Autologous gene‑engineered T cells expressing a mesothelin‑targeted CAR and providing local anti‑PD‑1 activity to block PD‑1/PD‑L1 signaling, enhancing T‑cell activation, cytotoxicity, and persistence in PD‑L1–positive, mesothelin‑expressing tumors.
Autologous T cells engineered to express a mesothelin-targeted chimeric antigen receptor that recognizes and kills mesothelin-positive tumor cells, while concurrently delivering local anti–PD-1 activity to block PD-1/PD-L1 signaling, enhancing T-cell activation, cytotoxicity, and persistence in the tumor microenvironment.
MSLN-targeted CAR T cells bind mesothelin on tumor cells, activating T-cell killing via perforin/granzyme release and death-receptor pathways; PD-1 blockade locally enhances this cytotoxic response.
Type II, glycoengineered humanized anti-CD20 IgG1 monoclonal antibody that depletes CD20+ B cells via enhanced antibody-dependent cellular cytotoxicity/phagocytosis and direct cell death, with limited complement activation.
Type II, glycoengineered humanized anti‑CD20 IgG1 that binds CD20 on B cells; afucosylated Fc increases FcγRIIIa affinity to enhance antibody‑dependent cellular cytotoxicity and phagocytosis, and it triggers direct, caspase‑independent cell death with minimal complement activation, leading to depletion of CD20+ B cells.
Obinutuzumab binds CD20 on B cells and kills via enhanced Fc gamma RIIIa (CD16a)-mediated ADCC by NK cells and antibody-dependent phagocytosis, plus direct caspase-independent cell death; complement involvement is minimal.
Antibody-drug conjugate targeting Trop-2; a humanized anti–Trop-2 monoclonal antibody linked to SN-38 (topoisomerase I inhibitor) to deliver cytotoxic payload to Trop-2–expressing tumor cells, causing DNA damage and bystander killing.
Humanized anti–Trop-2 monoclonal antibody conjugated to SN-38 (topoisomerase I inhibitor). After binding Trop-2 on tumor cells and internalization, the linker is cleaved to release SN-38, which stabilizes topo I–DNA complexes, causing DNA strand breaks, cell-cycle arrest, and apoptosis; the membrane-permeable payload can also produce bystander killing.
ADC binds TROP2, is internalized, and releases SN-38 (topoisomerase I inhibitor) that stabilizes topo I–DNA complexes, causing DNA damage, cell-cycle arrest, and apoptosis; the membrane-permeable payload can also cause bystander killing.
Autologous anti-CD19 chimeric antigen receptor (CAR) T-cell therapy in which a patient’s T cells are genetically engineered to express a CD19-specific scFv linked to CD28 costimulatory and CD3ζ activation domains; upon engagement with CD19 on malignant B cells, engineered T cells activate, expand, and mediate cytotoxicity.
Autologous T cells engineered to express an anti-CD19 chimeric antigen receptor with CD28 costimulatory and CD3zeta activation domains; binding to CD19 on malignant B cells activates and expands the T cells and induces perforin/granzyme-mediated cytotoxicity, depleting CD19-positive tumor cells.
Anti-CD19 CAR T cells bind CD19 on target cells, activate, form an immune synapse, and kill via perforin/granzyme-mediated cytotoxicity (and Fas–FasL apoptosis).
An anti-FOLR1 human IgG1 antibody-drug conjugate with a cleavable hemiasterlin payload (SC209); after FOLR1 binding and internalization, the payload inhibits tubulin polymerization, causing mitotic arrest and cell death.
Anti-FOLR1 human IgG1 antibody-drug conjugate that binds FOLR1 on tumor cells, is internalized, and releases a cleavable hemiasterlin payload (SC209) that inhibits tubulin polymerization, inducing mitotic arrest and cell death in FOLR1-expressing cells.
An anti-FOLR1 ADC binds FOLR1 on target cells, is internalized, and releases a hemiasterlin payload (SC209) that inhibits tubulin polymerization, causing mitotic arrest and apoptosis of FOLR1-expressing cells.