Human IgG1 monoclonal antibody targeting CD38 on myeloma cells; induces ADCC, CDC, ADCP, and direct apoptosis and modulates CD38 ectoenzyme activity.
Anti-CD38 human IgG1 monoclonal antibody that binds CD38 on myeloma cells, triggering ADCC, CDC, and ADCP, inducing direct apoptosis, and inhibiting CD38 ectoenzyme activity, resulting in depletion/lysis of CD38-expressing tumor cells.
Binds CD38 on target cells and induces killing via Fc-mediated ADCC (NK cells), CDC (complement), and ADCP (macrophages), and can also trigger direct apoptosis upon CD38 engagement.
Selective small-molecule BCL-2 inhibitor (BH3 mimetic) that triggers mitochondrial apoptosis in AML cells.
Selective BH3-mimetic inhibitor of BCL-2 that binds the BCL-2 hydrophobic groove, displaces pro-apoptotic BH3-only proteins, and restores mitochondrial apoptosis (BAX/BAK activation, MOMP, cytochrome c release) in AML cells; spares BCL-XL relative to navitoclax.
Venetoclax directly inhibits BCL-2, releasing BH3-only proteins to activate BAX/BAK, inducing mitochondrial outer membrane permeabilization, cytochrome c release, caspase activation, and apoptosis in BCL-2–dependent cells.
JCPyV-specific virus-specific T-cell therapy (adoptive cellular immunotherapy) consisting of HLA-restricted T cells infused IV (1×10^8 cells every 28 days for 4 doses) to restore antiviral cytotoxic T-lymphocyte responses (primarily CD8+) against JCPyV-infected CNS cells, control viral replication, and slow/stop PML progression.
Adoptive transfer of ex vivo expanded, HLA-restricted JCPyV-specific T cells (primarily CD8+ cytotoxic T lymphocytes) that recognize JCPyV antigens via native TCRs on infected CNS cells and eliminate them via cytotoxic effector functions and Th1 cytokines, restoring antiviral cellular immunity to control viral replication and slow or halt PML progression.
Adoptively transferred JCPyV-specific CD8+ T cells recognize LTAg-derived peptides on HLA class I and kill infected cells via perforin/granzyme cytolysis (and Fas/FasL), with supportive Th1 cytokines.
JCPyV-specific virus-specific T-cell therapy (adoptive cellular immunotherapy) consisting of HLA-restricted T cells infused IV (1×10^8 cells every 28 days for 4 doses) to restore antiviral cytotoxic T-lymphocyte responses (primarily CD8+) against JCPyV-infected CNS cells, control viral replication, and slow/stop PML progression.
Adoptive transfer of ex vivo expanded, HLA-restricted JCPyV-specific T cells (primarily CD8+ cytotoxic T lymphocytes) that recognize JCPyV antigens via native TCRs on infected CNS cells and eliminate them via cytotoxic effector functions and Th1 cytokines, restoring antiviral cellular immunity to control viral replication and slow or halt PML progression.
HLA-restricted, TCR-mediated recognition of JCPyV small t antigen peptides on infected cells by infused virus-specific CD8+ T cells, leading to perforin/granzyme-dependent cytolysis (and Fas–FasL apoptosis).
JCPyV-specific virus-specific T-cell therapy (adoptive cellular immunotherapy) consisting of HLA-restricted T cells infused IV (1×10^8 cells every 28 days for 4 doses) to restore antiviral cytotoxic T-lymphocyte responses (primarily CD8+) against JCPyV-infected CNS cells, control viral replication, and slow/stop PML progression.
Adoptive transfer of ex vivo expanded, HLA-restricted JCPyV-specific T cells (primarily CD8+ cytotoxic T lymphocytes) that recognize JCPyV antigens via native TCRs on infected CNS cells and eliminate them via cytotoxic effector functions and Th1 cytokines, restoring antiviral cellular immunity to control viral replication and slow or halt PML progression.
Adoptively transferred JCPyV-specific CD8+ T cells recognize VP1-derived peptides on HLA class I of infected cells and induce apoptosis via perforin/granzyme (and Fas–FasL) effector pathways.