Cetuximab-like anti-EGFR monoclonal antibody that binds EGFR to inhibit ligand-driven signaling and mediates Fc-dependent cytotoxicity (ADCC, ADCP).
Unconjugated monoclonal antibody that binds EGFR, blocks ligand-driven receptor activation and downstream signaling (e.g., RAS/MAPK, PI3K/AKT), and engages Fc receptors to elicit immune effector functions including ADCC and ADCP against EGFR-expressing tumor cells.
Antibody binding to EGFR opsonizes target cells and engages Fcγ receptors on effector cells, leading to ADCC by NK cells and ADCP by macrophages, killing EGFR+ cells.
Antibody–drug conjugate targeting HER2; trastuzumab linked via a cleavable linker to a topoisomerase I inhibitor payload (DXd). Binds HER2, internalizes, releases DXd to induce DNA damage, also blocks HER2 signaling and mediates ADCC with bystander killing.
HER2-directed monoclonal antibody (trastuzumab) linked via a cleavable linker to a membrane-permeable topoisomerase I inhibitor payload (DXd). After HER2 binding and internalization, the linker is cleaved to release DXd, which inhibits Top1, causing DNA damage, replication arrest, and apoptosis. The antibody also blocks HER2 signaling and mediates Fc-dependent ADCC, with a bystander killing effect from the released payload.
The ADC binds HER2, is internalized, and releases the DXd topoisomerase I inhibitor, causing DNA damage and apoptosis in HER2+ cells; Fc-mediated ADCC and a bystander effect can also contribute.
A subcutaneously administered bispecific antibody immunotherapy that binds CD20 on malignant B cells and an additional immune-effector target to redirect immune cell–mediated cytotoxicity for B-cell depletion in relapsed/refractory CD20+ B-cell non-Hodgkin lymphoma.
Subcutaneously administered bispecific antibody that binds CD20 on malignant B cells and a T‑cell effector target to recruit and activate T cells, forming an immune synapse and redirecting T‑cell–mediated cytotoxicity to deplete CD20+ B cells in relapsed/refractory non‑Hodgkin lymphoma.
The bispecific antibody binds CD20 on B cells and CD3 on T cells, forming an immune synapse and activating T cells to lyse CD20+ cells via perforin/granzyme-mediated cytotoxicity.
Autologous, gene-modified T lymphocytes engineered with a CD70-specific chimeric antigen receptor; a single IV infusion that targets CD70-positive tumor cells to trigger T-cell activation and cytotoxicity.
Autologous T cells genetically engineered to express a CD70-specific chimeric antigen receptor; upon binding CD70 on tumor cells, the CAR triggers T-cell activation and expansion, cytokine release, and perforin/granzyme-mediated cytotoxic killing of CD70-positive cells.
CAR-T cells bind CD70 on target cells, activate, and kill via perforin/granzyme-mediated cytolysis (and Fas/FasL apoptosis).
Antibody–drug conjugate: humanized anti-HER2 IgG1 (trastuzumab) linked to a topoisomerase I inhibitor payload (DXd); binds HER2, is internalized, releases DXd to inhibit topo I causing DNA damage/apoptosis; can mediate ADCC and has a bystander effect.
Humanized anti-HER2 IgG1 antibody–drug conjugate (trastuzumab linked via a cleavable linker to the topoisomerase I inhibitor DXd). Binds HER2 on tumor cells, is internalized, and releases DXd to inhibit topoisomerase I, causing DNA damage and apoptosis; the Fc can mediate ADCC, and the membrane-permeable payload enables a bystander killing effect.
The ADC binds HER2, is internalized, and releases the DXd topoisomerase I inhibitor inside the cell, causing DNA damage and apoptosis; Fc can also trigger ADCC, with a membrane-permeable payload allowing bystander killing.