Humanized, Fc‑engineered anti‑CD19 monoclonal antibody that binds B cells and enhances ADCC/ADCP and apoptosis.
Fc‑engineered humanized anti‑CD19 monoclonal antibody that binds CD19 on B cells and depletes CD19+ cells by enhancing FcγR‑mediated ADCC and ADCP, with additional direct pro‑apoptotic activity.
Binds CD19 on B cells and engages Fc-gamma receptors to trigger ADCC (e.g., NK cells) and ADCP (macrophages), with additional direct pro-apoptotic signaling in CD19+ cells.
Chimeric anti‑CD20 monoclonal antibody that induces complement-dependent cytotoxicity, ADCC, and apoptosis in B cells.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and induces complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, resulting in depletion of CD20-positive B cells.
Rituximab binds CD20 on B cells and induces complement-dependent cytotoxicity and Fc-mediated ADCC (and can trigger apoptosis), causing direct killing of CD20+ cells.
A subcutaneous human afucosylated IgG1 monoclonal antibody (also known as AMG 451/KHK4083) targeting OX40 (TNFRSF4). It blocks OX40–OX40L costimulatory signaling and depletes OX40-expressing activated effector/memory T cells via enhanced ADCC, reducing pathogenic T-cell activation, survival, and cytokine production in atopic dermatitis.
Afucosylated human IgG1 monoclonal antibody against OX40 (TNFRSF4) that blocks OX40–OX40L costimulatory signaling and depletes OX40-expressing activated effector/memory T cells via enhanced ADCC, thereby reducing T‑cell activation, survival, and inflammatory cytokine production in atopic dermatitis.
Afucosylated IgG1 binds OX40 on activated T cells and engages Fcγ receptors on effector cells (e.g., NK cells), triggering enhanced ADCC (and phagocytosis) to deplete OX40+ cells.
HER2-targeted antibody–drug conjugate (anti-HER2 mAb linked to MMAE) that binds HER2, is internalized, and releases MMAE to inhibit microtubules, causing mitotic arrest and apoptosis (with possible bystander effect).
HER2-targeted antibody–drug conjugate in which disitamab (anti-HER2 mAb) delivers the microtubule inhibitor MMAE. After HER2 binding and internalization, linker cleavage releases MMAE to block tubulin polymerization, causing G2/M arrest and apoptosis, with potential bystander killing.
Anti-HER2 ADC binds HER2, is internalized, and releases MMAE that inhibits tubulin polymerization, causing G2/M arrest and apoptosis (with possible bystander killing).
Genetically engineered autologous T cells expressing a chimeric antigen receptor targeting CD70 for MHC-independent recognition and killing of CD70-positive tumor cells; administered after lymphodepletion.
Autologous T cells are genetically engineered to express a chimeric antigen receptor that specifically binds CD70 on tumor cells, enabling MHC-independent recognition. CAR signaling (CD3ζ with costimulation) activates the T cells to proliferate, release cytokines, and deliver cytotoxic killing of CD70-positive tumor cells. Lymphodepletion prior to infusion enhances CAR-T expansion and persistence.
CD70 CAR-T cells bind CD70 on target cells and, upon CAR activation, kill via perforin/granzyme-mediated apoptosis (and Fas–FasL), lysing CD70-positive cells.