HER2-targeted antibody–drug conjugate delivering MMAE to HER2-positive tumor cells, causing microtubule disruption and apoptosis; may also mediate ADCC.
HER2-targeted antibody–drug conjugate that binds HER2 on tumor cells and is internalized; a cleavable linker releases the MMAE payload intracellularly to inhibit tubulin polymerization, causing G2/M arrest and apoptosis; the antibody Fc may also mediate ADCC and enable a bystander effect.
YES
DIRECT
ADC binds HER2 and is internalized; a cleavable linker releases MMAE, inhibiting tubulin and causing G2/M arrest and apoptosis. Fc engagement can also mediate ADCC; a bystander effect may occur.
HER2-targeted antibody–drug conjugate delivering MMAE to HER2-positive tumor cells, causing microtubule disruption and apoptosis; may also mediate ADCC.
HER2-targeted antibody–drug conjugate that binds HER2 on tumor cells and is internalized; a cleavable linker releases the MMAE payload intracellularly to inhibit tubulin polymerization, causing G2/M arrest and apoptosis; the antibody Fc may also mediate ADCC and enable a bystander effect.
NO
INDIRECT
The ADC binds HER2 (not beta‑tubulin), is internalized, and releases MMAE that binds the vinca site on beta‑tubulin to disrupt microtubules and trigger G2/M arrest and apoptosis in HER2+ cells; beta‑tubulin expression alone does not target cells for killing.
Type II anti-CD20 monoclonal antibody that depletes malignant B cells via ADCC/ADCP and direct cell death.
Glycoengineered humanized IgG1 type II anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes malignant CD20+ B cells primarily via enhanced FcγRIIIa-mediated ADCC and ADCP, with additional direct (caspase-independent) cell death; limited reliance on complement activation.
YES
DIRECT
Obinutuzumab binds CD20 on B cells and kills them via enhanced FcγRIIIa-mediated ADCC by NK cells and ADCP by macrophages, plus induction of direct caspase-independent cell death; limited complement involvement.
Type II anti-CD20 monoclonal antibody that depletes malignant B cells via ADCC/ADCP and direct cell death.
Glycoengineered humanized IgG1 type II anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes malignant CD20+ B cells primarily via enhanced FcγRIIIa-mediated ADCC and ADCP, with additional direct (caspase-independent) cell death; limited reliance on complement activation.
NO
INDIRECT
Obinutuzumab binds CD20 on B cells and engages FcγRIIIa (CD16A) on NK cells/monocytes to trigger ADCC/ADCP, killing CD20+ B cells. CD16A-expressing cells act as effectors, not targets, and are not directly killed.
Autologous, gene-edited tumor-infiltrating lymphocyte (TIL) therapy engineered to inactivate SOCS1 and Regnase-1 (ZC3H12A) to enhance T-cell activation, cytokine production, proliferation, persistence, and tumor killing.
Autologous tumor-infiltrating lymphocytes edited with CRISPR-Cas9 to inactivate SOCS1 and Regnase-1 (ZC3H12A), removing intrinsic brakes on cytokine/JAK-STAT signaling and mRNA stability. This enhances T-cell activation, cytokine production, proliferation, persistence, and cytotoxic killing of tumor cells after infusion.
NO
INDIRECT
SOCS1 is knocked out in the therapeutic TILs to enhance their function; the edited TILs then kill tumor cells they recognize via their native TCR (perforin/granzyme, Fas–FasL). Cells expressing SOCS1 are not specifically targeted or killed.