Anti-HER2 IgG1 antibody–drug conjugate that targets HER2-expressing tumor cells and delivers MMAE; internalization and linker cleavage release MMAE to inhibit tubulin polymerization, causing G2/M arrest and apoptosis; may also trigger ADCC and a bystander effect.
Disitamab vedotin is an anti-HER2 IgG1 antibody–drug conjugate that binds HER2 on tumor cells, is internalized, and releases the payload MMAE via a cleavable linker. MMAE inhibits tubulin polymerization, causing G2/M cell-cycle arrest and apoptosis. The IgG1 backbone may also mediate ADCC, and released MMAE can produce a bystander killing effect.
Anti-HER2 ADC binds HER2, is internalized, and releases MMAE via a cleavable linker; MMAE inhibits tubulin polymerization causing G2/M arrest and apoptosis. The IgG1 Fc can also mediate ADCC, and released MMAE may cause bystander killing.
Allogeneic, gene-edited chimeric antigen receptor T lymphocytes engineered to target CD19 on B-lineage cells; administered as a single IV infusion after lymphodepletion to deplete CD19+ B cells/plasmablasts and reduce autoantibody production.
Allogeneic, gene-edited T cells engineered with an anti-CD19 chimeric antigen receptor bind CD19 on B-lineage cells. CAR engagement activates T-cell cytotoxic pathways (e.g., perforin/granzyme, Fas–FasL), leading to targeted depletion of CD19+ B cells and plasmablasts, thereby reducing autoantibody production and modulating humoral immunity.
Anti-CD19 CAR-T cells recognize CD19 on target cells and induce killing via T-cell cytotoxic pathways, including perforin/granzyme-mediated lysis and Fas–FasL–triggered apoptosis.
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 G12V peptide presented by HLA-A*11, triggering TCR signaling and perforin/granzyme-mediated cytolysis (MHC-restricted killing).
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 G12V peptide presented by HLA-C*01:02 and, upon TCR engagement, directly kill target cells 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 G12V peptide presented by HLA-C*08:02 and directly kill target cells via TCR-triggered cytotoxicity, primarily through perforin/granzyme-mediated apoptosis.