Multikinase TKI targeting ROS1, NTRK, and ALK with CNS activity.
Oral multikinase tyrosine kinase inhibitor that targets TRKA/B/C (NTRK1/2/3), ROS1, and ALK. By binding the ATP site, it inhibits kinase signaling (e.g., MAPK and PI3K/AKT pathways), leading to tumor cell growth arrest and apoptosis in cancers driven by these fusions/rearrangements; demonstrates CNS penetration.
YES
DIRECT
ATP-competitive inhibition of ROS1 kinase blocks downstream MAPK/PI3K-AKT signaling in ROS1-driven tumor cells, causing growth arrest and apoptosis.
Multikinase TKI targeting ROS1, NTRK, and ALK with CNS activity.
Oral multikinase tyrosine kinase inhibitor that targets TRKA/B/C (NTRK1/2/3), ROS1, and ALK. By binding the ATP site, it inhibits kinase signaling (e.g., MAPK and PI3K/AKT pathways), leading to tumor cell growth arrest and apoptosis in cancers driven by these fusions/rearrangements; demonstrates CNS penetration.
YES
DIRECT
ATP-competitive inhibition of ALK blocks downstream MAPK and PI3K/AKT signaling, leading to growth arrest and apoptosis in ALK-driven tumor cells.
Autologous, gene-modified T cells transduced with a lentiviral vector to express a CD19-specific chimeric antigen receptor (CAR), enabling antigen-specific activation and cytotoxic killing of CD19-positive B-lineage cells; administered after lymphodepleting chemotherapy.
Autologous T cells are lentivirally transduced to express a CD19-specific chimeric antigen receptor that recognizes CD19 on B-lineage cells, triggering CAR signaling to activate, expand, and mediate cytotoxic killing of CD19-positive malignant and normal B cells after lymphodepleting chemotherapy.
YES
DIRECT
CD19-specific CAR T cells recognize CD19 on target cells and kill them via T-cell effector functions, primarily perforin/granzyme-mediated cytolysis and death receptor signaling.
Polyclonal antibody preparation that depletes T lymphocytes for induction immunosuppression.
Polyclonal anti–T-lymphocyte IgG that binds multiple T-cell surface antigens and depletes T cells via complement-dependent cytotoxicity and Fc-mediated ADCC, with additional T-cell apoptosis and functional inhibition, producing potent immunosuppression.
YES
DIRECT
ATG antibodies bind CD7 on T cells, inducing complement-dependent lysis and Fc-mediated ADCC/phagocytosis, and can also trigger apoptosis.
Anti-CD20 monoclonal antibody that depletes CD20+ B cells to reduce neutralizing antibody formation.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on pre-B and mature B cells and depletes them via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis, thereby suppressing humoral immunity and reducing anti-drug antibody formation.
YES
DIRECT
Rituximab binds CD20 on B cells and induces killing via Fc-mediated ADCC by NK cells/macrophages, complement-dependent cytotoxicity, and CD20 cross-linking–induced apoptosis.