An intravenous antibody–drug conjugate (ADC) targeting a tumor-associated antigen. Following antigen binding and internalization, a cleavable linker releases a cytotoxic payload that kills tumor cells (via microtubule disruption and/or DNA damage); Fc-mediated immune effector functions may contribute. Dosed every 3 weeks.
TROP-2-targeted monoclonal antibody linked via a cleavable linker to a topoisomerase I inhibitor; after antigen binding and internalization, linker cleavage releases the payload to inhibit topoisomerase I, blocking DNA replication and inducing DNA damage, cell-cycle arrest, and apoptosis in TROP-2-expressing tumor cells; Fc-mediated effector functions may contribute.
The ADC binds TROP-2 on tumor cells, is internalized, and its cleavable linker releases a topoisomerase I inhibitor that blocks DNA replication, causing DNA damage, cell-cycle arrest, and apoptosis; Fc-mediated effector functions (e.g., ADCC/CDC) may also contribute.
TROP2-directed antibody–drug conjugate that internalizes into TROP2-positive tumor cells to deliver a topoisomerase I inhibitor (DXd) payload, causing DNA damage and tumor cell death.
TROP2-directed antibody–drug conjugate that binds TROP2 on tumor cells, is internalized, and releases a lysosomally cleaved DXd (topoisomerase I inhibitor) payload, stabilizing the Topo I–DNA cleavable complex to induce DNA damage, inhibit replication, and trigger apoptosis in TROP2-expressing tumor cells.
ADC binds TROP2 on tumor cells, is internalized, and releases a DXd topoisomerase I inhibitor payload that causes DNA damage and apoptosis of the TROP2-expressing cells.
Cytokine immunotherapy that activates TNFR1/TNFR2 on tumor and tumor-associated endothelial cells to induce apoptosis/necrosis, disrupt tumor vasculature, increase vascular permeability, and enhance local immune responses.
Recombinant modified human TNF-alpha cytokine that binds TNFR1/TNFR2 on tumor cells and tumor-associated endothelial cells, inducing apoptotic/necrotic signaling, disrupting tumor vasculature and increasing vascular permeability, and enhancing local antitumor immune responses.
TNF-α binds TNFR1 on target cells, triggering death‑domain signaling (TRADD/FADD) that activates caspase‑8–mediated apoptosis or, if caspases are inhibited, RIPK1/RIPK3‑dependent necroptosis; it also kills tumor-associated endothelium via the same pathway, disrupting tumor vasculature.
Cytokine immunotherapy that activates TNFR1/TNFR2 on tumor and tumor-associated endothelial cells to induce apoptosis/necrosis, disrupt tumor vasculature, increase vascular permeability, and enhance local immune responses.
Recombinant modified human TNF-alpha cytokine that binds TNFR1/TNFR2 on tumor cells and tumor-associated endothelial cells, inducing apoptotic/necrotic signaling, disrupting tumor vasculature and increasing vascular permeability, and enhancing local antitumor immune responses.
rmhTNF binds TNFR2 (and TNFR1) on tumor and tumor-associated endothelial cells, triggering TNF-receptor signaling that induces apoptosis/necroptosis and vascular disruption.
Anti-CD38 monoclonal antibody that targets clonal plasma cells and mediates ADCC, CDC, apoptosis, and immunomodulatory effects.
Human IgG1κ anti‑CD38 monoclonal antibody that binds CD38 on clonal plasma cells, inducing direct cell death and immune‑mediated killing via ADCC, ADCP, and CDC; also depletes CD38+ immunosuppressive cells, contributing to antitumor immune modulation.
The antibody binds CD38 on target cells and triggers Fc-mediated ADCC (NK cells), ADCP (macrophages), and complement-dependent cytotoxicity (CDC), and can also induce direct apoptosis of CD38+ cells.