Autologous T cells engineered to express a chimeric antigen receptor targeting CD20 to recognize and kill CD20-positive B-cell lymphoma cells; part of a dual-target CAR T product.
Autologous T cells are genetically engineered to express a chimeric antigen receptor that binds CD20 on B cells. CAR engagement activates the T cells, leading to proliferation, cytokine release, and targeted cytotoxic killing (e.g., perforin/granzyme, death receptor pathways) of CD20-positive malignant and normal B cells; in some regimens paired with an anti-CD19 CAR to reduce antigen escape.
CAR T cells bind CD20 on target cells, activate, and kill via immunologic synapse with perforin/granzyme-mediated cytolysis and death-receptor (Fas/FasL) apoptosis.
Type II, humanized, glyco-engineered anti-CD20 monoclonal antibody that depletes CD20+ B cells via enhanced FcγRIIIa-mediated antibody-dependent cellular cytotoxicity and phagocytosis, and direct apoptosis; less reliant on complement-dependent cytotoxicity than rituximab. Administered as 1000 mg IV in this study.
A glycoengineered, humanized type II anti‑CD20 IgG1 that binds CD20 on B cells and depletes them primarily via enhanced FcγRIIIa‑mediated ADCC and antibody‑dependent phagocytosis, with potent direct (caspase‑independent) apoptosis and reduced reliance on complement‑dependent cytotoxicity.
Anti‑CD20 antibody binds CD20 on B cells and induces killing via enhanced FcγRIIIa-mediated ADCC (NK cells), antibody‑dependent phagocytosis (macrophages), and direct caspase‑independent apoptosis; complement has a minor role.
Gene-edited allogeneic anti-CD7 CAR T-cell therapy with CD7 knockout to prevent fratricide and TRAC knockout to ablate endogenous TCR signaling, targeting CD7 on malignant T/NK cells and a subset of AML blasts.
Off‑the‑shelf, donor-derived T cells gene-edited to express an anti‑CD7 chimeric antigen receptor that binds CD7 on malignant T/NK cells and some AML blasts, triggering CAR-driven cytotoxicity and cytokine release. CD7 is knocked out to prevent fratricide, and TRAC is knocked out to ablate endogenous TCR signaling and reduce graft‑versus‑host disease risk, restricting specificity to CD7 via the CAR.
Anti-CD7 CAR T cells bind CD7 on target cells, form an immune synapse, and kill via T cell–mediated cytotoxicity (perforin/granzyme release and death receptor pathways).
An autologous anti-CD20 chimeric antigen receptor T-cell (CAR-T) therapy in which a patient’s T cells are engineered ex vivo to express a CAR that binds CD20 on B cells; CAR activation triggers cytotoxic activity and cytokine release to eliminate CD20-positive malignant B cells, with expected on-target B-cell aplasia.
Autologous T cells are engineered ex vivo to express a chimeric antigen receptor that binds CD20 on B cells; CAR engagement activates T-cell cytotoxicity and cytokine release to eliminate CD20-positive malignant B cells, with expected on-target B-cell aplasia.
Anti-CD20 CAR-T cells bind CD20 on B cells and induce T-cell–mediated killing via perforin/granzyme and death-receptor pathways, leading to apoptosis/lysis.
An antibody–drug conjugate (ADC) consisting of a humanized anti–Trop-2 monoclonal antibody linked to SN-38 (the active metabolite of irinotecan), a topoisomerase I inhibitor. After binding Trop-2 on tumor cells, the ADC is internalized and releases SN-38 to inhibit topoisomerase I, leading to DNA damage and apoptosis. Administered IV at 10 mg/kg on days 1 and 8 of a 21-day cycle.
Humanized anti–Trop-2 monoclonal antibody linked to SN-38 (topoisomerase I inhibitor). After binding Trop-2 on tumor cells, the ADC is internalized and releases SN-38, which stabilizes Topo I–DNA complexes, causing DNA damage, S-phase arrest, and apoptosis; membrane-permeable SN-38 can produce a bystander effect.
ADC binds TROP2 on tumor cells, is internalized, and releases SN-38, a topoisomerase I inhibitor that causes DNA damage (Topo I–DNA complex stabilization), S‑phase arrest, and apoptosis; membrane-permeable SN‑38 can also cause a bystander effect.