US-licensed brand of rituximab; chimeric IgG1 anti-CD20 monoclonal antibody that depletes CD20+ B cells via ADCC, CDC, and apoptosis, reducing autoantibody production and B–T cell interactions.
Chimeric IgG1 monoclonal antibody targeting CD20 on pre‑B and mature B lymphocytes; depletes CD20+ B cells primarily via antibody‑dependent cellular cytotoxicity (ADCC), complement‑dependent cytotoxicity (CDC), and apoptosis, thereby reducing autoantibody production and B–T cell interactions (plasma cells largely spared).
NO
INDIRECT
Rituximab binds CD20 on B cells; its Fc engages Fcγ receptors (including CD64) on effector cells to mediate ADCC/ADCP and CDC against CD20+ cells. CD64+ cells act as effectors, not targets, and are not directly killed.
US-licensed brand of rituximab; chimeric IgG1 anti-CD20 monoclonal antibody that depletes CD20+ B cells via ADCC, CDC, and apoptosis, reducing autoantibody production and B–T cell interactions.
Chimeric IgG1 monoclonal antibody targeting CD20 on pre‑B and mature B lymphocytes; depletes CD20+ B cells primarily via antibody‑dependent cellular cytotoxicity (ADCC), complement‑dependent cytotoxicity (CDC), and apoptosis, thereby reducing autoantibody production and B–T cell interactions (plasma cells largely spared).
NO
INDIRECT
Rituximab targets CD20 on B cells; its Fc binds C1q to activate complement, leading to CDC (and ADCC/apoptosis) of CD20+ cells. C1q is not the antigen, so C1q-expressing cells are not directly targeted or killed.
An antibody–drug conjugate targeting N-glycosylated CEACAM5/6; the tumor-targeting monoclonal antibody is internalized and releases the cytotoxic payload monomethyl auristatin E (MMAE), a microtubule inhibitor that induces mitotic arrest and cell death.
Antibody binds N-glycosylated CEACAM5/6 on tumor cells, is internalized, and releases the MMAE payload, which binds tubulin and inhibits microtubule polymerization, leading to G2/M arrest and apoptotic cell death in CEACAM5/6-expressing cells.
YES
DIRECT
ADC antibody binds CEACAM5 on tumor cells, is internalized, and releases MMAE, which inhibits tubulin polymerization causing G2/M arrest and apoptotic cell death.
An antibody–drug conjugate targeting N-glycosylated CEACAM5/6; the tumor-targeting monoclonal antibody is internalized and releases the cytotoxic payload monomethyl auristatin E (MMAE), a microtubule inhibitor that induces mitotic arrest and cell death.
Antibody binds N-glycosylated CEACAM5/6 on tumor cells, is internalized, and releases the MMAE payload, which binds tubulin and inhibits microtubule polymerization, leading to G2/M arrest and apoptotic cell death in CEACAM5/6-expressing cells.
YES
DIRECT
ADC antibody binds N-glycosylated CEACAM6 on tumor cells, is internalized, and releases MMAE, which inhibits microtubule polymerization causing G2/M arrest and apoptosis.
An antibody–drug conjugate targeting N-glycosylated CEACAM5/6; the tumor-targeting monoclonal antibody is internalized and releases the cytotoxic payload monomethyl auristatin E (MMAE), a microtubule inhibitor that induces mitotic arrest and cell death.
Antibody binds N-glycosylated CEACAM5/6 on tumor cells, is internalized, and releases the MMAE payload, which binds tubulin and inhibits microtubule polymerization, leading to G2/M arrest and apoptotic cell death in CEACAM5/6-expressing cells.
NO
INDIRECT
EBC-129 targets CEACAM5/6 on tumor cells for internalization; once inside, MMAE binds beta‑tubulin to inhibit microtubules, causing G2/M arrest and apoptosis. Beta‑tubulin expression alone does not trigger targeting or killing.