A personalized neoantigen mRNA cancer vaccine designed to deliver patient-specific mRNA that is taken up by antigen-presenting cells, translated into neoantigen peptides, and presented via MHC I/II to prime CD8+ and CD4+ T-cell responses against tumor cells; administered by injection every 21 days (up to 9 cycles) after surgery alongside standard adjuvant therapy.
Personalized mRNA encoding patient-specific tumor neoantigens is injected and taken up by antigen-presenting cells (e.g., dendritic cells). The mRNA is translated into neoantigen peptides that are processed and presented on MHC I and II, priming and expanding tumor-specific CD8+ cytotoxic and CD4+ helper T cells to recognize and kill tumor cells expressing those neoantigens and establish immune memory.
YES
INDIRECT
The vaccine primes endogenous neoantigen-specific T cells; activated CTLs (and sometimes cytotoxic CD4+ T cells) recognize the neoantigen peptide–MHC on tumor cells and kill them via perforin/granzyme and/or Fas–FasL pathways.
Adoptive cell therapy using Vα24+ invariant natural killer T cells that recognize glycolipid antigens via CD1d, rapidly secrete IFN-γ and other cytokines, directly lyse tumor cells, activate NK and dendritic cells, and remodel the immunosuppressive microenvironment to overcome PD‑1 resistance.
Autologous invariant natural killer T (iNKT; Va24-Ja18) cells expanded ex vivo and reinfused. They recognize glycolipid antigens presented by CD1d via their invariant TCR, rapidly secrete IFN-gamma and other cytokines, directly lyse tumor cells (perforin/granzyme, Fas/FasL), and activate NK and dendritic cells to remodel the immunosuppressive tumor microenvironment, enhancing antitumor immunity and helping overcome PD-1 resistance.
YES
DIRECT
Adoptively transferred iNKT cells recognize glycolipid antigens presented by CD1d via their invariant TCR and directly kill CD1d+ cells through perforin/granzyme release and Fas–FasL–mediated apoptosis.
Adoptive cell therapy using Vα24+ invariant natural killer T cells that recognize glycolipid antigens via CD1d, rapidly secrete IFN-γ and other cytokines, directly lyse tumor cells, activate NK and dendritic cells, and remodel the immunosuppressive microenvironment to overcome PD‑1 resistance.
Autologous invariant natural killer T (iNKT; Va24-Ja18) cells expanded ex vivo and reinfused. They recognize glycolipid antigens presented by CD1d via their invariant TCR, rapidly secrete IFN-gamma and other cytokines, directly lyse tumor cells (perforin/granzyme, Fas/FasL), and activate NK and dendritic cells to remodel the immunosuppressive tumor microenvironment, enhancing antitumor immunity and helping overcome PD-1 resistance.
YES
DIRECT
iNKT cells recognize CD1d-presented glycolipid antigens via their invariant TCR and directly kill target cells through perforin/granzyme release and Fas–FasL–mediated apoptosis.
Adoptive cell therapy using Vα24+ invariant natural killer T cells that recognize glycolipid antigens via CD1d, rapidly secrete IFN-γ and other cytokines, directly lyse tumor cells, activate NK and dendritic cells, and remodel the immunosuppressive microenvironment to overcome PD‑1 resistance.
Autologous invariant natural killer T (iNKT; Va24-Ja18) cells expanded ex vivo and reinfused. They recognize glycolipid antigens presented by CD1d via their invariant TCR, rapidly secrete IFN-gamma and other cytokines, directly lyse tumor cells (perforin/granzyme, Fas/FasL), and activate NK and dendritic cells to remodel the immunosuppressive tumor microenvironment, enhancing antitumor immunity and helping overcome PD-1 resistance.
YES
DIRECT
iNKT cells express FasL and engage Fas (CD95) on target cells, triggering death receptor–mediated (caspase-8) apoptosis; they can also kill via perforin/granzyme.
A humanized IgG4 bispecific T‑cell–engager monoclonal antibody that binds CD3 on T cells and BCMA on malignant plasma cells to trigger T‑cell cytotoxicity (brand: TECVAYLI).
Humanized IgG4 bispecific antibody that binds CD3 on T cells and BCMA on malignant plasma cells, crosslinking T cells to tumor cells to activate cytotoxic T-cell responses (perforin/granzyme release and cytokine-mediated killing) against BCMA-expressing myeloma cells.
NO
INDIRECT
Teclistamab uses CD3 on T cells to engage and activate them; the activated T cells kill BCMA-expressing myeloma cells via perforin/granzyme and cytokine-mediated cytotoxicity. CD3E+ T cells are not the targets of killing.