Humanized IgG1 monoclonal antibody against EGFR; inhibits EGFR signaling and mediates antibody-dependent cellular cytotoxicity (ADCC).
Humanized IgG1 monoclonal antibody targeting EGFR; binds the receptor’s extracellular domain to block ligand binding and receptor activation, suppressing downstream signaling (e.g., RAS/MAPK, PI3K/AKT) and tumor cell proliferation/survival. The IgG1 Fc also engages immune effector cells to mediate ADCC against EGFR-expressing tumor cells.
YES
DIRECT
IgG1 anti-EGFR antibody binds EGFR on target cells and its Fc engages Fcγ receptors on NK cells/macrophages to mediate ADCC (and some CDC), leading to lysis/apoptosis of EGFR+ cells; signaling blockade is antiproliferative.
Engineered natural killer cells expressing a chimeric antigen receptor specific for CD123 (IL-3 receptor α), administered intravenously as cellular immunotherapy to eliminate CD123-positive AML/BPDCN cells.
Engineered natural killer cells expressing a chimeric antigen receptor that binds CD123 (IL‑3 receptor α) on AML/BPDCN cells. CAR engagement activates NK signaling and triggers cytotoxicity (perforin/granzyme release and cytokine secretion), leading to targeted lysis of CD123-positive malignant blasts and stem-like leukemic cells.
YES
DIRECT
CAR-engineered NK cells bind CD123 on target cells, triggering NK activation and degranulation (perforin/granzyme) and death-receptor signaling, causing lysis/apoptosis of CD123-positive cells.
Autologous T lymphocytes genetically engineered to express a chimeric antigen receptor targeting CD70; binding to CD70 on tumor cells triggers T-cell activation, cytokine release, and cytotoxic killing.
Autologous T cells engineered to express a chimeric antigen receptor recognizing CD70. CAR engagement of CD70 on tumor cells triggers CD3ζ/co-stimulatory signaling, leading to T‑cell activation, expansion, cytokine release, and perforin/granzyme‑mediated cytotoxic killing of CD70‑expressing cancer cells.
YES
DIRECT
CAR engagement of CD70 activates CAR‑T cells to release perforin and granzymes (and other cytotoxic pathways), inducing apoptosis/lysis of CD70‑expressing cells.
Fully humanized IgG4 monoclonal antibody targeting CD47 that blocks the CD47/SIRPα innate immune checkpoint to enhance macrophage-mediated phagocytosis of AML/MDS cells.
Fully humanized IgG4 monoclonal antibody against CD47 that blocks the CD47–SIRPα innate immune checkpoint, removing the tumor cell 'don’t‑eat‑me' signal to enable macrophage activation and phagocytosis of cancer cells.
YES
INDIRECT
Blocking CD47–SIRPα lifts the anti-phagocytic signal, enabling macrophage activation and antibody-dependent cellular phagocytosis of CD47-expressing cells.
An antibody-drug conjugate carrying a topoisomerase I inhibitor payload; binds a tumor cell-surface antigen, is internalized, and releases the payload to induce DNA damage and tumor cell death.
An anti-nectin-4 IgG1 antibody-drug conjugate that binds nectin-4 on tumor cells, is internalized, and via a cleavable linker releases a topoisomerase I inhibitor payload. The payload inhibits topoisomerase I, disrupting DNA replication and causing DNA damage, cell-cycle arrest, and apoptosis in nectin-4–expressing cancer cells.
YES
DIRECT
ADC binds Nectin-4 on tumor cells, is internalized, and a cleavable linker releases a topoisomerase I inhibitor intracellularly, causing DNA damage, cell-cycle arrest, and apoptosis of Nectin-4–expressing cells.