Chimeric anti-CD20 IgG1 monoclonal antibody that depletes B cells via complement-dependent cytotoxicity (CDC), ADCC, and apoptosis.
Chimeric anti-CD20 IgG1 monoclonal antibody that binds CD20 on B cells and induces cell killing via complement-dependent cytotoxicity (CDC), antibody-dependent cellular cytotoxicity (ADCC), and apoptosis, resulting in depletion of CD20-positive B cells.
YES
DIRECT
Anti-CD20 IgG1 binds CD20 on B cells and triggers complement-dependent cytotoxicity (CDC), antibody-dependent cellular cytotoxicity (ADCC) via Fcγ receptor–bearing effector cells, and can induce apoptosis, killing CD20+ cells.
Autologous, genetically modified CAR T-cell therapy targeting CLEC12A (CD371/CLL-1) on AML cells; incorporates CD3ζ-based CAR signaling with costimulation and is "armored" to secrete IL-18 to enhance expansion/persistence, Th1 polarization, and recruitment/activation of innate immune cells, thereby broadening anti-leukemia activity. Administered after lymphodepleting chemotherapy in relapsed/refractory AML.
Autologous T cells engineered with a CAR that binds CLEC12A (CD371/CLL-1) on AML cells. CAR signaling via CD3zeta with costimulation triggers T-cell cytotoxicity against leukemic blasts and stem cells. The construct is armored to secrete IL-18, which enhances CAR T expansion and persistence, promotes Th1 polarization and IFN-gamma–driven immunity, and recruits/activates innate immune cells (e.g., NK cells, macrophages), broadening anti-leukemia activity after lymphodepletion.
YES
DIRECT
CAR T cells recognize CLEC12A on AML cells and induce T-cell cytotoxicity, primarily via perforin/granzyme-mediated apoptosis and Fas/FasL signaling; IL-18 enhances CAR T activity and can recruit innate effectors.
Autologous, genetically modified CAR T-cell therapy targeting CLEC12A (CD371/CLL-1) on AML cells; incorporates CD3ζ-based CAR signaling with costimulation and is "armored" to secrete IL-18 to enhance expansion/persistence, Th1 polarization, and recruitment/activation of innate immune cells, thereby broadening anti-leukemia activity. Administered after lymphodepleting chemotherapy in relapsed/refractory AML.
Autologous T cells engineered with a CAR that binds CLEC12A (CD371/CLL-1) on AML cells. CAR signaling via CD3zeta with costimulation triggers T-cell cytotoxicity against leukemic blasts and stem cells. The construct is armored to secrete IL-18, which enhances CAR T expansion and persistence, promotes Th1 polarization and IFN-gamma–driven immunity, and recruits/activates innate immune cells (e.g., NK cells, macrophages), broadening anti-leukemia activity after lymphodepletion.
NO
INDIRECT
CAR T cells recognize and kill CLEC12A+ AML cells via CAR-mediated cytolysis. The IL-18 secreted by the CAR T cells signals through IL18R1 on immune cells to enhance activation but does not target IL18R1+ cells for killing.
Rabbit polyclonal anti-thymocyte globulin that depletes T cells to prevent rejection and GVHD.
Rabbit polyclonal anti-thymocyte IgG that binds multiple T-cell surface antigens and depletes T cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, producing immunosuppression to prevent rejection and GVHD.
NO
INDIRECT
Thymoglobulin binds multiple T‑cell surface antigens (not HLA‑A) and depletes T cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis.
Autologous, genetically modified CAR T-cell therapy targeting CLEC12A (CD371/CLL-1) on AML cells; incorporates CD3ζ-based CAR signaling with costimulation and is "armored" to secrete IL-18 to enhance expansion/persistence, Th1 polarization, and recruitment/activation of innate immune cells, thereby broadening anti-leukemia activity. Administered after lymphodepleting chemotherapy in relapsed/refractory AML.
Autologous T cells engineered with a CAR that binds CLEC12A (CD371/CLL-1) on AML cells. CAR signaling via CD3zeta with costimulation triggers T-cell cytotoxicity against leukemic blasts and stem cells. The construct is armored to secrete IL-18, which enhances CAR T expansion and persistence, promotes Th1 polarization and IFN-gamma–driven immunity, and recruits/activates innate immune cells (e.g., NK cells, macrophages), broadening anti-leukemia activity after lymphodepletion.
NO
INDIRECT
CAR T cells kill CLEC12A (CD371)-positive AML cells. IL-18 secretion signals via IL18RAP to activate immune cells, but IL18RAP-expressing cells are not targeted or killed.