Rabbit-derived polyclonal IgG targeting human T-cell antigens; depletes T cells (and some B/NK cells) via complement-dependent cytotoxicity, ADCC, and apoptosis.
Rabbit-derived polyclonal IgG that binds multiple human T‑cell antigens and depletes T cells (with some B/NK cell effects) via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and induction of apoptosis, producing profound lymphodepletion.
Polyclonal antibodies in rATG bind CD52 on lymphocytes, triggering complement-dependent cytotoxicity and Fc receptor–mediated ADCC, and can also induce apoptosis, directly depleting CD52+ cells.
Rabbit-derived polyclonal IgG targeting human T-cell antigens; depletes T cells (and some B/NK cells) via complement-dependent cytotoxicity, ADCC, and apoptosis.
Rabbit-derived polyclonal IgG that binds multiple human T‑cell antigens and depletes T cells (with some B/NK cell effects) via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and induction of apoptosis, producing profound lymphodepletion.
Polyclonal antibodies in rATG bind CD95 (Fas) on T cells, leading to complement-dependent lysis, antibody-dependent cellular cytotoxicity, and Fas cross-linking–induced apoptosis.
Rabbit-derived polyclonal IgG targeting human T-cell antigens; depletes T cells (and some B/NK cells) via complement-dependent cytotoxicity, ADCC, and apoptosis.
Rabbit-derived polyclonal IgG that binds multiple human T‑cell antigens and depletes T cells (with some B/NK cell effects) via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and induction of apoptosis, producing profound lymphodepletion.
rATG contains antibodies that bind CD25 on T cells, leading to depletion via complement-dependent cytotoxicity and Fc-mediated ADCC, with additional apoptosis induction.
Chimeric anti-CD20 monoclonal antibody that depletes CD20+ B cells (including memory B cells) via CDC, ADCC, and apoptosis; spares plasma cells.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on pre-B and mature B cells and depletes them via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis; spares CD20-negative plasma cells.
Anti-CD20 mAb binds CD20 on B cells and triggers complement-dependent cytotoxicity and Fc-mediated ADCC by NK/macrophages, and can directly induce apoptosis.
Adoptive cellular therapy using engineered T cells (commonly CD19‑targeted) to mediate cytotoxicity against B‑cell malignancies.
Engineered autologous T cells expressing a chimeric antigen receptor (commonly targeting CD19) recognize B‑cell antigens independent of MHC, triggering T‑cell activation and cytotoxic killing of malignant B cells via perforin/granzyme release and cytokine production.
CAR T cells recognize CD19 on target cells via the CAR and kill them through perforin/granzyme-mediated cytolysis (and death receptor signaling), inducing apoptosis.