Chimeric IgG1 monoclonal antibody targeting EGFR; blocks ligand binding and receptor activation and can mediate ADCC.
Chimeric IgG1 monoclonal antibody against EGFR that binds the extracellular domain to block ligand binding and prevent receptor activation and dimerization, inhibiting downstream signaling (e.g., RAS/MAPK, PI3K/AKT) and tumor cell proliferation; its Fc region can engage immune effector cells to mediate ADCC.
NO
INDIRECT
Cetuximab binds EGFR on tumor cells; its Fc engages CD16a (FcγRIIIa) on NK cells to trigger ADCC, killing EGFR-expressing cells. CD16a+ immune cells act as effectors and are not killed.
Humanized anti-HER2 monoclonal antibody that inhibits HER2 signaling/dimerization and mediates ADCC.
Humanized anti-HER2 (ERBB2) IgG1 monoclonal antibody that binds the HER2 extracellular domain, blocks receptor activation and dimerization, downregulates HER2 signaling, and engages Fcγ-mediated antibody-dependent cellular cytotoxicity (ADCC), leading to tumor cell death.
YES
DIRECT
Trastuzumab binds HER2 on target cells and engages Fcγ receptor–bearing immune effectors (e.g., NK cells) to mediate ADCC, killing the cells; it also inhibits HER2 signaling, promoting apoptosis.
Autologous TCR-engineered T cells (TCR-T) expressing an NY-ESO-1–specific, HLA-A2–restricted T-cell receptor to recognize NY-ESO-1 peptides on HLA-A2 and kill tumor cells via TCR-mediated cytotoxicity.
Autologous T cells are genetically engineered to express an NY-ESO-1–specific, HLA-A2–restricted T-cell receptor. They recognize NY-ESO-1 peptide presented on HLA-A2 on tumor cells and, upon TCR engagement, activate and kill target cells via perforin/granzyme-mediated cytotoxicity and associated effector functions.
YES
DIRECT
Engineered TCR-T cells recognize the NY-ESO-1(157–165) peptide presented on HLA-A*02 and kill target cells via TCR-triggered perforin/granzyme-mediated cytotoxicity.
Autologous TCR-engineered T cells (TCR-T) expressing an NY-ESO-1–specific, HLA-A2–restricted T-cell receptor to recognize NY-ESO-1 peptides on HLA-A2 and kill tumor cells via TCR-mediated cytotoxicity.
Autologous T cells are genetically engineered to express an NY-ESO-1–specific, HLA-A2–restricted T-cell receptor. They recognize NY-ESO-1 peptide presented on HLA-A2 on tumor cells and, upon TCR engagement, activate and kill target cells via perforin/granzyme-mediated cytotoxicity and associated effector functions.
YES
DIRECT
Engineered TCR-T cells recognize the NY-ESO-1 peptide presented by HLA-A2 and kill target cells via TCR-triggered perforin/granzyme-mediated cytotoxicity (apoptosis).
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).
NO
INDIRECT
Vaccine primes TAA-specific CD8+ T cells; CTLs kill tumor cells presenting TAA-derived peptides on HLA-A2 via perforin/granzyme cytolysis. HLA-A2 itself is not the cytotoxic target.