Immune-stimulating antibody conjugate (ISAC) comprising a trastuzumab-biosimilar monoclonal antibody linked via a non-cleavable, cell-impermeable linker to a TLR7/8 agonist; binds HER2 on tumor cells to localize TLR7/8 activation and trigger innate and adaptive anti-tumor immunity.
Immune-stimulating antibody conjugate: a trastuzumab-biosimilar mAb targets HER2 on tumor cells to localize a linked TLR7/8 agonist to the tumor microenvironment, activating TLR7/8 on dendritic and other antigen-presenting cells. This triggers innate immune activation, pro-inflammatory cytokine production, enhanced antigen presentation, and subsequent cytotoxic T-cell and B-cell responses leading to anti-tumor activity.
NO
INDIRECT
The drug activates TLR8 on antigen-presenting cells to stimulate innate immunity and prime cytotoxic T cells; the resulting immune response kills HER2-positive tumor cells, not the TLR8-expressing cells.
Humanized IgG1 monoclonal antibody against EGFR that inhibits ligand binding and downstream EGFR signaling (MAPK/ERK, PI3K/AKT), reducing proliferation and potentially promoting ADCC.
Humanized IgG1 monoclonal antibody targeting EGFR; blocks ligand binding and receptor activation to inhibit downstream MAPK/ERK and PI3K/AKT signaling, reducing tumor cell proliferation and survival, with potential Fc-mediated ADCC.
YES
DIRECT
IgG1 anti-EGFR antibody binds EGFR on tumor cells and engages FcγR-bearing effector cells (e.g., NK cells) to mediate ADCC (and possibly CDC); EGFR signaling blockade is mainly cytostatic but can contribute to apoptosis.
Chimeric IgG1 monoclonal antibody targeting EGFR to inhibit EGFR signaling and promote Fc-mediated ADCC against tumor cells.
Chimeric IgG1 monoclonal antibody that binds the extracellular domain of EGFR, blocking ligand binding and receptor dimerization to inhibit downstream EGFR signaling and tumor cell proliferation; its Fc region also engages Fcγ receptors to promote ADCC against EGFR-expressing tumor cells.
YES
DIRECT
IgG1 Fc of cetuximab engages Fcγ receptors on NK cells and other effectors to mediate ADCC (and ADCP/CDC), directly killing EGFR-expressing cells; EGFR blockade also inhibits proliferation.
Antibody–drug conjugate targeting nectin‑4; the monoclonal antibody delivers the microtubule-disrupting payload MMAE (vedotin) to tumor cells, causing apoptosis.
Monoclonal antibody targets nectin-4 on tumor cells, is internalized, and releases the cytotoxic payload MMAE via a cleavable linker; MMAE binds tubulin, inhibits microtubule polymerization, causes G2/M arrest, and induces apoptosis in nectin-4–expressing cells.
YES
DIRECT
The ADC binds Nectin-4, is internalized, and releases MMAE via a cleavable linker; MMAE inhibits tubulin polymerization, causing G2/M arrest and apoptosis of Nectin-4–expressing cells.
Fully humanized IgG4 monoclonal antibody that blocks the CD47–SIRPα innate immune checkpoint. By preventing CD47 on tumor cells from engaging SIRPα on macrophages, it abrogates the anti-phagocytic “don’t eat me” signal and promotes macrophage activation and calreticulin–LRP1–mediated phagocytosis of tumor cells, enhancing innate antitumor activity.
YES
INDIRECT
CD47–SIRPα blockade removes the “don’t eat me” signal, enabling macrophage Fc/CR-dependent antibody-dependent cellular phagocytosis (ADCP) of CD47+ tumor cells.