Autologous T cells engineered to express a chimeric antigen receptor targeting CD19 to recognize and kill CD19-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 CD19 on B cells. CAR engagement activates the T cells via CD3ζ/co-stimulatory signaling, driving proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing, resulting in depletion of CD19-positive malignant B cells (and normal B cells).
YES
DIRECT
CAR T cells bind CD19 on target cells, become activated via CD3ζ/co-stimulatory signaling, and kill through immunologic synapse formation with perforin/granzyme release (and death-receptor pathways), leading to apoptosis of CD19+ cells.
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.
YES
DIRECT
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.
YES
DIRECT
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.
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.
NO
INDIRECT
CD16a (FcγRIIIa) on NK cells/macrophages binds the Fc of obinutuzumab to mediate ADCC/phagocytosis against CD20+ B cells; the CD16a-expressing effector cells are not targeted or killed by the drug.
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.
YES
DIRECT
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).