An intravenous antibody–drug conjugate consisting of a humanized anti‑TROP2 monoclonal antibody linked to a topoisomerase I–inhibiting cytotoxic payload that is delivered to TROP2‑expressing tumor cells, inducing DNA damage and cell death; indicated for metastatic triple‑negative breast cancer.
Humanized anti‑TROP2 (TACSTD2) monoclonal antibody conjugated to SN‑38 binds TROP2‑expressing tumor cells, is internalized, and releases SN‑38 to inhibit topoisomerase I, stabilizing Topo I–DNA complexes and causing DNA damage, replication arrest, and apoptosis.
Anti‑TROP2 ADC binds TROP2, is internalized, and releases SN‑38, a topoisomerase I inhibitor, causing DNA damage/replication arrest and apoptosis of the target cell.
CD70-targeting monoclonal antibody that blocks CD70–CD27 signaling on AML blasts and leukemia stem cells and promotes immune-mediated killing (e.g., ADCC/CDC).
Defucosylated humanized IgG1 monoclonal antibody targeting CD70 that blocks CD70–CD27 signaling on AML blasts and leukemia stem cells and promotes immune-mediated killing (e.g., ADCC/CDC, ADCP) of CD70-expressing cells.
Anti-CD70 IgG1 binds CD70 and engages Fc-mediated effector functions (ADCC by NK cells, CDC, and ADCP), leading to killing of CD70-expressing cells.
Oral small-molecule BCL-2 inhibitor (BH3 mimetic) that restores mitochondrial apoptosis in AML cells.
Selective oral BCL-2 inhibitor (BH3 mimetic) that binds the BH3-binding groove of BCL-2, blocks its anti-apoptotic function, releases pro-apoptotic factors to activate BAX/BAK and restore mitochondrial apoptosis; sparing BCL-XL.
BH3-mimetic inhibition of BCL-2 releases pro-apoptotic factors, activates BAX/BAK, induces mitochondrial outer membrane permeabilization and caspase-dependent apoptosis in BCL-2–dependent cells.
Polyclonal antibody preparation that depletes and suppresses T lymphocytes to reduce autoimmune marrow destruction.
Polyclonal anti-lymphocyte immunoglobulin that binds multiple T‑cell surface antigens and depletes/suppresses T lymphocytes via complement-dependent cytolysis and Fc-mediated clearance, reducing autoreactive T‑cell–mediated marrow destruction.
ALG antibodies bind CD2 on T cells, triggering complement-dependent lysis and Fc receptor–mediated ADCC/phagocytic clearance of the opsonized cells.
Polyclonal antibody preparation that depletes and suppresses T lymphocytes to reduce autoimmune marrow destruction.
Polyclonal anti-lymphocyte immunoglobulin that binds multiple T‑cell surface antigens and depletes/suppresses T lymphocytes via complement-dependent cytolysis and Fc-mediated clearance, reducing autoreactive T‑cell–mediated marrow destruction.
ALG binds CD3E on T cells and induces complement-dependent lysis and Fc-mediated effector clearance (ADCC/ADCP), depleting CD3+ T cells.