Autologous, lentivirally transduced second-generation CAR T-cell therapy (CD4+ and CD8+) targeting B7-H3 (CD276), EGFR806 epitope on EGFR/EGFRvIII, HER2 (ERBB2), and IL13Rα2 via an IL13-zetakine design; administered locoregionally via intraventricular catheter to drive CAR-mediated cytotoxic killing of CNS tumor cells and mitigate antigen escape.
Autologous CD4+/CD8+ T cells are lentivirally engineered to express four second-generation CARs targeting B7-H3 (CD276), the tumor-restricted EGFR806 epitope on EGFR/EGFRvIII, HER2, and IL13Ra2 (via an IL13-zetakine design). Following locoregional intraventricular delivery, CAR engagement drives antigen-specific T-cell activation, cytokine release, and cytotoxic killing of CNS tumor cells, with multi-antigen targeting intended to mitigate antigen escape.
CAR T cells recognizing the EGFR806 epitope on EGFR/EGFRvIII bind target cells and, upon CAR engagement, execute cytolytic killing via perforin/granzyme release and death-receptor pathways.
Autologous, lentivirally transduced second-generation CAR T-cell therapy (CD4+ and CD8+) targeting B7-H3 (CD276), EGFR806 epitope on EGFR/EGFRvIII, HER2 (ERBB2), and IL13Rα2 via an IL13-zetakine design; administered locoregionally via intraventricular catheter to drive CAR-mediated cytotoxic killing of CNS tumor cells and mitigate antigen escape.
Autologous CD4+/CD8+ T cells are lentivirally engineered to express four second-generation CARs targeting B7-H3 (CD276), the tumor-restricted EGFR806 epitope on EGFR/EGFRvIII, HER2, and IL13Ra2 (via an IL13-zetakine design). Following locoregional intraventricular delivery, CAR engagement drives antigen-specific T-cell activation, cytokine release, and cytotoxic killing of CNS tumor cells, with multi-antigen targeting intended to mitigate antigen escape.
CAR T cells engineered to recognize HER2 bind HER2 on target cells, triggering T-cell activation and direct killing via perforin/granzyme-mediated cytolysis (and death receptor pathways).
Autologous, lentivirally transduced second-generation CAR T-cell therapy (CD4+ and CD8+) targeting B7-H3 (CD276), EGFR806 epitope on EGFR/EGFRvIII, HER2 (ERBB2), and IL13Rα2 via an IL13-zetakine design; administered locoregionally via intraventricular catheter to drive CAR-mediated cytotoxic killing of CNS tumor cells and mitigate antigen escape.
Autologous CD4+/CD8+ T cells are lentivirally engineered to express four second-generation CARs targeting B7-H3 (CD276), the tumor-restricted EGFR806 epitope on EGFR/EGFRvIII, HER2, and IL13Ra2 (via an IL13-zetakine design). Following locoregional intraventricular delivery, CAR engagement drives antigen-specific T-cell activation, cytokine release, and cytotoxic killing of CNS tumor cells, with multi-antigen targeting intended to mitigate antigen escape.
CAR T cells engineered with an IL13-zetakine bind IL13Ralpha2 on tumor cells, triggering T-cell activation and perforin/granzyme-mediated cytolysis and apoptosis (with possible Fas–FasL/cytokine contributions).
An antibody–drug conjugate targeting Nectin-4 that delivers the cytotoxic payload MMAE (a microtubule inhibitor), leading to internalization, microtubule disruption, and tumor cell death in Nectin-4–expressing urothelial cancer cells.
A Nectin-4–targeted monoclonal antibody linked via a cleavable linker to the microtubule inhibitor MMAE; upon binding Nectin-4 on tumor cells, the ADC is internalized and MMAE is released to inhibit tubulin polymerization, causing G2/M arrest and apoptosis in Nectin-4–expressing cancer cells.
The ADC binds Nectin-4 on target cells, is internalized, and releases MMAE after linker cleavage; MMAE inhibits tubulin polymerization, causing G2/M arrest and apoptosis of Nectin-4–expressing cells.
Autologous adoptive T-cell therapy expanded from tumor-associated lymph nodes; tumor-reactive T cells that recognize tumor antigens via TCRs and mediate cytotoxicity.
Autologous T cells expanded from tumor-associated lymph nodes that retain native TCRs specific for tumor antigens. After infusion, they recognize peptide–MHC on tumor cells via their endogenous TCRs and mediate antitumor activity through cytotoxic granule release and cytokine secretion.
TAL-T cells recognize the tumor peptide–HLA-I complex via their endogenous TCRs and directly kill target cells through cytotoxic degranulation (perforin/granzymes) and death-receptor pathways (e.g., Fas/FasL).