Autologous gene-modified T cells expressing a chimeric antigen receptor targeting CD19, CD20, and BCMA; infused after lymphodepletion to treat relapsed/refractory B-cell NHL.
Autologous T cells are genetically engineered to express chimeric antigen receptors that bind CD19, CD20, and BCMA on malignant B-lineage cells. Antigen engagement activates CAR signaling (CD3ζ with co‑stimulatory domains), driving T‑cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of target cells. Multi-antigen targeting reduces antigen escape, and prior lymphodepletion supports in vivo expansion and persistence.
CAR T cells recognize CD19 on target cells, triggering T-cell activation and perforin/granzyme-mediated lysis (and death receptor signaling), killing CD19+ cells.
Autologous GPC3-targeted chimeric antigen receptor T-cell therapy; patient T cells engineered with an anti-GPC3 scFv, costimulatory domains (4-1BB/CD28), and CD3zeta, plus immune microenvironment-activating elements; delivered via hepatic arterial infusion for HCC.
Autologous T cells are engineered to express a chimeric antigen receptor with an anti-GPC3 scFv, 4-1BB/CD28 costimulatory domains, and CD3ζ, enabling MHC-independent recognition and killing of GPC3-positive hepatocellular carcinoma cells via cytotoxic granule release and cytokine secretion. Added immune microenvironment–activating elements are intended to enhance CAR-T activation, expansion, and recruitment/activation of bystander immune cells to overcome the suppressive HCC tumor microenvironment; delivery via hepatic arterial infusion increases exposure to liver tumors.
CAR-T cells bind GPC3 via the CAR and directly kill target cells through perforin/granzyme-mediated apoptosis (and Fas/FasL).
Autologous gene-modified T cells expressing a chimeric antigen receptor targeting CD19, CD20, and BCMA; infused after lymphodepletion to treat relapsed/refractory B-cell NHL.
Autologous T cells are genetically engineered to express chimeric antigen receptors that bind CD19, CD20, and BCMA on malignant B-lineage cells. Antigen engagement activates CAR signaling (CD3ζ with co‑stimulatory domains), driving T‑cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of target cells. Multi-antigen targeting reduces antigen escape, and prior lymphodepletion supports in vivo expansion and persistence.
CAR T cells bind CD20 on target cells, triggering activation and degranulation with perforin/granzymes (and Fas–FasL), inducing apoptosis of CD20+ cells.
Autologous gene-modified T cells expressing a chimeric antigen receptor targeting CD19, CD20, and BCMA; infused after lymphodepletion to treat relapsed/refractory B-cell NHL.
Autologous T cells are genetically engineered to express chimeric antigen receptors that bind CD19, CD20, and BCMA on malignant B-lineage cells. Antigen engagement activates CAR signaling (CD3ζ with co‑stimulatory domains), driving T‑cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of target cells. Multi-antigen targeting reduces antigen escape, and prior lymphodepletion supports in vivo expansion and persistence.
CAR T cells bind BCMA on target cells, triggering CAR signaling and direct cytolysis via perforin/granzyme (and death-receptor) pathways.
A glycoengineered type I anti-CD20 monoclonal antibody that depletes B cells via high-affinity Fc-mediated ADCC and complement-dependent cytotoxicity, with secondary induction of apoptosis; reduces B-cell antigen presentation, cytokine production, and T–B cell costimulation in multiple sclerosis.
Ublituximab is a glycoengineered type I anti‑CD20 IgG1 monoclonal antibody that binds CD20 on B cells and depletes them via enhanced Fc‑mediated antibody‑dependent cellular cytotoxicity (ADCC), complement‑dependent cytotoxicity (CDC), and induction of apoptosis, leading to reduced B‑cell antigen presentation, cytokine production, and T–B costimulation.
Binds CD20 on B cells and triggers Fc-mediated ADCC by effector cells, activates complement for CDC, and can induce apoptosis via CD20 crosslinking.