A human monoclonal antibody targeting HBsAg that neutralizes HBV virions/subviral particles and, via Fc engineering, enhances Fcγ receptor–mediated effector functions (ADCC/ADCP) to promote clearance of HBsAg-expressing hepatocytes.
Human monoclonal antibody to HBsAg that neutralizes circulating HBV virions and subviral particles and, via Fc engineering, enhances Fc gamma receptor–mediated effector functions (ADCC/ADCP) to promote clearance of HBsAg-expressing hepatocytes and reduce HBsAg levels.
Fc-engineered anti-HBsAg antibody opsonizes HBsAg+ hepatocytes and engages Fcγ receptors on NK cells/macrophages to trigger ADCC/ADCP, leading to killing/clearance of target cells.
An antibody–drug conjugate targeting CEACAM5; after binding and internalization it releases the maytansinoid payload DM4 (ravtansine), a microtubule inhibitor that induces mitotic arrest and tumor cell death.
Monoclonal antibody targets CEACAM5 on tumor cells; after binding and internalization, the linker is cleaved to release the DM4 (ravtansine) maytansinoid payload, a microtubule inhibitor, causing mitotic arrest and tumor cell death.
ADC binds CEACAM5, is internalized, and releases the DM4 (ravtansine) microtubule inhibitor, causing mitotic arrest and apoptosis of the target-expressing cells.
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.
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.
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.
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.
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).