A bispecific tetravalent monoclonal antibody immune cell engager that binds CD123 on AML cells and CD16A on innate immune cells (primarily NK cells) to trigger ADCC and kill CD123+ leukemic cells; administered weekly IV.
A tetravalent bispecific IgG1–scFv that simultaneously binds CD123 on leukemic cells and CD16A (FcγRIIIa) on innate immune cells—primarily NK cells—cross-linking them to activate NK cell–mediated ADCC and lyse CD123+ tumor cells.
NO
INDIRECT
AFM28 binds CD16A on NK/macrophages to engage them against CD123+ tumor cells, triggering NK-cell ADCC that kills the CD123+ targets; CD16A-expressing effector cells are not killed.
Autologous TCR-T cell therapy engineered to express a high-affinity T-cell receptor recognizing an AFP-derived peptide presented by HLA-A*02:03 on tumor cells, inducing MHC-restricted T-cell activation and cytotoxic killing; administered after lymphodepleting chemotherapy to enhance engraftment, expansion, and persistence.
Autologous T cells are genetically engineered to express a high-affinity T-cell receptor that recognizes an AFP-derived peptide presented by HLA-A*02:03 on tumor cells. Engagement of the AFP/HLA complex triggers MHC-restricted T-cell activation and cytotoxic killing via perforin/granzyme release and cytokine secretion. Lymphodepleting chemotherapy is given pre-infusion to enhance engraftment, expansion, and persistence of the infused TCR-T cells.
YES
DIRECT
Engineered TCR-T cells recognize the AFP peptide presented by HLA-A*02:03 and directly induce MHC-restricted killing of target cells via perforin/granzyme-mediated apoptosis (with contributions from Fas–FasL and cytokines).
Anti-EGFR IgG1 monoclonal antibody that blocks ligand binding and downstream EGFR signaling, can mediate ADCC, and may enhance radiosensitivity.
Humanized IgG1 monoclonal antibody against EGFR that binds the receptor’s extracellular domain, blocks ligand binding and receptor activation, suppressing downstream RAS/RAF/MEK/ERK and PI3K/AKT signaling to inhibit tumor cell proliferation; can mediate ADCC against EGFR-expressing cells and may enhance radiosensitivity.
YES
DIRECT
IgG1 anti-EGFR antibody binds EGFR on target cells and engages Fcγ receptors on effector cells to trigger ADCC (and potentially CDC), leading to immune-mediated killing of EGFR-expressing cells; it also blocks EGFR signaling (growth inhibition).
Autologous TCR-engineered T-cell therapy expressing a transgenic TCR specific for the KRAS G12D neoantigen presented by HLA-C*08:02; infused cells recognize the KRAS G12D peptide–HLA complex on tumor cells and mediate cytotoxic killing.
Autologous T cells are genetically engineered to express an HLA-C*08:02–restricted TCR that recognizes the KRAS G12D neoantigen. After infusion, these TCR-T cells bind the KRAS G12D peptide–HLA complex on tumor cells, become activated, and mediate cytotoxic T-lymphocyte killing of KRAS G12D–expressing cancer cells.
YES
DIRECT
Engineered TCR-T cells recognize the KRAS G12D peptide presented by HLA-C*08:02 on tumor cells and directly induce CTL-mediated killing via perforin/granzyme and Fas–FasL apoptosis.
Autologous TCR-engineered T-cell therapy expressing a transgenic TCR specific for the KRAS G12D neoantigen presented by HLA-C*08:02; infused cells recognize the KRAS G12D peptide–HLA complex on tumor cells and mediate cytotoxic killing.
Autologous T cells are genetically engineered to express an HLA-C*08:02–restricted TCR that recognizes the KRAS G12D neoantigen. After infusion, these TCR-T cells bind the KRAS G12D peptide–HLA complex on tumor cells, become activated, and mediate cytotoxic T-lymphocyte killing of KRAS G12D–expressing cancer cells.
NO
DIRECT
Engineered TCR-T cells kill cells that present the KRAS G12D peptide on HLA-C*08:02 via CTL perforin/granzyme release; expression of HLA-C*08:02 alone is not sufficient.