Chimeric IgG1 monoclonal antibody against EGFR that blocks ligand binding and downstream signaling (e.g., RAS/RAF/MEK/ERK, PI3K/AKT), inhibits proliferation, and mediates ADCC.
Chimeric IgG1 monoclonal antibody against EGFR that binds the extracellular domain to block ligand binding and receptor activation/dimerization, suppressing downstream RAS/RAF/MEK/ERK and PI3K/AKT signaling to inhibit tumor cell proliferation; additionally mediates Fc-dependent ADCC against EGFR-expressing cells.
YES
DIRECT
Cetuximab coats EGFR-expressing cells and engages Fcγ receptors on NK cells to trigger antibody-dependent cellular cytotoxicity (ADCC), with possible complement-dependent cytotoxicity (CDC); signaling blockade is mainly cytostatic.
An intravenous SIRPα–Fc fusion protein biologic that acts as a decoy to bind CD47 on tumor cells, blocking the CD47–SIRPα innate immune checkpoint to restore macrophage-mediated phagocytosis and, via its Fc region, engage Fcγ receptors to enhance myeloid effector functions and dendritic cell antigen presentation, supporting downstream T-cell priming.
HCB101 is an IV SIRPalpha-Fc fusion protein that binds CD47 on tumor cells and blocks the CD47-SIRPalpha innate immune checkpoint, removing the 'don't-eat-me' signal. This restores macrophage-mediated phagocytosis and, via its IgG4 Fc domain, engages Fc-gamma receptors to enhance myeloid effector functions and dendritic cell antigen presentation, supporting downstream T-cell priming.
YES
INDIRECT
Blocks CD47–SIRPα signaling to remove the “don’t-eat-me” signal; Fc engagement of Fcγ receptors promotes macrophage-mediated phagocytosis (ADCP) of CD47+ cells and enhances antigen presentation, leading to downstream T-cell killing.
An intravenous SIRPα–Fc fusion protein biologic that acts as a decoy to bind CD47 on tumor cells, blocking the CD47–SIRPα innate immune checkpoint to restore macrophage-mediated phagocytosis and, via its Fc region, engage Fcγ receptors to enhance myeloid effector functions and dendritic cell antigen presentation, supporting downstream T-cell priming.
HCB101 is an IV SIRPalpha-Fc fusion protein that binds CD47 on tumor cells and blocks the CD47-SIRPalpha innate immune checkpoint, removing the 'don't-eat-me' signal. This restores macrophage-mediated phagocytosis and, via its IgG4 Fc domain, engages Fc-gamma receptors to enhance myeloid effector functions and dendritic cell antigen presentation, supporting downstream T-cell priming.
NO
INDIRECT
The drug’s Fc engages CD64 on myeloid cells to activate them while the SIRPα domain blocks CD47 on tumor cells, leading to macrophage-mediated phagocytosis and T-cell priming. CD64+ cells are effector cells, not killed.
An intravenous SIRPα–Fc fusion protein biologic that acts as a decoy to bind CD47 on tumor cells, blocking the CD47–SIRPα innate immune checkpoint to restore macrophage-mediated phagocytosis and, via its Fc region, engage Fcγ receptors to enhance myeloid effector functions and dendritic cell antigen presentation, supporting downstream T-cell priming.
HCB101 is an IV SIRPalpha-Fc fusion protein that binds CD47 on tumor cells and blocks the CD47-SIRPalpha innate immune checkpoint, removing the 'don't-eat-me' signal. This restores macrophage-mediated phagocytosis and, via its IgG4 Fc domain, engages Fc-gamma receptors to enhance myeloid effector functions and dendritic cell antigen presentation, supporting downstream T-cell priming.
NO
INDIRECT
HCB101 binds CD47 on tumor cells to block the CD47–SIRPα checkpoint, enabling macrophage-mediated phagocytosis; its IgG4 Fc engages Fcγ receptors (including CD32A) to enhance myeloid effector function, but CD32A-expressing cells are not targeted or killed.
An intravenous SIRPα–Fc fusion protein biologic that acts as a decoy to bind CD47 on tumor cells, blocking the CD47–SIRPα innate immune checkpoint to restore macrophage-mediated phagocytosis and, via its Fc region, engage Fcγ receptors to enhance myeloid effector functions and dendritic cell antigen presentation, supporting downstream T-cell priming.
HCB101 is an IV SIRPalpha-Fc fusion protein that binds CD47 on tumor cells and blocks the CD47-SIRPalpha innate immune checkpoint, removing the 'don't-eat-me' signal. This restores macrophage-mediated phagocytosis and, via its IgG4 Fc domain, engages Fc-gamma receptors to enhance myeloid effector functions and dendritic cell antigen presentation, supporting downstream T-cell priming.
NO
INDIRECT
HCB101 binds CD47 on tumor cells to block the CD47–SIRPα checkpoint and promote macrophage-mediated phagocytosis via Fcγ receptor engagement. CD32B is an Fcγ receptor on immune cells and is not the antigen targeted for killing; CD32B+ cells are not directly killed.