Autologous, gene-engineered T-cell receptor (TCR) T cells that recognize KRAS G12V or G12D neoantigen peptides presented on HLA-A*11, C*01:02, or C*08:02; infused IV after lymphodepletion to mediate MHC-restricted tumor killing.
Autologous T cells are genetically engineered to express a T-cell receptor that recognizes KRAS G12V or G12D neoantigen peptides presented on HLA-A*11, C*01:02, or C*08:02. Following lymphodepletion and infusion, these TCR-T cells engage peptide–HLA complexes on KRAS-mutant tumor cells and mediate MHC-restricted cytotoxic killing via TCR signaling with perforin/granzyme release and cytokine production.
Engineered TCR-T cells recognize the KRAS G12D peptide presented by HLA-A*11 and, upon TCR engagement, kill target cells via cytolytic granule release (perforin/granzyme) and MHC-restricted CTL apoptosis-inducing mechanisms.
Autologous, gene-engineered T-cell receptor (TCR) T cells that recognize KRAS G12V or G12D neoantigen peptides presented on HLA-A*11, C*01:02, or C*08:02; infused IV after lymphodepletion to mediate MHC-restricted tumor killing.
Autologous T cells are genetically engineered to express a T-cell receptor that recognizes KRAS G12V or G12D neoantigen peptides presented on HLA-A*11, C*01:02, or C*08:02. Following lymphodepletion and infusion, these TCR-T cells engage peptide–HLA complexes on KRAS-mutant tumor cells and mediate MHC-restricted cytotoxic killing via TCR signaling with perforin/granzyme release and cytokine production.
Engineered TCR-T cells recognize the KRAS G12D peptide presented by HLA-C*01:02 and, upon TCR engagement, kill the target cell via perforin/granzyme-mediated cytotoxicity (MHC-restricted).
Autologous, gene-engineered T-cell receptor (TCR) T cells that recognize KRAS G12V or G12D neoantigen peptides presented on HLA-A*11, C*01:02, or C*08:02; infused IV after lymphodepletion to mediate MHC-restricted tumor killing.
Autologous T cells are genetically engineered to express a T-cell receptor that recognizes KRAS G12V or G12D neoantigen peptides presented on HLA-A*11, C*01:02, or C*08:02. Following lymphodepletion and infusion, these TCR-T cells engage peptide–HLA complexes on KRAS-mutant tumor cells and mediate MHC-restricted cytotoxic killing via TCR signaling with perforin/granzyme release and cytokine production.
Engineered TCR-T cells recognize the KRAS G12D peptide–HLA-C*08:02 complex and kill target cells via MHC-restricted cytolysis through perforin/granzyme release.
Bispecific IgG1 monoclonal antibody targeting EGFR and MET; blocks ligand–receptor interactions, induces receptor internalization and degradation, and engages immune effector functions (ADCC/ADCP).
Human bispecific IgG1 monoclonal antibody that targets EGFR and MET on tumor cells, blocking ligand binding and receptor phosphorylation, promoting receptor internalization and degradation to inhibit downstream signaling; additionally engages Fc-mediated immune effector functions (ADCC/ADCP) to kill target-expressing cells.
Amivantamab binds EGFR on target cells and its IgG1 Fc engages Fcγ receptor–bearing immune cells, leading to antibody-dependent cellular cytotoxicity (ADCC) and phagocytosis (ADCP). Receptor internalization/degradation inhibits signaling but killing is primarily immune-mediated.
Bispecific IgG1 monoclonal antibody targeting EGFR and MET; blocks ligand–receptor interactions, induces receptor internalization and degradation, and engages immune effector functions (ADCC/ADCP).
Human bispecific IgG1 monoclonal antibody that targets EGFR and MET on tumor cells, blocking ligand binding and receptor phosphorylation, promoting receptor internalization and degradation to inhibit downstream signaling; additionally engages Fc-mediated immune effector functions (ADCC/ADCP) to kill target-expressing cells.
Amivantamab binds MET on target cells and its Fc region engages immune effector cells (e.g., NK cells, macrophages) via Fcγ receptors, inducing ADCC and ADCP to kill MET-expressing cells; it also promotes receptor internalization/degradation and signaling blockade (antiproliferative).