Rituximab‑pvvr biosimilar; anti‑CD20 monoclonal antibody that depletes CD20+ B cells via ADCC, CDC, and apoptosis.
Ruxience (rituximab‑pvvr) is an anti‑CD20 monoclonal antibody that binds CD20 on B lymphocytes and depletes CD20+ B cells via antibody‑dependent cellular cytotoxicity (ADCC), complement‑dependent cytotoxicity (CDC), and induction of apoptosis.
YES
DIRECT
Anti-CD20 antibody binds CD20 on B cells and triggers killing via antibody-dependent cellular cytotoxicity (effector cells), complement-dependent cytotoxicity, and direct apoptosis signaling.
Rituximab‑arrx biosimilar; anti‑CD20 monoclonal antibody that depletes CD20+ B cells via ADCC, CDC, and apoptosis.
Riabni (rituximab-arrx) is an anti-CD20 monoclonal antibody that binds CD20 on B cells and mediates B-cell depletion via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and induction of apoptosis.
YES
DIRECT
Anti-CD20 mAb binds CD20 on B cells and induces killing via Fc-mediated ADCC, complement-dependent cytotoxicity (CDC), and can trigger apoptosis upon CD20 engagement.
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.
YES
DIRECT
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.
YES
DIRECT
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.
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.
NO
INDIRECT
T-DM1 binds HER2 and is internalized; the DM1 payload then binds beta-tubulin to disrupt microtubules, causing mitotic arrest and apoptosis. Beta-tubulin expression alone does not target cells for killing.