Chimeric IgG monoclonal antibody against EGFR that blocks ligand binding and downstream MAPK/PI3K signaling.
Chimeric IgG1 monoclonal antibody that binds the extracellular domain of EGFR, blocking ligand binding and receptor dimerization/activation, thereby inhibiting downstream MAPK and PI3K signaling and tumor cell proliferation.
YES
DIRECT
Cetuximab binds EGFR on target cells and engages Fcγ receptors on immune effectors to mediate ADCC (and some CDC), leading to lysis; it also blocks EGFR signaling (cytostatic).
An autologous, fully human, dual-target CAR-T cell therapy engineered to recognize BCMA (TNFRSF17) and GPRC5D on malignant plasma cells; administered as a single infusion at approximately 1–6 × 10^5 CAR-T cells/kg. Binding to targets triggers CAR signaling, activating T-cell cytotoxicity and cytokine release to lyse tumor cells.
Autologous dual-target CAR-T cells engineered to recognize BCMA and GPRC5D on malignant plasma cells. Antigen binding activates CAR signaling, leading to T-cell activation, proliferation, cytokine release, and cytotoxic killing of tumor cells, aiming to overcome antigen escape via dual targeting.
YES
DIRECT
BCMA recognition by the dual-target CAR on T cells triggers T‑cell activation and cytolytic killing of BCMA+ cells via perforin/granzyme release (and Fas/FasL), with supportive cytokine-mediated effects.
An autologous, fully human, dual-target CAR-T cell therapy engineered to recognize BCMA (TNFRSF17) and GPRC5D on malignant plasma cells; administered as a single infusion at approximately 1–6 × 10^5 CAR-T cells/kg. Binding to targets triggers CAR signaling, activating T-cell cytotoxicity and cytokine release to lyse tumor cells.
Autologous dual-target CAR-T cells engineered to recognize BCMA and GPRC5D on malignant plasma cells. Antigen binding activates CAR signaling, leading to T-cell activation, proliferation, cytokine release, and cytotoxic killing of tumor cells, aiming to overcome antigen escape via dual targeting.
YES
DIRECT
CAR-T cells recognize GPRC5D on target cells and, upon engagement, kill them via T-cell cytotoxic pathways (perforin/granzyme and Fas–FasL), causing apoptotic/lytic death.
An antibody–drug conjugate targeting Trop-2 that delivers SN-38 (active metabolite of irinotecan), a topoisomerase I inhibitor, causing DNA damage and tumor cell death; cleavable linker enables a bystander effect. Used here as neoadjuvant therapy in triple-negative breast cancer.
Anti-Trop-2 monoclonal antibody linked via a cleavable linker to SN-38 (active metabolite of irinotecan). Binding to Trop-2 on tumor cells leads to internalization and linker cleavage, releasing SN-38 to inhibit topoisomerase I, induce DNA breaks, and trigger apoptosis; some extracellular release enables a bystander killing effect.
YES
DIRECT
The anti–TROP-2 antibody–drug conjugate binds and is internalized; linker cleavage releases SN-38, a topoisomerase I inhibitor, causing DNA breaks and apoptosis in TROP-2–positive cells. Some extracellular SN-38 can also mediate bystander killing.
An antibody–drug conjugate targeting Trop-2 that delivers SN-38 (active metabolite of irinotecan), a topoisomerase I inhibitor, causing DNA damage and tumor cell death; cleavable linker enables a bystander effect. Used here as neoadjuvant therapy in triple-negative breast cancer.
Anti-Trop-2 monoclonal antibody linked via a cleavable linker to SN-38 (active metabolite of irinotecan). Binding to Trop-2 on tumor cells leads to internalization and linker cleavage, releasing SN-38 to inhibit topoisomerase I, induce DNA breaks, and trigger apoptosis; some extracellular release enables a bystander killing effect.
NO
INDIRECT
The ADC targets Trop-2 on the cell surface; after internalization it releases SN-38, which inhibits topoisomerase I to cause DNA damage and apoptosis. Expression of topoisomerase I alone does not lead to targeted killing; cytotoxicity depends on Trop-2–mediated delivery (with some bystander effect).