Autologous gene-modified T cells expressing an anti-CD19 chimeric antigen receptor with added metabolic armoring to enhance fitness, persistence, and function against CD19+ B-cell malignancies.
Autologous T cells engineered to express an anti-CD19 chimeric antigen receptor that recognizes CD19 on malignant B cells, activating T-cell signaling to induce cytotoxic killing and cytokine release; added metabolic armoring enhances T-cell metabolic fitness, persistence, and function within the tumor microenvironment.
YES
DIRECT
Anti-CD19 CAR-T cells bind CD19 on target B cells and, upon CAR signaling, kill them via perforin/granzyme-mediated cytolysis and apoptotic pathways (e.g., Fas–FasL), with cytokine release.
Anti-CD20 IgG1 monoclonal antibody that depletes malignant B cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis.
Chimeric anti-CD20 IgG1 monoclonal antibody that binds CD20 on B cells and induces cell death via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and direct apoptosis, leading to depletion of CD20-positive malignant B cells.
YES
DIRECT
Rituximab binds CD20 on B cells and induces killing via antibody-dependent cellular cytotoxicity (NK/macrophages via Fcγ receptors), complement-dependent cytotoxicity (C1q/MAC), and can trigger direct apoptosis upon CD20 ligation.
Donor-derived, partially HLA-matched virus-specific T lymphocytes enriched for IFN-γ–secreting CD8+/CD4+ T cells reactive to adenovirus, CMV, and EBV antigens; manufactured using CliniMACS cytokine capture and infused to restore antiviral immunity by HLA-restricted recognition and cytotoxic killing of infected cells.
Adoptive transfer of donor-derived, partially HLA-matched virus-specific CD8+/CD4+ T cells selected for IFN-γ secretion. These unengineered T cells use native TCRs to recognize HLA-presented adenovirus/CMV/EBV peptides on infected cells, secrete Th1 cytokines, and kill targets via perforin/granzyme, restoring antiviral immunity.
YES
DIRECT
Virus-specific T cells recognize HLA-presented adenoviral peptides via their native TCRs and directly kill the infected cells by perforin/granzyme-mediated apoptosis (and related cytotoxic pathways).
Donor-derived, partially HLA-matched virus-specific T lymphocytes enriched for IFN-γ–secreting CD8+/CD4+ T cells reactive to adenovirus, CMV, and EBV antigens; manufactured using CliniMACS cytokine capture and infused to restore antiviral immunity by HLA-restricted recognition and cytotoxic killing of infected cells.
Adoptive transfer of donor-derived, partially HLA-matched virus-specific CD8+/CD4+ T cells selected for IFN-γ secretion. These unengineered T cells use native TCRs to recognize HLA-presented adenovirus/CMV/EBV peptides on infected cells, secrete Th1 cytokines, and kill targets via perforin/granzyme, restoring antiviral immunity.
YES
DIRECT
Virus-specific T cells recognize CMV peptide–HLA complexes via native TCRs and kill infected cells by CTL degranulation (perforin/granzyme), with possible Fas–FasL engagement.
Donor-derived, partially HLA-matched virus-specific T lymphocytes enriched for IFN-γ–secreting CD8+/CD4+ T cells reactive to adenovirus, CMV, and EBV antigens; manufactured using CliniMACS cytokine capture and infused to restore antiviral immunity by HLA-restricted recognition and cytotoxic killing of infected cells.
Adoptive transfer of donor-derived, partially HLA-matched virus-specific CD8+/CD4+ T cells selected for IFN-γ secretion. These unengineered T cells use native TCRs to recognize HLA-presented adenovirus/CMV/EBV peptides on infected cells, secrete Th1 cytokines, and kill targets via perforin/granzyme, restoring antiviral immunity.
YES
DIRECT
Virus-specific T cells recognize HLA-presented EBV peptides via native TCRs and kill target cells through CTL cytotoxicity (perforin/granzyme; Fas–FasL).