Autologous GPC3-targeted chimeric antigen receptor T-cell (CAR-T) therapy for advanced/recurrent hepatocellular carcinoma; patient T cells are collected via leukapheresis, engineered ex vivo to express a GPC3-specific CAR, and reinfused to mediate antigen-directed cytotoxicity.
Autologous T cells engineered with a GPC3-specific chimeric antigen receptor recognize glypican-3 on tumor cells, triggering T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxicity against GPC3-positive cells. The cells are armored with a dominant-negative TGF-beta receptor II to block TGF-beta signaling in the tumor microenvironment, increasing resistance to immunosuppression and enhancing antitumor activity.
NO
INDIRECT
AZD5851 CAR-T cells target GPC3, not TGF-β3. The dnTGFβRII armors T cells by blocking TGF-β signaling without inducing killing of TGF-β3–expressing cells. Cytotoxicity is only against GPC3+ cells via perforin/granzyme after CAR engagement.
A glycoengineered type II anti-CD20 monoclonal antibody (brand name Gazyva) given IV that depletes CD20+ B cells through enhanced direct cell death and Fc-mediated ADCC, with relatively reduced complement activation, to modulate humoral autoimmunity and increase platelet counts in pediatric ITP.
Glycoengineered type II anti-CD20 humanized IgG1 that binds CD20 on B cells and depletes them via enhanced Fc-gamma RIII–mediated ADCC and direct, caspase-independent type II cell death, with relatively reduced complement-dependent cytotoxicity; used to suppress pathogenic CD20+ B cells (e.g., in ITP).
YES
DIRECT
Binds CD20 on B cells and depletes them via enhanced Fc gamma RIIIa–mediated ADCC (NK cells/monocytes) and induction of type II, caspase-independent direct cell death; complement lysis is relatively reduced.
Chimeric anti-CD20 monoclonal antibody (IV then SC) that depletes CD20-positive B cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity/phagocytosis, and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes them via complement-dependent cytotoxicity, Fc-mediated antibody-dependent cellular cytotoxicity/phagocytosis, and apoptosis.
YES
DIRECT
Anti-CD20 antibody binds CD20 on B cells and triggers complement-dependent cytotoxicity and Fc receptor–mediated ADCC/ADCP, with additional direct apoptosis signaling.
A glycoengineered type II anti-CD20 monoclonal antibody (brand name Gazyva) given IV that depletes CD20+ B cells through enhanced direct cell death and Fc-mediated ADCC, with relatively reduced complement activation, to modulate humoral autoimmunity and increase platelet counts in pediatric ITP.
Glycoengineered type II anti-CD20 humanized IgG1 that binds CD20 on B cells and depletes them via enhanced Fc-gamma RIII–mediated ADCC and direct, caspase-independent type II cell death, with relatively reduced complement-dependent cytotoxicity; used to suppress pathogenic CD20+ B cells (e.g., in ITP).
NO
INDIRECT
Obinutuzumab binds CD20 on B cells; its Fc engages FcγRIIIa (CD16a) on NK cells to trigger ADCC, killing CD20+ B cells. CD16a-expressing effector cells are not killed by the drug.
A glycoengineered type II anti-CD20 monoclonal antibody (brand name Gazyva) given IV that depletes CD20+ B cells through enhanced direct cell death and Fc-mediated ADCC, with relatively reduced complement activation, to modulate humoral autoimmunity and increase platelet counts in pediatric ITP.
Glycoengineered type II anti-CD20 humanized IgG1 that binds CD20 on B cells and depletes them via enhanced Fc-gamma RIII–mediated ADCC and direct, caspase-independent type II cell death, with relatively reduced complement-dependent cytotoxicity; used to suppress pathogenic CD20+ B cells (e.g., in ITP).
NO
INDIRECT
CD16b is an Fc receptor on neutrophils. Obinutuzumab binds CD20 on B cells and engages CD16 (including CD16b) via its Fc to recruit ADCC/ADCP, plus induces direct type II cell death of CD20+ cells; CD16b+ cells are not targeted or killed.