An anti-HER2 antibody–drug conjugate (ADC) composed of a humanized anti‑HER2 monoclonal antibody linked to the microtubule inhibitor MMAE (vedotin); upon HER2 binding and internalization, releases MMAE to disrupt microtubules, causing cell-cycle arrest and apoptosis, and may mediate ADCC.
Humanized anti‑HER2 monoclonal antibody linked to the microtubule inhibitor MMAE (vedotin). After binding HER2 on tumor cells and internalization, the linker is cleaved to release MMAE, which binds tubulin and inhibits microtubule polymerization, causing G2/M arrest and apoptosis; the IgG1 antibody may also mediate ADCC.
ADC binds HER2, is internalized, and releases MMAE that inhibits microtubule polymerization causing G2/M arrest and apoptosis; the IgG1 Fc can also mediate ADCC.
An individualized, autologous, gene-modified TCR-T cellular immunotherapy. Patient T cells are engineered ex vivo to express a tumor-specific T-cell receptor identified from the patient’s lesion and then reinfused to mediate HLA-restricted recognition of tumor peptide antigens, triggering TCR/CD3 signaling, activation, proliferation, and perforin/granzyme-dependent cytotoxic killing of tumor cells in refractory/relapsed solid tumors.
Autologous patient T cells are gene-modified ex vivo to express a tumor-specific T-cell receptor. After reinfusion, these TCR-T cells recognize peptide antigens presented by patient HLA on tumor cells, initiating TCR/CD3 signaling, activation and expansion, cytokine release, and perforin/granzyme-mediated cytotoxic killing of tumor cells.
Engineered TCR-T cells recognize the patient-specific peptide–HLA class I complex via their TCR, triggering cytotoxic effector functions (perforin/granzyme release and Fas–FasL–mediated apoptosis) that kill the target-expressing cells.
Also known as SYS6010, an EGFR-targeting antibody–drug conjugate (ADC). A monoclonal antibody binds EGFR on tumor cells, is internalized, and releases a linked cytotoxic payload to kill the cancer cell. Administered intravenously every 3 weeks in Phase 1 dose escalation/expansion for EGFR-expressing solid tumors (e.g., EGFR-mutant NSCLC, head and neck, KRAS–wild-type colorectal, and breast cancers).
An EGFR-targeted monoclonal antibody delivers an attached cytotoxic payload to EGFR-expressing tumor cells. After binding EGFR on the cell surface, the ADC is internalized and the payload is released intracellularly, inducing cancer cell death (specific payload/mechanism not disclosed).
The EGFR-targeted ADC binds EGFR, is internalized, and releases an intracellular cytotoxic payload that kills the EGFR-expressing cell (specific payload mechanism not disclosed).
Chimeric IgG1 anti-CD20 monoclonal antibody that binds CD20 on B cells (pre-B to mature, not plasma cells) and depletes them via ADCC, CDC, and apoptosis; reduces B-cell antigen presentation, proinflammatory cytokines, and autoantibody activity. Used off-label in MS.
Chimeric IgG1 monoclonal antibody against CD20 on pre-B to mature B cells (not plasma cells); depletes CD20+ B cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis, reducing B-cell antigen presentation, proinflammatory cytokines, and autoantibody activity.
Rituximab binds CD20 on B cells and depletes them via Fc-mediated ADCC by NK/macrophages, complement-dependent cytotoxicity, and induction of apoptosis.
Humanized IgG1 anti-CD20 monoclonal antibody that binds CD20 on B cells (pre-B to mature, not plasma cells) and depletes them via ADCC, CDC, and apoptosis; diminishes B-cell–driven adaptive immune activity. Approved for RRMS.
Humanized IgG1 monoclonal antibody targeting CD20 on pre-B to mature B cells (sparing plasma cells), depleting them via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis to suppress B cell–mediated adaptive immunity.
Anti-CD20 IgG1 binds CD20 on B cells and induces Fc-mediated ADCC by NK cells/macrophages and complement-dependent cytotoxicity, with some apoptosis, depleting CD20+ cells.