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.
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.
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.
Adoptive γδ T‑cell therapy using Vγ9Vδ2 T cells expanded from healthy donors and administered intraventricularly/intracavitary via an Ommaya reservoir. These innate‑like cytotoxic lymphocytes recognize tumor phosphoantigens via BTN3A1/BTN2A1 independent of MHC, triggering perforin/granzyme‑mediated killing and cytokine release; they can also respond via NKG2D and mediate ADCC.
Allogeneic Vγ9Vδ2 T cells recognize tumor-derived phosphoantigens generated by dysregulated mevalonate metabolism via BTN3A1/BTN2A1 in an MHC-independent manner, triggering perforin/granzyme-mediated cytotoxicity and cytokine release. They also respond to stress ligands through NKG2D and can mediate ADCC.
Vγ9Vδ2 T cells sense phosphoantigen-induced BTN3A1/BTN2A1 on target cells via their TCR, triggering activation and perforin/granzyme-mediated cytolysis (with NKG2D co-stimulation).
Autologous TCR-engineered T-cell therapy targeting KRAS G12D presented by HLA-A*11:01 or HLA-A*11:02; infused cells recognize the KRAS G12D peptide–HLA complex on tumor cells and mediate cytotoxic killing.
Autologous T cells are genetically engineered to express a T-cell receptor that recognizes the KRAS G12D peptide presented by HLA-A*11:01 or HLA-A*11:02 on tumor cells. Upon antigen recognition, the engineered T cells become activated and mediate cytotoxic killing of KRAS G12D–positive tumor cells via TCR signaling, cytokine release, and perforin/granzyme pathways.
Engineered TCR T cells recognize the KRAS G12D peptide–HLA-A*11:01 complex and kill target cells via TCR-activated cytotoxic pathways, primarily perforin/granzyme-mediated apoptosis (with supportive cytokine effects).
Autologous TCR-engineered T-cell therapy targeting KRAS G12D presented by HLA-A*11:01 or HLA-A*11:02; infused cells recognize the KRAS G12D peptide–HLA complex on tumor cells and mediate cytotoxic killing.
Autologous T cells are genetically engineered to express a T-cell receptor that recognizes the KRAS G12D peptide presented by HLA-A*11:01 or HLA-A*11:02 on tumor cells. Upon antigen recognition, the engineered T cells become activated and mediate cytotoxic killing of KRAS G12D–positive tumor cells via TCR signaling, cytokine release, and perforin/granzyme pathways.
Engineered TCR T cells recognize the KRAS G12D–HLA-A*11:02 complex and directly lyse target cells via TCR activation leading to perforin/granzyme-mediated apoptosis (with supportive cytokine effects).