Autologous T cells genetically engineered to express a chimeric antigen receptor targeting the EGFRvIII mutant epitope; administered locally to the CNS via an Ommaya reservoir to eliminate EGFRvIII-positive glioblastoma cells through HLA-independent T-cell activation, cytokine release, and cytotoxic killing.
Autologous T cells are genetically engineered to express a chimeric antigen receptor that specifically binds the tumor-specific EGFRvIII epitope on glioblastoma cells, enabling HLA-independent recognition. CAR signaling activates the T cells (via CD3ζ and costimulatory domains), inducing cytokine release, proliferation, and targeted cytotoxic killing of EGFRvIII-positive tumor cells; administered locally to the CNS via an Ommaya reservoir.
YES
DIRECT
CAR-T cells recognize EGFRvIII on tumor cells and, upon CAR activation (CD3ζ/costimulatory), kill targets via perforin/granzyme-mediated cytolysis and apoptosis (HLA-independent).
Humanized IgG1 monoclonal antibody against HER2/ErbB2 that binds the extracellular domain to block receptor dimerization and activation, downregulating PI3K/AKT/MAPK signaling and promoting receptor internalization; additionally mediates antibody-dependent cellular cytotoxicity (ADCC) against HER2-overexpressing cells.
YES
DIRECT
Trastuzumab binds HER2 on target cells and engages Fcγ receptors on NK cells/macrophages to trigger antibody-dependent cellular cytotoxicity (perforin/granzyme-mediated lysis); complement activation may also contribute.
T cells from a newly matched donor engineered to express an anti-CD5 chimeric antigen receptor to bind CD5 on malignant T cells and trigger CAR-mediated cytotoxic killing, with anticipated on-target depletion of normal CD5+ T cells.
Allogeneic donor T cells engineered to express an anti-CD5 chimeric antigen receptor bind CD5 on malignant T cells, triggering CAR-mediated activation (CD3ζ/costimulatory signaling), proliferation, and perforin/granzyme-dependent cytotoxic killing; on-target depletion of normal CD5+ T cells is anticipated.
YES
DIRECT
Anti-CD5 CAR T cells bind CD5, triggering CAR (CD3ζ/costimulatory) activation and directly killing CD5+ cells via perforin/granzyme-mediated cytolysis (and related death receptor pathways).
CUSP06 is a cadherin-6 (CDH6)–directed antibody–drug conjugate (ADC). Its monoclonal antibody binds CDH6 on tumor cells, is internalized, and releases an intracellular cytotoxic payload (type not specified) to induce DNA damage and apoptosis in CDH6-positive tumors, including platinum-refractory/resistant ovarian cancer and other advanced solid tumors.
CUSP06 is an anti‑CDH6 antibody–drug conjugate that binds CDH6 on tumor cells, is internalized, and releases the exatecan payload via a protease‑cleavable linker. Exatecan inhibits topoisomerase I, stabilizing the topo I–DNA cleavable complex, causing DNA breaks, replication arrest, and apoptosis, with potential bystander killing of neighboring tumor cells.
YES
DIRECT
An anti-CDH6 ADC binds CDH6 on tumor cells, is internalized, and releases exatecan via a protease-cleavable linker; exatecan inhibits topoisomerase I, causing DNA breaks, replication arrest, and apoptosis (with potential bystander effect).
Autologous dendritic cells ex vivo loaded with survivin peptides; administered intradermally and intravenously to prime/expand tumor-specific CD8+ and CD4+ T cells against survivin-expressing glioblastoma cells.
Autologous dendritic cells are ex vivo loaded with survivin peptides and, after intradermal/IV administration, present survivin epitopes on MHC I/II to activate and expand survivin-specific CD8+ cytotoxic T cells and CD4+ helper T cells, driving targeted immune-mediated killing of survivin-expressing glioblastoma cells.
YES
INDIRECT
Dendritic-cell vaccination primes survivin-specific CD8+ T cells, which recognize survivin peptide–HLA class I complexes on target cells and kill them via perforin/granzyme-mediated cytotoxicity (and Fas/FasL apoptosis).