CRISPR-edited, allogeneic off-the-shelf CAR T-cell therapy targeting CLL-1 (CLEC12A); redirects donor T cells to bind CLL-1 on AML cells and trigger T-cell activation and cytotoxic killing.
Allogeneic CRISPR-edited anti-CLL-1 (CLEC12A) CAR T cells that bind CLL-1 on AML cells to induce CAR-mediated T-cell activation and cytotoxic killing; TRAC knockout removes endogenous TCR to reduce GvHD, PD-1 knockout limits exhaustion, and B2M deletion with HLA-E fusion reduces host T- and NK-cell rejection to enhance persistence.
Anti-CLL-1 CAR T cells recognize CLL-1 on target cells, activate, and kill them via T cell cytotoxic mechanisms (perforin/granzyme and death-receptor pathways).
HER2-targeted antibody–drug conjugate in which trastuzumab binds HER2, inhibits HER2 signaling and mediates ADCC; internalization releases the DM1 maytansinoid microtubule inhibitor, causing mitotic arrest and cytotoxicity.
HER2-targeted monoclonal antibody–drug conjugate: trastuzumab binds HER2, inhibits HER2 signaling and mediates ADCC; upon receptor-mediated internalization, the DM1 (maytansinoid) microtubule inhibitor is released, disrupting microtubules to induce mitotic arrest and tumor cell death.
Trastuzumab binds HER2 on target cells, is internalized, and releases the DM1 microtubule inhibitor, causing mitotic arrest and cell death; its Fc also engages immune effectors to mediate ADCC against HER2+ cells.
Humanized IgG1 monoclonal antibody targeting HER2/ERBB2; blocks HER2 signaling and mediates ADCC in HER2-positive breast cancer.
Humanized IgG1 monoclonal antibody that binds HER2/ERBB2 on tumor cells, inhibits receptor dimerization and downstream PI3K/AKT/MAPK signaling, and engages Fc receptors to elicit antibody-dependent cell-mediated cytotoxicity (ADCC) against HER2-overexpressing cells.
Trastuzumab binds HER2 on tumor cells and engages Fcγ receptors on immune effectors (e.g., NK cells) to mediate ADCC, killing HER2+ cells; signaling blockade may also promote apoptosis.
Antibody–drug conjugate linking trastuzumab to the cytotoxic microtubule inhibitor DM1 to deliver targeted chemotherapy to HER2-overexpressing tumor cells.
Trastuzumab (anti-HER2 IgG1) is conjugated to the maytansinoid DM1. The antibody binds HER2 on tumor cells and is internalized; lysosomal processing releases DM1, which inhibits microtubule assembly, causing mitotic arrest and apoptosis. The trastuzumab moiety also blocks HER2 signaling and can mediate ADCC.
T-DM1 binds HER2, is internalized, and releases the DM1 payload intracellularly; DM1 inhibits microtubule assembly causing mitotic arrest and apoptosis. The Fc can also mediate ADCC.
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.
ATG contains polyclonal antibodies that bind T-cell receptor components (including TCRβ) on T cells, leading to complement-dependent lysis, Fc-mediated ADCC, and apoptosis, thereby depleting TCRβ+ cells.