivers a cytotoxic payload.
Trastuzumab-based anti-HER2 antibody-drug conjugate linked via a cleavable linker to a camptothecin-derived topoisomerase I inhibitor (rezetecan). After HER2 binding and internalization, linker cleavage releases the payload, which stabilizes Topo I-DNA complexes, causing DNA strand breaks, replication arrest, and apoptosis in HER2-expressing tumor cells.
NO
INDIRECT
The ADC targets HER2 on the cell surface, is internalized, and then releases a camptothecin payload that inhibits Topoisomerase I, causing DNA damage and apoptosis in HER2-positive cells; Topoisomerase I itself is not the cell-selective (direct) target.