TROP2-directed antibody–drug conjugate targeting TACSTD2 on epithelial tumor cells; internalization and payload release lead to cytotoxicity in TROP2-expressing cells.
TROP2 (TACSTD2)-directed IgG1 antibody–drug conjugate linked via a cleavable linker to SHR9265 (an exatecan-derived topoisomerase I inhibitor). After binding TROP2 on tumor cells and internalization, linker cleavage releases the payload, inhibiting topoisomerase I, blocking DNA replication and inducing cell cycle arrest and apoptosis in TROP2-expressing cells.
ADC binds TROP2 on target cells, is internalized, and releases an exatecan-derived topoisomerase I inhibitor, causing DNA damage/replication block leading to cell cycle arrest and apoptosis in TROP2-expressing cells.
Type I anti-CD20 monoclonal antibody that depletes CD20+ B cells via complement-dependent cytotoxicity (CDC) and ADCC.
Type I anti-CD20 chimeric monoclonal antibody that binds CD20 on B cells and depletes them via complement-dependent cytotoxicity (CDC), antibody-dependent cellular cytotoxicity (ADCC), and phagocytosis.
Rituximab binds CD20 on B cells and induces killing via complement-dependent cytotoxicity (CDC), Fc-mediated antibody-dependent cellular cytotoxicity (ADCC) by NK cells, and antibody-dependent phagocytosis by macrophages.
A bispecific T‑cell engager (BiTE) antibody that binds CD19 on B‑lymphoblasts and CD3 on T cells to create an immune synapse, activate TCR/CD3 signaling, and induce perforin/granzyme‑mediated cytotoxic killing of CD19+ leukemia cells.
Bispecific single‑chain antibody that binds CD19 on B‑lymphoblasts and CD3 on T cells, bringing them into proximity to form an immune synapse, activate TCR/CD3 signaling, and induce perforin/granzyme‑mediated cytotoxic killing of CD19+ leukemia cells.
Blinatumomab links CD3 on T cells to CD19 on target cells, forming an immune synapse and activating T cells to release perforin and granzymes that induce apoptosis of CD19+ cells.
Recombinant humanized anti-EGFR monoclonal antibody that blocks EGFR signaling (MAPK/PI3K) and may induce ADCC.
Glycoengineered humanized anti-EGFR monoclonal antibody that binds the extracellular domain of EGFR, preventing ligand-induced activation and dimerization to block downstream MAPK/PI3K signaling and inhibit tumor cell proliferation; Fc optimization enhances antibody-dependent cell-mediated cytotoxicity (ADCC) against EGFR-expressing cells.
Binds EGFR on target cells and engages Fcγ receptor–bearing effector cells (e.g., NK cells) to induce ADCC (and possibly ADCP), leading to lysis of EGFR+ cells; EGFR blockade mainly inhibits proliferation.
Autologous genetically modified TCR-engineered SPEAR T-cell therapy expressing an affinity-enhanced TCR specific for the MAGE-A4 peptide presented by HLA-A2 and co-expressing CD8αβ to enhance class I–restricted cytotoxicity; designed to recognize HLA-A2/MAGE-A4 on tumor cells and kill them.
Autologous T cells genetically modified to express an affinity-enhanced TCR specific for the MAGE-A4 peptide presented by HLA-A2 and co-express CD8alpha/beta; following infusion they recognize HLA-A2/MAGE-A4 on tumor cells and mediate class I-restricted cytotoxic killing.
Engineered TCR T cells recognize the HLA-A2/MAGE-A4 peptide complex on target cells and kill them via CTL effector mechanisms, primarily perforin/granzyme-mediated apoptosis (and Fas–FasL).