Allogeneic cord blood–derived NK cells engineered to express a CD70-targeted chimeric antigen receptor and an IL-15 transgene to support survival, proliferation, and persistence; designed for antigen-specific cytotoxicity against CD70-expressing tumors.
Allogeneic cord blood–derived NK cells engineered to express a CD70-specific chimeric antigen receptor and an IL-15 transgene. The CAR redirects NK cells to CD70-expressing tumor cells to trigger antigen-specific NK activation and cytotoxicity (perforin/granzyme release and death receptor pathways), while IL-15 provides autocrine support for survival, proliferation, and persistence in vivo.
NO
INDIRECT
The CAR-NK cells kill CD70-expressing cells via CAR-mediated recognition with perforin/granzyme release and death receptor pathways. IL-15Rα is not a recognition target; IL-15 signaling is supportive/autocrine and does not trigger cytotoxicity against IL-15Rα-expressing cells.
Allogeneic cord blood–derived NK cells engineered to express a CD70-targeted chimeric antigen receptor and an IL-15 transgene to support survival, proliferation, and persistence; designed for antigen-specific cytotoxicity against CD70-expressing tumors.
Allogeneic cord blood–derived NK cells engineered to express a CD70-specific chimeric antigen receptor and an IL-15 transgene. The CAR redirects NK cells to CD70-expressing tumor cells to trigger antigen-specific NK activation and cytotoxicity (perforin/granzyme release and death receptor pathways), while IL-15 provides autocrine support for survival, proliferation, and persistence in vivo.
NO
INDIRECT
The CAR-NK cells kill CD70-positive tumor cells via CAR-triggered cytotoxicity (perforin/granzyme and death receptor pathways). IL-2Rβ is part of the IL-15 receptor on the engineered NK cells and provides survival/proliferation signals; cells expressing IL-2Rβ are not targeted for killing.
Allogeneic cord blood–derived NK cells engineered to express a CD70-targeted chimeric antigen receptor and an IL-15 transgene to support survival, proliferation, and persistence; designed for antigen-specific cytotoxicity against CD70-expressing tumors.
Allogeneic cord blood–derived NK cells engineered to express a CD70-specific chimeric antigen receptor and an IL-15 transgene. The CAR redirects NK cells to CD70-expressing tumor cells to trigger antigen-specific NK activation and cytotoxicity (perforin/granzyme release and death receptor pathways), while IL-15 provides autocrine support for survival, proliferation, and persistence in vivo.
NO
INDIRECT
Cytotoxicity is directed to CD70-expressing cells via CAR-activated NK killing (perforin/granzyme and death receptor pathways). The IL-15 transgene signals through the common gamma chain to support NK survival/proliferation, not to kill gamma chain–expressing cells.
IgG1κ anti-CD38 monoclonal antibody that depletes CD38-expressing plasma cells, plasmablasts, and B cells via ADCC, CDC, and apoptosis to remove anti-donor alloantibodies prior to transplant.
Human IgG1κ anti-CD38 monoclonal antibody that binds CD38 on plasma cells, plasmablasts, and other CD38+ immune cells and depletes them via Fc-mediated ADCC and ADCP, complement-dependent cytotoxicity (CDC), and direct apoptosis, thereby reducing antibody-secreting cells and pathogenic/alloantibody levels.
YES
DIRECT
Anti-CD38 IgG1 mAb binds CD38 on target cells and induces Fc-mediated ADCC (NK cells) and ADCP (macrophages), complement-dependent cytotoxicity (CDC), and can trigger direct apoptosis upon crosslinking.
Anti-CD52 monoclonal antibody that induces broad depletion of T and B lymphocytes for conditioning before hematopoietic cell transplantation.
Humanized IgG1 anti-CD52 monoclonal antibody that binds CD52 on T and B lymphocytes (and other CD52+ leukocytes), inducing antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis to deplete lymphocytes and provide immunosuppression for transplant conditioning.
YES
DIRECT
Alemtuzumab binds CD52 on lymphocytes and induces killing via Fc-mediated ADCC, complement-dependent cytotoxicity (CDC), and direct apoptosis of CD52+ cells.