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.
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.
Anti–CTLA-4 monoclonal antibody (IgG1) that blocks CTLA-4 to enhance CD28-mediated costimulation and T-cell priming; its IgG1 Fc may deplete intratumoral regulatory T cells (Tregs).
Anti–CTLA-4 IgG1 monoclonal antibody that blocks CTLA-4 checkpoint signaling on T cells, enhancing CD28-mediated costimulation and T-cell priming/activation; its IgG1 Fc can mediate depletion of intratumoral regulatory T cells, collectively boosting cytotoxic antitumor T-cell responses.
IgG1 anti-CTLA-4 engages Fcγ receptors on NK cells/macrophages to deplete CTLA-4–high Tregs via ADCC/ADCP, killing CTLA-4–expressing cells.
An anti-HER2 antibody–drug conjugate (ADC) consisting of trastuzumab linked to a cleavable topoisomerase I inhibitor payload (DXd). It binds ERBB2/HER2 on tumor cells, is internalized, and releases the cytotoxic payload in lysosomes to induce tumor cell death.
Trastuzumab deruxtecan is a HER2-targeted monoclonal antibody linked via a cleavable linker to a topoisomerase I inhibitor payload (deruxtecan, DXd). After binding ERBB2/HER2 on tumor cells, the complex is internalized and the payload is released in lysosomes, inhibiting Top1 to cause DNA damage, replication arrest, and apoptosis. It also mediates ADCC and produces a bystander killing effect due to a membrane-permeable payload.
The ADC binds HER2, is internalized, and releases a topoisomerase I inhibitor (deruxtecan) that causes DNA damage and apoptosis in HER2+ cells; Fc engagement can also trigger ADCC.
Recombinant humanized bispecific IgG antibody that binds EGFR on tumor cells and agonizes 4-1BB (CD137) on activated T cells/NK cells to provide costimulatory signaling and enhance antitumor immunity.
HLX35 is a bispecific IgG that binds EGFR on tumor cells and 4-1BB (CD137) on activated T/NK cells, crosslinking them to deliver tumor-localized 4-1BB costimulatory signaling while concurrently blocking EGFR signaling. This conditional 4-1BB agonism enhances T-cell proliferation, survival, and cytotoxicity, and can activate NK and dendritic cells, promoting antitumor immunity.
HLX35 binds EGFR on tumor cells and 4-1BB on activated T/NK cells, providing localized 4-1BB costimulation that enhances effector function and leads to T/NK cell–mediated lysis (perforin/granzyme) of EGFR+ cells; concurrent EGFR blockade adds antiproliferative effects.
Polyclonal antibody preparation that depletes T lymphocytes for induction immunosuppression.
Polyclonal anti–T-lymphocyte IgG that binds multiple T-cell surface antigens and depletes T cells via complement-dependent cytotoxicity and Fc-mediated ADCC, with additional T-cell apoptosis and functional inhibition, producing potent immunosuppression.
ATG contains polyclonal IgG that binds CD18 (LFA-1β) on T cells; bound antibody triggers complement-dependent lysis and Fc-mediated ADCC, and can also induce apoptosis, directly depleting the target cells.