An autologous CD19-directed CAR-T cell therapy generated by retroviral transduction; the CAR contains CD3ζ and costimulatory domains that enhance cytokine-driven JAK/STAT signaling to promote T-cell activation, proliferation, and cytotoxic killing of CD19-positive malignant B cells.
Autologous T cells are retrovirally transduced to express a CD19-specific chimeric antigen receptor containing CD3ζ and costimulatory domains. Engagement of CD19 on malignant B cells triggers CAR-mediated signaling (including cytokine-driven JAK/STAT pathways), leading to T-cell activation, proliferation, and targeted cytotoxic killing of CD19-positive cells.
YES
DIRECT
CD19-directed CAR-T cells bind CD19 on target cells, become activated, and kill them via perforin/granzyme release and death-receptor (Fas/FasL)–mediated apoptosis.
Patient-derived T cells genetically engineered to express a chimeric antigen receptor that specifically recognizes Claudin18.2 (CLDN18.2), activating and expanding T cells to mediate targeted cytotoxicity against CLDN18.2-positive tumor cells; administered as up to three infusions.
Autologous T cells are genetically engineered to express a chimeric antigen receptor targeting Claudin18.2 (CLDN18.2). Antigen engagement triggers CAR signaling, activating and expanding the T cells to mediate targeted cytotoxicity and cytokine release, leading to selective killing of CLDN18.2-positive tumor cells.
YES
DIRECT
CAR T cells bind CLDN18.2 on target cells and kill them via T‑cell effector mechanisms (perforin/granzyme-mediated cytolysis and Fas–FasL apoptosis).
Autologous TH1-polarizing dendritic cell vaccine loaded with patient tumor lysate and mRNA-encoded antigens to enhance antigen presentation (MHC I/II) and prime CD8+ cytotoxic T cells and CD4+ TH1 responses, boosting IFN-γ–mediated antitumor immunity.
Autologous TH1-polarized dendritic cells are loaded ex vivo with patient tumor lysate and mRNA-encoded tumor antigens. The DCs process/translate antigens and present peptides on MHC class I and II to cross-prime tumor-specific CD8+ cytotoxic T cells and activate CD4+ TH1 cells, enhancing IFN-γ–mediated antitumor immunity.
YES
INDIRECT
Ex vivo–loaded dendritic cells prime tumor-specific CD8+ T cells, which recognize neoantigen–MHC I on tumor cells and kill them via perforin/granzyme and Fas–FasL pathways with TH1/IFN-γ support.
Autologous TH1-polarizing dendritic cell vaccine loaded with patient tumor lysate and mRNA-encoded antigens to enhance antigen presentation (MHC I/II) and prime CD8+ cytotoxic T cells and CD4+ TH1 responses, boosting IFN-γ–mediated antitumor immunity.
Autologous TH1-polarized dendritic cells are loaded ex vivo with patient tumor lysate and mRNA-encoded tumor antigens. The DCs process/translate antigens and present peptides on MHC class I and II to cross-prime tumor-specific CD8+ cytotoxic T cells and activate CD4+ TH1 cells, enhancing IFN-γ–mediated antitumor immunity.
YES
INDIRECT
The DC vaccine primes tumor‑specific T cells. CD4 TH1/CTL recognize MHC II–restricted neoantigens on MHC II–positive tumor cells and can directly lyse them (perforin/granzyme, Fas–FasL), while also helping CD8 CTLs; the dendritic cells themselves do not kill tumor cells.
Autologous, gene-modified CD19-directed CAR T-cell therapy (also known as CNCT19) in which a patient’s T cells are engineered to express a CAR targeting CD19, leading to T-cell activation, cytotoxic killing of CD19+ B-cell malignancies, and B-cell aplasia.
Autologous T cells are genetically modified to express a CD19-directed chimeric antigen receptor; upon binding CD19 on B-cell malignancies, CAR signaling (CD3zeta with costimulation) activates T-cell cytotoxicity and cytokine release, resulting in perforin/granzyme-mediated killing of CD19+ cells and on-target B-cell aplasia.
YES
DIRECT
CD19-directed CAR T cells bind CD19 and activate T-cell effector killing, primarily via perforin/granzyme-mediated apoptosis (and Fas–FasL).