Humanized anti-EGFR IgG1 monoclonal antibody that blocks ligand binding, inhibits downstream EGFR signaling (RAS/RAF/MEK/ERK; PI3K/AKT), enhances radiosensitivity, and can induce ADCC.
Humanized IgG1 monoclonal antibody against EGFR that blocks ligand binding and receptor activation, suppressing downstream RAS/RAF/MEK/ERK and PI3K/AKT signaling to inhibit proliferation and survival; its Fc can mediate ADCC and it enhances radiosensitivity in EGFR-overexpressing tumors.
YES
DIRECT
EGFR+ cells can be killed via Fc-mediated ADCC (primarily NK cells/macrophages; possible CDC), while EGFR signaling blockade is mainly cytostatic.
TROP-2–targeted antibody–drug conjugate that delivers SN-38, a topoisomerase I inhibitor.
TROP-2-targeted monoclonal antibody conjugated to SN-38 (topoisomerase I inhibitor). After binding TROP-2 on tumor cells and internalization, the linker is cleaved to release SN-38, which stabilizes topoisomerase I–DNA complexes, causing DNA damage, inhibition of DNA replication, and apoptosis.
YES
DIRECT
The ADC binds TROP-2, is internalized, and releases SN-38, which inhibits topoisomerase I, causing DNA damage, replication arrest, and apoptosis.
Personalized mRNA cancer vaccine encoding patient-specific tumor neoantigens; taken up by antigen-presenting cells and presented on MHC I/II to prime CD8+ and CD4+ T-cell responses.
Personalized lipid‑nanoparticle mRNA vaccine encoding patient-specific tumor neoantigens. After uptake by antigen‑presenting cells, the mRNA is translated and neoantigen peptides are presented on MHC I/II, priming and expanding tumor‑specific CD8+ cytotoxic and CD4+ helper T cells to drive antitumor immunity.
YES
INDIRECT
The mRNA vaccine is taken up by APCs, which present neoantigens and expand neoantigen-specific CD8+ T cells; these T cells recognize neoantigen–MHC on tumor cells and kill them via perforin/granzyme and Fas–FasL pathways.
TROP-2–targeted antibody–drug conjugate that delivers SN-38, a topoisomerase I inhibitor.
TROP-2-targeted monoclonal antibody conjugated to SN-38 (topoisomerase I inhibitor). After binding TROP-2 on tumor cells and internalization, the linker is cleaved to release SN-38, which stabilizes topoisomerase I–DNA complexes, causing DNA damage, inhibition of DNA replication, and apoptosis.
NO
INDIRECT
Sacituzumab govitecan targets TROP-2 on tumor cells, is internalized, and releases SN-38, which inhibits topoisomerase I to cause DNA damage and apoptosis. Topoisomerase I is the payload’s enzymatic target, not the antigen determining cell selectivity.
An autologous CD7-directed CAR T-cell therapy in which a patient’s T cells are engineered to express a CAR targeting CD7; engagement triggers cytotoxic activity to eliminate CD7-positive malignant T lymphoblasts and also depletes normal CD7+ T and NK cells.
Autologous T cells are engineered ex vivo to express a CD7-specific chimeric antigen receptor; after infusion, CAR T cells bind CD7 on target cells, activate, and mediate cytotoxic killing of CD7-positive malignant T lymphoblasts, with on-target depletion of normal CD7+ T and NK cells.
YES
DIRECT
Anti-CD7 CAR T cells bind CD7 on target cells, activate, and induce T-cell cytotoxic killing (perforin/granzyme-mediated apoptosis, plus death receptor pathways).