Fc-enhanced anti-CTLA-4 monoclonal antibody that promotes T-cell priming and depletes intratumoral Tregs via ADCC, boosting CD8+ T-cell responses.
Fc-enhanced anti-CTLA-4 monoclonal antibody that blocks CTLA-4 to promote T-cell priming/activation and leverages Fc-mediated ADCC to deplete intratumoral Tregs, boosting CD8+ T-cell responses.
Antibody binds CTLA-4 on target cells; its Fc engages FcγR-bearing effectors (e.g., NK cells/macrophages) to mediate ADCC/ADCP, depleting CTLA-4+ cells such as intratumoral Tregs.
Autologous tumor-infiltrating lymphocyte (TIL) adoptive cell therapy administered intravenously after lymphodepleting chemotherapy to mediate TCR-dependent cytotoxicity against tumor cells.
Autologous TILs expanded ex vivo are reinfused after lymphodepleting chemotherapy. They recognize patient-specific tumor antigens via TCR-MHC and kill tumor cells through perforin/granzyme-mediated cytotoxicity and cytokine release, with IL-2 supporting T-cell activation, proliferation, and persistence.
Autologous TILs recognize the tumor-associated peptide–MHC II complex via their TCRs and directly kill target cells through perforin/granzyme-mediated cytolysis (with possible Fas–FasL and cytokine-mediated effects).
TROP2-targeting antibody-drug conjugate that delivers a topoisomerase I inhibitor payload to TROP2-expressing tumor cells.
TROP2-targeting monoclonal antibody linked via a cleavable linker to a topoisomerase I inhibitor payload. Binding to TROP2 on tumor cells triggers internalization and intracellular release of the payload, which inhibits topoisomerase I to induce DNA damage and replication stress, leading to apoptosis, with potential bystander killing of adjacent tumor cells.
The anti-TROP2 ADC binds TROP2, is internalized, and releases a topoisomerase I inhibitor that induces DNA damage and apoptosis, with possible bystander killing.
Humanized IgG1 monoclonal antibody targeting EGFR; blocks ligand binding and receptor activation, inhibiting RAS–RAF–MEK–ERK and PI3K–AKT signaling, and can induce antibody-dependent cellular cytotoxicity (ADCC).
Humanized IgG1 monoclonal antibody against EGFR that blocks ligand binding and receptor activation, inhibiting downstream RAS-RAF-MEK-ERK and PI3K-AKT signaling to suppress tumor cell proliferation and survival; can also mediate antibody-dependent cellular cytotoxicity (ADCC).
The IgG1 antibody binds EGFR on target cells and its Fc engages Fc gamma receptors on immune effectors (e.g., NK cells, macrophages) to trigger ADCC, killing EGFR-positive cells; EGFR blockade can also promote apoptosis/growth arrest.
Chimeric IgG1 anti–TNF-α monoclonal antibody that neutralizes soluble and transmembrane TNF-α, suppressing TNF-driven signaling, cytokine release, leukocyte recruitment, and inducing apoptosis of activated immune cells.
Chimeric IgG1 monoclonal antibody that binds and neutralizes soluble and transmembrane TNF-α, blocking TNF receptor signaling (e.g., NF-κB activation), thereby reducing pro-inflammatory cytokine release and leukocyte recruitment, and can induce apoptosis of activated TNF-expressing immune cells.
Infliximab binds transmembrane TNF-α on activated immune cells; its IgG1 Fc recruits effector functions (ADCC by NK/myeloid cells and CDC) and crosslinking of tmTNF triggers reverse-signaling–mediated apoptosis of the TNF-expressing cells.