Antibody fusion protein combining an anti-CD20 monoclonal antibody with the CD47-binding domain of SIRPα; blocks the CD47–SIRPα checkpoint to promote macrophage phagocytosis and engages Fcγ receptors to enhance ADCC against CD20+ B cells.
Bispecific antibody fusion that targets CD20 on B cells while presenting a SIRPα domain to bind CD47, locally blocking the CD47–SIRPα innate immune checkpoint. This removes the “don’t‑eat‑me” signal to promote macrophage-mediated phagocytosis (ADCP) and, via its IgG1 Fc, engages Fcγ receptors to enhance NK cell/macrophage ADCC against CD20+ B cells, with secondary activation of adaptive anti-tumor immunity.
YES
DIRECT
The bispecific antibody binds CD20 on B cells and presents SIRPα to block CD47, removing the “don’t‑eat‑me” signal and promoting macrophage phagocytosis (ADCP). Its IgG1 Fc engages Fcγ receptors to recruit NK cells/macrophages for ADCC, leading to direct immune effector killing of CD20+ cells.
Antibody fusion protein combining an anti-CD20 monoclonal antibody with the CD47-binding domain of SIRPα; blocks the CD47–SIRPα checkpoint to promote macrophage phagocytosis and engages Fcγ receptors to enhance ADCC against CD20+ B cells.
Bispecific antibody fusion that targets CD20 on B cells while presenting a SIRPα domain to bind CD47, locally blocking the CD47–SIRPα innate immune checkpoint. This removes the “don’t‑eat‑me” signal to promote macrophage-mediated phagocytosis (ADCP) and, via its IgG1 Fc, engages Fcγ receptors to enhance NK cell/macrophage ADCC against CD20+ B cells, with secondary activation of adaptive anti-tumor immunity.
NO
INDIRECT
IMM0306 anchors to CD20 on B cells and locally blocks CD47–SIRPalpha, removing the don't-eat-me signal to enable macrophage phagocytosis and Fc receptor–mediated ADCC of CD20+ cells; CD47 expression alone is not sufficient for targeting.
Type II glycoengineered anti-CD20 monoclonal antibody (Gazyva) that binds CD20 on mature/memory B cells, enhancing ADCC and direct cell death with reduced CDC versus rituximab, resulting in B-cell depletion and reduced antiplatelet autoantibody production.
Glycoengineered type II anti‑CD20 IgG1 that binds CD20 on mature/memory B cells with increased FcγRIII affinity, driving enhanced ADCC/ADCP and direct, caspase‑independent cell death (with reduced CDC), resulting in B‑cell depletion and decreased pathogenic autoantibody production.
YES
DIRECT
Obinutuzumab binds CD20 on B cells, inducing type II direct (caspase‑independent) cell death and engaging FcγRIIIa on effector cells to drive ADCC/ADCP (with reduced CDC), leading to B‑cell killing.
Type II glycoengineered anti-CD20 monoclonal antibody (Gazyva) that binds CD20 on mature/memory B cells, enhancing ADCC and direct cell death with reduced CDC versus rituximab, resulting in B-cell depletion and reduced antiplatelet autoantibody production.
Glycoengineered type II anti‑CD20 IgG1 that binds CD20 on mature/memory B cells with increased FcγRIII affinity, driving enhanced ADCC/ADCP and direct, caspase‑independent cell death (with reduced CDC), resulting in B‑cell depletion and decreased pathogenic autoantibody production.
NO
INDIRECT
Obinutuzumab binds CD20 on B cells; its Fc engages FcγRIIIa (CD16a) on NK cells/macrophages to trigger ADCC/ADCP against CD20+ cells. CD16a+ cells act as effectors and are not targeted or killed.
Anti-CD20 monoclonal antibody that depletes B cells, including memory B cells.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on pre-B and mature B cells, inducing depletion via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, thereby reducing B cells (including memory B cells) and antibody production.
YES
DIRECT
Rituximab binds CD20 on B cells and induces killing via Fc-mediated ADCC (NK cells/macrophages), complement-dependent cytotoxicity (CDC), and can directly trigger apoptosis of CD20+ cells.