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.
ADC binds B7-H3 on tumor cells, is internalized, and releases a topoisomerase I inhibitor payload that induces DNA damage, leading to apoptosis and cell death.
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.
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.
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.
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.
Autologous mesothelin-targeted CAR T-cell therapy in which a patient's T cells are lentivirally transduced to express an anti-mesothelin M5 scFv fused to 4-1BB and CD3ζ signaling domains; administered intratumorally (3e6 or 3e7 cells). Binding to mesothelin triggers T-cell activation and costimulation, leading to targeted cytotoxicity and local immune modulation.
Autologous T cells are lentivirally engineered to express an anti-mesothelin CAR (M5 scFv) with 4-1BB costimulatory and CD3ζ activation domains. Upon binding mesothelin on tumor cells, the CAR triggers T-cell activation, proliferation, and cytotoxic killing, with 4-1BB enhancing persistence; intratumoral delivery promotes localized immune modulation.
Anti-mesothelin CAR T cells bind mesothelin, activating CD3ζ/4-1BB signaling and inducing T-cell cytotoxicity (perforin/granzyme-mediated apoptosis, possibly Fas/FasL), killing mesothelin+ cells.
An antibody–drug conjugate (ADC) targeting Claudin 18.2; upon tumor binding and internalization, it releases the cytotoxic payload monomethyl auristatin E (MMAE) to disrupt microtubules and induce mitotic arrest/apoptosis in CLDN18.2-positive tumor cells.
RC118 is an anti‑CLDN18.2 antibody–drug conjugate that binds CLDN18.2 on tumor cells, is internalized, and releases the cytotoxic payload MMAE, which disrupts microtubule polymerization, causing G2/M arrest and apoptosis in CLDN18.2‑expressing cells.
The ADC binds CLDN18.2 on target cells, is internalized, and releases the MMAE payload that disrupts microtubules, causing G2/M arrest and apoptosis.