Human IgG1 anti-PD-L1 monoclonal antibody immune checkpoint inhibitor that blocks PD-1/PD-L1 and PD-L1/CD80 interactions and can trigger ADCC to enhance T-cell and NK-cell activity.
Human IgG1 anti-PD-L1 checkpoint-blocking monoclonal antibody that prevents PD-L1 interaction with PD-1 and CD80, releasing PD-1-mediated inhibitory signaling to restore T-cell function; Fc-competent IgG1 also triggers antibody-dependent cellular cytotoxicity against PD-L1-expressing cells, enhancing T-cell and NK-cell antitumor activity.
Avelumab binds PD-L1 on target cells and, via its IgG1 Fc, engages FcγR on NK cells/macrophages to trigger antibody-dependent cellular cytotoxicity (ADCC), killing PD-L1–expressing cells.
An antibody-drug conjugate (Blenrep) consisting of a humanized anti-BCMA IgG1 monoclonal antibody linked to the microtubule toxin MMAF; binds BCMA on myeloma cells, is internalized, and releases MMAF to disrupt microtubules and induce apoptosis; can also engage immune effector functions (ADCC/ADCP).
Belantamab mafodotin is an anti-BCMA IgG1 antibody-drug conjugate that binds BCMA on myeloma cells, is internalized, and releases the auristatin payload MMAF to inhibit tubulin polymerization, causing G2/M arrest and apoptosis; the afucosylated Fc can also mediate ADCC/ADCP.
ADC binds BCMA, is internalized, and releases MMAF to inhibit tubulin, causing G2/M arrest and apoptosis; afucosylated Fc also triggers ADCC/ADCP.
Engineered TCR T-cell therapy targeting MAGE-A4; autologous T cells transduced to express a T-cell receptor recognizing MAGE-A4 peptide–HLA complexes on tumor cells.
Autologous T cells are transduced to express an affinity‑enhanced T‑cell receptor specific for an HLA‑A2–restricted MAGE‑A4 peptide. After infusion, these TCR‑T cells recognize the peptide–HLA complex on tumor cells, activate, and kill MAGE‑A4–expressing cancer cells via cytotoxic mechanisms (e.g., perforin/granzyme).
Engineered TCR-T cells recognize the HLA-A2–restricted MAGE-A4 peptide–HLA complex on target cells and kill them via cytotoxic T-cell effector functions (perforin/granzyme-mediated apoptosis, plus Fas–FasL).
Engineered TCR T-cell therapy targeting NY-ESO-1; autologous T cells modified to express a T-cell receptor recognizing NY-ESO-1 peptide–HLA complexes on tumor cells.
Autologous T cells are transduced to express a high‑affinity TCR specific for NY‑ESO‑1/LAGE‑1 peptide–HLA complexes on tumor cells. After infusion, these TCR‑engineered T cells recognize antigen-presenting tumor cells and mediate cytotoxic killing and cytokine-driven anti-tumor responses.
Engineered TCR T cells recognize NY-ESO-1 peptide–HLA complexes on tumor cells and directly kill them via CTL mechanisms (perforin/granzyme and Fas–FasL apoptosis).
Engineered TCR T-cell therapy targeting NY-ESO-1; autologous T cells modified to express a T-cell receptor recognizing NY-ESO-1 peptide–HLA complexes on tumor cells.
Autologous T cells are transduced to express a high‑affinity TCR specific for NY‑ESO‑1/LAGE‑1 peptide–HLA complexes on tumor cells. After infusion, these TCR‑engineered T cells recognize antigen-presenting tumor cells and mediate cytotoxic killing and cytokine-driven anti-tumor responses.
Autologous TCR-engineered T cells recognize LAGE-1/NY-ESO-1 peptide–HLA complexes on tumor cells and induce CTL-mediated killing via perforin/granzyme and apoptosis pathways.