Autologous genetically engineered TCR-T cell product; patient T cells are transduced with a TCR recognizing the KRAS G12V neoepitope presented by HLA-A*11:01 to mediate MHC class I–restricted cytotoxic killing of KRAS G12V–mutant tumor cells.
Autologous T cells are genetically engineered to express a T-cell receptor specific for the KRAS G12V neoepitope presented by HLA-A*11:01. Upon peptide-HLA recognition, TCR signaling activates cytotoxic effector functions, leading to MHC class I-restricted killing of KRAS G12V–mutant tumor cells.
NO
INDIRECT
Engineered TCR-T cells kill only cells presenting the KRAS G12V peptide bound to HLA-A*11:01 via TCR engagement, triggering perforin/granzyme-mediated cytotoxicity (MHC I–restricted). HLA-A*11:01 alone is not sufficient.
Humanized anti-GD2 monoclonal antibody that binds GD2 on neuroblastoma cells and induces immune-mediated killing via ADCC and CDC.
Humanized anti-GD2 monoclonal antibody that binds GD2 on neuroblastoma cells, inducing immune-mediated killing via Fc-dependent antibody-dependent cellular cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC).
YES
DIRECT
Anti-GD2 mAb binds GD2 on tumor cells and recruits immune effectors to kill via Fc-mediated ADCC (e.g., NK cells) and complement-dependent cytotoxicity (CDC).
HER2-targeted antibody–drug conjugate; the anti-HER2 monoclonal antibody binds ERBB2 (HER2), is internalized, and releases an unspecified cytotoxic payload while retaining trastuzumab-like HER2 signaling inhibition and Fc-mediated ADCC.
HER2-targeted antibody–drug conjugate. The anti‑HER2 monoclonal antibody binds ERBB2 (HER2) on tumor cells, is internalized, and a cleavable linker releases a camptothecin/topoisomerase I–inhibitor payload (rezetecan), which stabilizes TOP1–DNA complexes to induce DNA strand breaks, block replication, and trigger apoptosis. The antibody component also retains trastuzumab-like HER2 signaling inhibition and Fc-mediated ADCC.
YES
DIRECT
An anti-HER2 ADC binds ERBB2 on tumor cells, is internalized, and releases a camptothecin/topoisomerase I–inhibitor payload (rezetecan) that causes DNA strand breaks leading to apoptosis; the antibody Fc can also trigger ADCC.
HER2-targeted antibody–drug conjugate; the anti-HER2 monoclonal antibody binds ERBB2 (HER2), is internalized, and releases an unspecified cytotoxic payload while retaining trastuzumab-like HER2 signaling inhibition and Fc-mediated ADCC.
HER2-targeted antibody–drug conjugate. The anti‑HER2 monoclonal antibody binds ERBB2 (HER2) on tumor cells, is internalized, and a cleavable linker releases a camptothecin/topoisomerase I–inhibitor payload (rezetecan), which stabilizes TOP1–DNA complexes to induce DNA strand breaks, block replication, and trigger apoptosis. The antibody component also retains trastuzumab-like HER2 signaling inhibition and Fc-mediated ADCC.
NO
INDIRECT
SHR-A1811 targets HER2 on the cell surface; after internalization it releases a TOP1 inhibitor that traps TOP1–DNA complexes and induces DNA damage and apoptosis in HER2-positive cells. Topoisomerase I itself is not the recognition target, so TOP1-expressing cells are not specifically killed unless they are HER2-positive.
HER2-targeted antibody–drug conjugate linking trastuzumab to the maytansinoid DM1 via a non-cleavable linker; inhibits HER2 signaling, mediates ADCC, and delivers DM1 to disrupt microtubules, causing mitotic arrest and apoptosis.
HER2-targeted antibody–drug conjugate: the trastuzumab antibody binds HER2, inhibits HER2 signaling and mediates ADCC, is internalized, and via a non-cleavable linker delivers the microtubule inhibitor DM1, which binds tubulin to disrupt microtubule dynamics, causing mitotic arrest and apoptosis in HER2-overexpressing tumor cells.
YES
DIRECT
The ADC binds HER2, is internalized, and delivers the DM1 microtubule inhibitor inside HER2+ cells, disrupting microtubules to cause mitotic arrest and apoptosis; trastuzumab’s Fc can also mediate ADCC.