An oral, bacteria-based personalized DNA cancer vaccine encoding patient-specific neoantigens; delivers neoantigen DNA to antigen-presenting cells to drive MHC I/II presentation and expand neoantigen-specific CD8+/CD4+ T cells.
An oral, live-attenuated Salmonella (Ty21a) vector delivering plasmid DNA encoding patient-specific tumor neoantigens to antigen-presenting cells in the gut-associated lymphoid tissue, leading to intracellular expression and MHC I/II presentation of the neoantigens and expansion/activation of neoantigen-specific CD8+ and CD4+ T cells for anti-tumor immunity.
YES
INDIRECT
The vaccine primes neoantigen-specific T cells. CD8+ CTLs kill tumor cells presenting the neoantigen via MHC I (perforin/granzyme, Fas–FasL), and CD4+ T cells recognizing the MHC II epitope provide help and can directly lyse MHC II–positive tumor cells.
Subcutaneous T-cell–engaging trispecific antibody that binds BCMA and GPRC5D on myeloma cells and CD3 on T cells, redirecting T-cell cytotoxicity.
Subcutaneous trispecific antibody that binds BCMA and GPRC5D on myeloma cells and CD3 on T cells, bridging them to activate CD3 signaling and redirect T-cell cytotoxicity for targeted lysis of malignant plasma cells.
YES
DIRECT
The trispecific T-cell engager binds GPRC5D on myeloma cells and CD3 on T cells, forming an immunologic synapse that activates T-cell killing via perforin/granzyme-mediated cytolysis and apoptosis of GPRC5D-positive cells.
Patient-derived T cells genetically modified to express an HLA-A–restricted T-cell receptor recognizing mutant KRAS G12V/G12D neoantigens; administered as adoptive cellular therapy to mediate MHC-restricted cytotoxic tumor killing.
Autologous T cells are genetically engineered to express an HLA-A–restricted T-cell receptor specific for mutant KRAS G12V/G12D peptides. After infusion, these TCR-T cells recognize KRAS neoantigens presented on tumor MHC, become activated, and mediate MHC-restricted cytotoxic killing via perforin/granzyme release and cytokine secretion, leading to selective elimination of KRAS-mutant tumor cells.
YES
DIRECT
Engineered TCR-T cells recognize the KRAS G12V neoantigen peptide presented on HLA-A on tumor cells and induce MHC-restricted killing via perforin/granzyme release (and Fas–FasL), causing apoptosis/lysis.
Patient-derived T cells genetically modified to express an HLA-A–restricted T-cell receptor recognizing mutant KRAS G12V/G12D neoantigens; administered as adoptive cellular therapy to mediate MHC-restricted cytotoxic tumor killing.
Autologous T cells are genetically engineered to express an HLA-A–restricted T-cell receptor specific for mutant KRAS G12V/G12D peptides. After infusion, these TCR-T cells recognize KRAS neoantigens presented on tumor MHC, become activated, and mediate MHC-restricted cytotoxic killing via perforin/granzyme release and cytokine secretion, leading to selective elimination of KRAS-mutant tumor cells.
YES
DIRECT
TCR-engineered T cells recognize the HLA-presented KRAS G12D neoantigen on tumor cells and directly induce cytolysis via perforin/granzyme-mediated apoptosis (and related CTL effector pathways).
Patient-derived T cells genetically modified to express an HLA-A–restricted T-cell receptor recognizing mutant KRAS G12V/G12D neoantigens; administered as adoptive cellular therapy to mediate MHC-restricted cytotoxic tumor killing.
Autologous T cells are genetically engineered to express an HLA-A–restricted T-cell receptor specific for mutant KRAS G12V/G12D peptides. After infusion, these TCR-T cells recognize KRAS neoantigens presented on tumor MHC, become activated, and mediate MHC-restricted cytotoxic killing via perforin/granzyme release and cytokine secretion, leading to selective elimination of KRAS-mutant tumor cells.
NO
INDIRECT
Engineered TCR-T cells kill only when mutant KRAS G12V/G12D peptides are presented by HLA-A; recognition of the peptide–HLA complex triggers perforin/granzyme-mediated cytolysis. HLA-A expression alone is not sufficient.