Type II anti‑CD20 monoclonal antibody given prior to glofitamab to debulk B cells and mitigate CRS; induces direct B‑cell death and Fc‑mediated ADCC/ADCP.
Type II anti-CD20 humanized IgG1 monoclonal antibody that binds CD20 on B cells; glycoengineering increases Fc-gamma RIIIa affinity to enhance antibody-dependent cellular cytotoxicity (ADCC) and antibody-dependent cellular phagocytosis (ADCP), and it also induces direct, caspase-independent B-cell death, depleting CD20+ B cells (used pre-glofitamab to debulk and mitigate CRS).
NO
INDIRECT
Obinutuzumab binds CD20 on B cells; its Fc engages Fcγ receptors (e.g., CD16a on NK cells and CD16b on neutrophils) to mediate ADCC/ADCP against CD20+ B cells and also induces direct B‑cell death. CD16b+ cells act as effectors, not targets, and are not killed by the drug.
IV humanized anti-HER2 monoclonal antibody that inhibits HER2 signaling/dimerization and mediates antibody-dependent cellular cytotoxicity (ADCC).
Humanized monoclonal antibody against HER2 (ErbB2) that binds the extracellular domain, blocks HER2 signaling and dimerization, promotes receptor downregulation, and triggers immune-mediated killing via antibody-dependent cellular cytotoxicity (ADCC), thereby inhibiting PI3K/AKT and MAPK pathways in HER2-overexpressing tumor cells.
YES
DIRECT
Trastuzumab binds HER2 on target cells and its Fc engages Fcγ receptor–bearing effector cells (e.g., NK cells) to mediate antibody‑dependent cellular cytotoxicity (ADCC); HER2 signaling blockade can also promote apoptosis.
Allogeneic cord blood–derived natural killer cells genetically engineered to express a chimeric antigen receptor targeting CD70, designed to bind CD70 on tumor cells and induce NK-mediated cytotoxicity while potentially modulating the CD70/CD27 pathway in CD70-positive T-cell lymphoma and acute myeloid leukemia.
Allogeneic cord blood–derived NK cells engineered to express a CD70-directed chimeric antigen receptor bind CD70 on tumor cells, triggering NK activation and cytotoxic killing (perforin/granzyme) of CD70-positive cells and potentially disrupting CD70/CD27 signaling in TCL and AML.
YES
DIRECT
CD70-directed CAR-NK cells bind CD70 on target cells, activating NK degranulation (perforin/granzymes) and death-receptor pathways to lyse/apoptose CD70+ cells.
Autologous CD19-directed CAR T-cell therapy with 4-1BB costimulation/CD3ζ signaling used to target and eliminate CD19+ malignant B cells.
Autologous T cells engineered to express a CD19‑directed chimeric antigen receptor with 4‑1BB costimulation and CD3ζ signaling. Binding to CD19 on B cells activates the CAR T cells, driving proliferation, cytokine release, and perforin/granzyme‑mediated cytotoxic killing of CD19+ malignant B cells, leading to depletion of CD19+ cells.
YES
DIRECT
CD19-directed CAR T cells bind CD19 on target cells, become activated, and kill via perforin/granzyme cytotoxicity (and Fas/FasL apoptosis), depleting CD19+ cells.
Allogeneic cord blood–derived NK cells engineered to express a CD70-targeted chimeric antigen receptor and an IL-15 transgene to support survival, proliferation, and persistence; designed for antigen-specific cytotoxicity against CD70-expressing tumors.
Allogeneic cord blood–derived NK cells engineered to express a CD70-specific chimeric antigen receptor and an IL-15 transgene. The CAR redirects NK cells to CD70-expressing tumor cells to trigger antigen-specific NK activation and cytotoxicity (perforin/granzyme release and death receptor pathways), while IL-15 provides autocrine support for survival, proliferation, and persistence in vivo.
YES
DIRECT
CD70-specific CAR on engineered NK cells binds CD70 on target cells, activating NK cytotoxicity via perforin/granzyme-mediated lysis and death receptor pathways (e.g., TRAIL/FasL).