Investigational anticancer immunotherapy drug administered intravenously; specific molecular target/mechanism not disclosed in the registry entry.
Bispecific antibody that binds CEA (CEACAM5) on tumor cells and 4-1BB (CD137) on activated T cells and NK cells, crosslinking them to deliver localized 4-1BB costimulation in the tumor microenvironment. This enhances cytotoxic T-cell activity and leads to lysis of CEA-expressing tumor cells; may also interfere with CEA-mediated signaling.
BGB-B167 binds CEA on tumor cells and 4-1BB on T/NK cells, providing localized 4-1BB costimulation that activates cytotoxic lymphocytes to lyse CEA-expressing cells (perforin/granzyme-mediated killing).
Oral BCL-2 inhibitor (BH3 mimetic) that triggers mitochondrial apoptosis.
Selective oral BCL-2 inhibitor (BH3 mimetic) that binds the BCL-2 hydrophobic groove to block its anti-apoptotic function, restoring intrinsic (mitochondrial) apoptosis via MOMP and caspase activation; spares BCL-XL.
Venetoclax directly inhibits BCL-2, releasing pro-apoptotic effectors (BAX/BAK) to cause mitochondrial outer membrane permeabilization, cytochrome c release, caspase activation, and apoptosis of BCL-2-dependent cells.
A tumor-targeted superantigen fusion protein (anti-5T4 Fab linked to a bacterial superantigen) that binds 5T4 on tumor cells and polyclonally activates T cells via TCR Vβ engagement at the tumor site.
A tumor‑targeted superantigen fusion protein in which an anti‑5T4 Fab directs the molecule to 5T4‑expressing tumor cells while the staphylococcal enterotoxin E (SEA/E‑120) moiety binds T‑cell receptors (TCR Vβ) and MHC class II, driving potent, polyclonal T‑cell activation at the tumor site and T‑cell–mediated killing of 5T4+ cancer cells.
The anti-5T4 Fab targets 5T4+ cells and presents a superantigen (SEA/E-120) that engages TCR Vβ (with MHC II), polyclonally activating T cells to kill 5T4-expressing tumor cells via cytotoxic T-cell mechanisms.
A type II anti-CD20 glycoengineered monoclonal antibody used to deplete B cells and reduce anti-drug antibodies/modify the immune milieu.
Type II anti-CD20 glycoengineered humanized IgG1 that binds CD20 on B cells with enhanced FcγRIII affinity, driving potent ADCC/ADCP and direct, caspase‑independent cell death to deplete CD20+ B cells and modulate the immune milieu.
Obinutuzumab binds CD20 on B cells and, via enhanced FcγRIIIa engagement, triggers NK cell–mediated ADCC and macrophage ADCP; it also induces direct, caspase‑independent cell death of CD20+ cells (with limited CDC).