TROP-2–directed antibody–drug conjugate delivering SN-38 (topoisomerase I inhibitor).
Humanized anti-TROP2 monoclonal antibody linked to SN-38 (active metabolite of irinotecan). After binding TROP2 on tumor cells and internalization, the linker is cleaved to release SN-38, which inhibits topoisomerase I by stabilizing the Topo I–DNA complex, leading to DNA damage, replication arrest, and apoptosis (with potential bystander effect).
ADC binds TROP-2 on target cells, is internalized, and releases SN-38, which inhibits topoisomerase I, causing DNA damage and apoptosis (with possible bystander effect).
TROP-2–directed antibody–drug conjugate with a topoisomerase I payload.
TROP-2–targeting humanized IgG1 ADC; after binding and internalization, pH/enzymatic cleavage of the linker releases the topoisomerase I inhibitor tirumotecan, inhibiting DNA replication and causing cell-cycle arrest and apoptosis, with a bystander killing effect.
The ADC binds TROP-2 on target cells, is internalized, and linker cleavage releases the topoisomerase I inhibitor tirumotecan, inhibiting DNA replication and inducing cell-cycle arrest and apoptosis (with a bystander effect).
Investigational TROP-2–directed antibody–drug conjugate with a topoisomerase I payload.
TROP‑2–targeted monoclonal antibody delivers a topoisomerase I inhibitor payload to TROP‑2–expressing tumor cells. After binding and internalization, linker cleavage releases the topo I inhibitor, causing DNA damage (single‑strand breaks) and tumor cell death, with potential bystander effect depending on linker permeability.
An anti–TROP-2 antibody–drug conjugate binds TROP-2 on tumor cells, is internalized, and releases a topoisomerase I inhibitor that induces DNA damage (single-strand breaks) leading to cell death; membrane-permeable payload can cause bystander killing.
Nectin-4–directed monoclonal antibody linked via a cleavable linker to the microtubule inhibitor MMAE (vedotin). After binding Nectin-4 and internalization, the linker is cleaved to release MMAE, which inhibits tubulin polymerization, causing G2/M arrest and apoptosis in Nectin-4–expressing tumor cells.
ADC binds Nectin-4, is internalized, and releases MMAE, which inhibits tubulin polymerization causing G2/M arrest and apoptosis of Nectin-4–expressing cells.
Intravenous broadly neutralizing monoclonal antibody targeting conserved HIV-1 Env epitopes; blocks viral entry and enables Fc-mediated clearance of infected cells.
Broadly neutralizing monoclonal antibody targeting conserved HIV-1 envelope epitopes; blocks Env-mediated attachment/fusion to prevent viral entry and leverages Fc-mediated effector functions (e.g., ADCC/ADCP) to help clear virus and infected cells.
The antibody binds Env on infected cells and engages FcγR-bearing effectors to trigger ADCC (NK cells) and ADCP (macrophages; ± complement), killing Env-expressing cells.