Beta-emitting therapeutic radionuclide conjugated to AKIR001 to deliver localized ionizing radiation, causing DNA damage and tumor cell death with potential cross-fire effects.
Lutetium-177 is a beta-emitting radionuclide linked to the CD44v6-targeting monoclonal antibody AKIR001. Upon binding CD44v6 on tumor cells, it delivers localized ionizing radiation that induces DNA double-strand breaks and tumor cell death, with cross-fire effects on neighboring tumor cells.
YES
DIRECT
CD44v6-binding antibody delivers 177Lu beta radiation to target cells, inducing DNA double‑strand breaks and tumor cell death (with cross‑fire to nearby cells).
Chimeric anti-CD20 monoclonal antibody that depletes circulating CD20+ B cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, aiming to reduce glucocorticoid exposure and achieve steroid-free remission in polymyalgia rheumatica.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on pre-B and mature B lymphocytes and depletes CD20+ B cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, thereby suppressing B cell–mediated immune activation and inflammation.
YES
DIRECT
Anti-CD20 antibody binds CD20 on B cells and triggers complement-dependent cytotoxicity and Fc-mediated ADCC/ADCP (NK cells/macrophages), and can induce apoptosis, leading to lysis/depletion of CD20+ cells.
An autologous, gene‑modified cellular immunotherapy consisting of CD19‑directed CAR T cells that incorporate an anti‑CD19 scFv with 4‑1BB costimulatory and CD3ζ signaling domains. Engagement of CD19 on B cells triggers T‑cell activation, proliferation, and cytotoxic killing of CD19+ leukemic blasts; the 4‑1BB domain supports expansion and persistence.
Autologous CD19-directed CAR T cells bearing an anti-CD19 scFv with 4-1BB costimulatory and CD3ζ signaling domains; engagement of CD19 on B cells activates the CAR T cells, driving proliferation and cytotoxic killing of CD19+ malignant cells, with 4-1BB supporting expansion and persistence.
YES
DIRECT
CD19-directed CAR T cells recognize CD19 on target cells and kill them via T-cell effector mechanisms (perforin/granzyme-mediated lysis and death-receptor apoptosis).
An autologous, gene‑modified cellular immunotherapy consisting of CD19‑directed CAR T cells that incorporate an anti‑CD19 scFv with 4‑1BB costimulatory and CD3ζ signaling domains. Engagement of CD19 on B cells triggers T‑cell activation, proliferation, and cytotoxic killing of CD19+ leukemic blasts; the 4‑1BB domain supports expansion and persistence.
Autologous CD19-directed CAR T cells bearing an anti-CD19 scFv with 4-1BB costimulatory and CD3ζ signaling domains; engagement of CD19 on B cells activates the CAR T cells, driving proliferation and cytotoxic killing of CD19+ malignant cells, with 4-1BB supporting expansion and persistence.
NO
INDIRECT
Tisagenlecleucel’s CAR recognizes CD19, not 4-1BB. 4-1BB serves as an internal costimulatory signaling domain in the CAR T cell. Killing is directed at CD19+ cells via T‑cell cytotoxic mechanisms (perforin/granzyme), not at 4-1BB–expressing cells.
An autologous, gene‑modified cellular immunotherapy consisting of CD19‑directed CAR T cells that incorporate an anti‑CD19 scFv with 4‑1BB costimulatory and CD3ζ signaling domains. Engagement of CD19 on B cells triggers T‑cell activation, proliferation, and cytotoxic killing of CD19+ leukemic blasts; the 4‑1BB domain supports expansion and persistence.
Autologous CD19-directed CAR T cells bearing an anti-CD19 scFv with 4-1BB costimulatory and CD3ζ signaling domains; engagement of CD19 on B cells activates the CAR T cells, driving proliferation and cytotoxic killing of CD19+ malignant cells, with 4-1BB supporting expansion and persistence.
NO
INDIRECT
CD3zeta (CD247) is an intracellular signaling domain in T cells used within the CAR; it is not the recognized antigen. Tisagenlecleucel targets CD19 and kills CD19+ cells via CAR-T cytolysis (perforin/granzyme and Fas–FasL) upon CD19 engagement.