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.
YES
DIRECT
Polyclonal antibodies in rATG bind CD25 on T cells, activating complement and engaging Fc receptors to mediate CDC and ADCC/phagocytosis (and apoptosis), depleting CD25+ cells.
Autologous, gene-modified CD19-directed CAR T-cell therapy co-expressing an engineered orthogonal IL-2 receptor beta (hoRb); eliminates CD19+ B cells and can be selectively expanded/activated via hoRb signaling.
Autologous T cells engineered with a CD19-directed CAR (CD28 costimulation + CD3ζ signaling) to recognize and kill CD19+ B cells via T-cell activation and cytolytic pathways. The cells co-express an engineered orthogonal IL-2 receptor β (hoRb), enabling selective expansion and activation upon administration of the matching orthogonal IL-2 (e.g., STK-009), which signals through JAK/STAT in the modified T cells only, enhancing proliferation, persistence, and antitumor activity while limiting systemic IL-2–mediated effects.
YES
DIRECT
CD19-directed CAR T cells bind CD19 on target B cells, become activated via CD28/CD3ζ signaling, and kill via perforin/granzyme and Fas–FasL apoptotic pathways; orthogonal IL-2 selectively expands the CAR T cells.
Autologous, gene-modified CD19-directed CAR T-cell therapy co-expressing an engineered orthogonal IL-2 receptor beta (hoRb); eliminates CD19+ B cells and can be selectively expanded/activated via hoRb signaling.
Autologous T cells engineered with a CD19-directed CAR (CD28 costimulation + CD3ζ signaling) to recognize and kill CD19+ B cells via T-cell activation and cytolytic pathways. The cells co-express an engineered orthogonal IL-2 receptor β (hoRb), enabling selective expansion and activation upon administration of the matching orthogonal IL-2 (e.g., STK-009), which signals through JAK/STAT in the modified T cells only, enhancing proliferation, persistence, and antitumor activity while limiting systemic IL-2–mediated effects.
NO
INDIRECT
STK-009 is a soluble orthogonal IL-2 that activates the engineered hoRb on SYNCAR-001 T cells to expand/persist; killing is directed against CD19+ cells via CAR-mediated cytolytic pathways, not against cells expressing STK-009.
Gene-modified autologous T-cell immunotherapy using an integrating lentiviral vector to express a chimeric antigen receptor (CAR). The CAR targets a tumor-associated surface antigen (unspecified), triggering CD3ζ and costimulatory signaling to activate T cells, drive clonal expansion, cytokine release, and antigen-specific cytotoxicity; persistence and safety (e.g., replication-competent lentivirus, insertional events) are monitored.
Autologous T cells are gene-modified with an integrating lentiviral vector to express a chimeric antigen receptor that recognizes a tumor-associated surface antigen. Antigen binding triggers TCR-independent CD3ζ and costimulatory signaling, leading to T-cell activation, clonal expansion, cytokine release, and antigen-specific cytotoxic killing; persistence and safety (e.g., replication-competent lentivirus, insertional events) are monitored.
YES
DIRECT
CAR T cells bind the tumor-associated surface antigen and, upon CAR signaling, directly kill antigen-positive cells via perforin/granzyme-mediated cytolysis and apoptosis (e.g., Fas/FasL).
Type II anti-CD20 monoclonal antibody that depletes CD20+ B cells via antibody-dependent cellular cytotoxicity, complement-mediated cytotoxicity, and direct cell death.
Glycoengineered type II anti-CD20 humanized IgG1 monoclonal antibody that binds CD20 on B cells and depletes them via enhanced antibody-dependent cellular cytotoxicity (increased FcγRIIIa affinity), complement-dependent cytotoxicity, and direct caspase-independent apoptosis.
YES
DIRECT
Binds CD20 on B cells and induces killing via Fc-enhanced ADCC (NK cells/macrophages), complement-dependent cytotoxicity, and direct caspase-independent apoptosis/type II signaling.