Rabbit polyclonal antilymphocyte globulin used for in vivo T-cell depletion to reduce graft-versus-host disease risk.
Rabbit polyclonal IgG against multiple human T‑cell surface antigens (e.g., CD2, CD3, CD4, CD8, HLA) that depletes T lymphocytes via complement-dependent cytotoxicity, Fc-mediated ADCC/phagocytosis, and apoptosis, producing in vivo T‑cell immunosuppression to reduce GVHD risk.
rATG contains antibodies to CD3 that bind CD3E on T cells and deplete them via complement-dependent cytotoxicity and Fc-mediated effector functions (ADCC/phagocytosis), with additional apoptosis upon cross-linking.
Anti‑CD20 monoclonal antibody that depletes B cells via ADCC, CDC, and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on pre-B and mature B cells, depleting CD20+ cells via ADCC, CDC, antibody-dependent phagocytosis, and induction of apoptosis.
Rituximab binds CD20 on B cells and triggers killing via Fc-mediated ADCC (NK cells), antibody-dependent phagocytosis (macrophages), complement-dependent cytotoxicity (CDC), and can induce apoptosis upon CD20 cross-linking.
Glycoengineered type II anti‑CD20 monoclonal antibody with enhanced ADCC and direct cell death.
Glycoengineered humanized IgG1 type II anti‑CD20 monoclonal antibody that binds CD20 on B cells; afucosylated Fc increases FcγRIIIa binding to enhance ADCC (and ADCP), and it triggers strong direct, largely caspase‑independent cell death, leading to depletion of CD20+ malignant B cells.
Binds CD20 on B cells, triggering direct caspase-independent cell death and engaging Fc-gamma RIIIa–bearing effector cells (NK cells/macrophages) to mediate ADCC/ADCP, depleting CD20+ cells.
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.
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.
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.