An intravenous antibody–drug conjugate (ADC) targeting B7-H3 (CD276), linked to a cytotoxic topoisomerase I inhibitor payload. After binding B7-H3 on tumor cells, it is internalized and releases the payload to inhibit topoisomerase I, causing DNA damage and tumor cell death; dosed every 3 weeks in advanced solid tumors.
Monoclonal antibody targeting B7-H3 (CD276) that is internalized upon binding and releases a linked topoisomerase I inhibitor payload inside tumor cells, inhibiting topo I, inducing DNA damage, and causing tumor cell death.
NO
INDIRECT
The ADC binds B7-H3 (CD276) on tumor cells, is internalized, and releases a topoisomerase I inhibitor that induces DNA damage and cell death. Topoisomerase I is the intracellular enzyme inhibited by the payload, not the surface antigen targeted for cell killing.
Fc‑engineered humanized anti‑CD19 monoclonal antibody that targets CD19 on B cells and induces tumor cell death via ADCC, ADCP, and direct pro‑apoptotic effects; used here with lenalidomide for induction followed by tafasitamab monotherapy.
Fc‑engineered humanized anti‑CD19 monoclonal antibody that binds CD19 on B cells and depletes CD19+ tumor cells by enhancing FcγR‑mediated ADCC and ADCP and by triggering direct pro‑apoptotic signaling.
YES
DIRECT
Anti-CD19 antibody binds CD19 on B cells, recruits Fc-gamma receptor–bearing effector cells to mediate ADCC and ADCP, and can trigger direct pro-apoptotic signaling in CD19+ cells.
Anti-BCMA antibody–drug conjugate that delivers the microtubule inhibitor MMAF; binds BCMA, is internalized, disrupts microtubules to kill malignant plasma cells, and also mediates ADCC/ADCP.
Afucosylated anti-BCMA antibody–drug conjugate linked to MMAF (auristatin). Binds BCMA on malignant plasma cells, is internalized, and delivers MMAF to inhibit tubulin polymerization causing G2/M arrest and apoptosis; Fc afucosylation enhances ADCC/ADCP.
NO
INDIRECT
Belantamab mafodotin targets BCMA on the cell surface; after BCMA-mediated internalization, the MMAF payload binds beta‑tubulin to disrupt microtubules causing G2/M arrest and apoptosis. Tubulin expression alone does not cause cells to be targeted or killed.
CT-P13 is a biosimilar to infliximab, a chimeric IgG1 monoclonal antibody that inhibits TNF-α. It neutralizes soluble and transmembrane TNF-α, blocks TNFR1/TNFR2 signaling, can mediate ADCC and CDC and induce apoptosis of TNF-expressing immune cells, and downregulates NF-κB–driven cytokines, chemokines, and adhesion molecules.
CT-P13 is a biosimilar to infliximab, a chimeric IgG1 monoclonal antibody that binds and neutralizes soluble and transmembrane TNF-α, blocking TNFR1/TNFR2 signaling. It can mediate ADCC and CDC and induce apoptosis of TNF-expressing immune cells, leading to downregulation of NF-κB–driven proinflammatory cytokines, chemokines, and adhesion molecules and reduced inflammation.
NO
INDIRECT
The antibody neutralizes soluble TNF-α in the extracellular space, blocking TNFR signaling. Because the target is not cell-bound, there is no ADCC/CDC engagement and no direct killing of TNF-producing cells.
CT-P13 is a biosimilar to infliximab, a chimeric IgG1 monoclonal antibody that inhibits TNF-α. It neutralizes soluble and transmembrane TNF-α, blocks TNFR1/TNFR2 signaling, can mediate ADCC and CDC and induce apoptosis of TNF-expressing immune cells, and downregulates NF-κB–driven cytokines, chemokines, and adhesion molecules.
CT-P13 is a biosimilar to infliximab, a chimeric IgG1 monoclonal antibody that binds and neutralizes soluble and transmembrane TNF-α, blocking TNFR1/TNFR2 signaling. It can mediate ADCC and CDC and induce apoptosis of TNF-expressing immune cells, leading to downregulation of NF-κB–driven proinflammatory cytokines, chemokines, and adhesion molecules and reduced inflammation.
YES
DIRECT
The antibody binds transmembrane TNF-alpha on target cells, engaging Fc-dependent ADCC and CDC and can trigger apoptosis via reverse signaling, leading to killing of TNF-expressing cells.