Type II anti-CD20 monoclonal antibody; used for B-cell debulking and to mitigate cytokine release syndrome risk.
Glycoengineered humanized IgG1 type II anti-CD20 monoclonal antibody that binds CD20 on B cells, enhancing FcγRIIIa engagement to drive strong ADCC/ADCP and inducing direct, caspase-independent apoptosis, resulting in rapid B‑cell depletion (with relatively low CDC). Used clinically for B‑cell debulking and to mitigate CRS risk with CD20×CD3 bispecifics.
Obinutuzumab binds CD20 on B cells, engaging FcγRIIIa on NK cells/macrophages to drive ADCC/ADCP and also triggers direct, caspase‑independent apoptosis (with relatively low CDC).
A HER3-directed antibody–drug conjugate consisting of a fully human anti-HER3 IgG1 linked via a cleavable linker to deruxtecan (DXd), a topoisomerase I inhibitor. It binds HER3, is internalized, and releases DXd to induce DNA damage and apoptosis; evaluated at 5.6 mg/kg IV every 3 weeks in advanced solid tumors with NRG1 fusions.
Patritumab deruxtecan is a HER3-directed monoclonal antibody linked via a cleavable linker to the topoisomerase I inhibitor deruxtecan (DXd). Upon binding HER3 on tumor cells, the ADC is internalized and the linker is cleaved intracellularly to release DXd, causing topoisomerase I–mediated DNA damage that leads to cell-cycle arrest and apoptosis, with potential bystander killing; it may also inhibit NRG1–HER3 signaling.
HER3-targeted ADC binds HER3, is internalized, and releases the topoisomerase I inhibitor deruxtecan (DXd), causing DNA damage, cell-cycle arrest, and apoptosis in HER3-expressing cells (with possible bystander killing).
HER2-targeted antibody–drug conjugate with a cathepsin-cleavable linker delivering MMAE, a microtubule inhibitor, to HER2-overexpressing tumor cells.
Disitamab vedotin (RC48) is a HER2-targeted antibody–drug conjugate that binds HER2 on tumor cells and is internalized. A cathepsin-cleavable linker releases the payload MMAE inside lysosomes, leading to microtubule depolymerization, G2/M cell-cycle arrest, and apoptotic cell death; the membrane-permeable MMAE can also cause a bystander effect. Fc effector functions may contribute.
The ADC binds HER2 and is internalized; lysosomal cleavage releases MMAE, which disrupts microtubules, causing G2/M arrest and apoptosis. Membrane-permeable MMAE can also cause bystander killing; Fc effector functions may contribute.
HER2-targeted antibody-drug conjugate (T-DXd) that binds HER2, internalizes, and releases a cleavable deruxtecan topoisomerase I inhibitor payload causing DNA damage with a bystander effect.
HER2-targeted antibody–drug conjugate: the trastuzumab antibody binds HER2 on tumor cells, is internalized, and a cleavable linker releases the deruxtecan (DXd) topoisomerase I inhibitor payload, causing DNA damage, cell-cycle arrest, and apoptosis with a bystander effect; additionally can mediate ADCC.
The HER2-targeted ADC binds HER2, is internalized, and releases a cleavable deruxtecan (DXd) topoisomerase I inhibitor payload that induces DNA damage and apoptosis in HER2+ cells; Fc-mediated ADCC and a bystander effect can also contribute.
TROP2-targeted antibody-drug conjugate (Dato-DXd) that binds TROP2, internalizes, and releases a cleavable deruxtecan topoisomerase I inhibitor payload causing DNA damage with a bystander effect.
TROP2-targeted antibody-drug conjugate that binds TROP2 on tumor cells, internalizes, and releases a cleavable deruxtecan (DXd) topoisomerase I inhibitor payload, stabilizing Topo I–DNA complexes to induce DNA breaks and cytotoxicity with a bystander effect.
ADC binds TROP2 on tumor cells, is internalized, and releases the DXd topoisomerase I inhibitor that induces DNA breaks and apoptosis; also enables a bystander effect.