Autologous T cells genetically engineered to express a single CAR with tandem scFvs targeting CD19 and CD20, incorporating a 4-1BB co-stimulatory and CD3ζ signaling domain to activate, expand, and mediate cytotoxic killing of malignant B cells; dual targeting aims to reduce antigen-loss escape.
Autologous T cells are genetically engineered to express a single CAR with tandem scFvs targeting CD19 and CD20, incorporating a 4-1BB co-stimulatory and CD3zeta signaling domain. Binding to CD19 or CD20 activates and expands the CAR T cells, driving targeted cytotoxic killing of malignant B cells and reducing antigen-loss escape.
CAR T cells bind CD20 via the tandem CAR, become activated through CD3ζ/4-1BB signaling, and kill CD20+ cells via perforin/granzyme-mediated cytolysis (and death-receptor pathways).
Autologous humanized CD19-specific CAR T cells enriched for naïve/memory T cells; the CAR signals via CD28 and CD3ζ for activation/expansion and includes a truncated EGFR (EGFRt) safety tag enabling on‑demand ablation.
Autologous humanized CD19-directed CAR T cells enriched for naïve/memory T cells. The CAR uses a humanized anti-CD19 scFv for target recognition and CD28/CD3ζ signaling domains to drive T‑cell activation, proliferation, cytokine release, and cytolytic killing of CD19‑positive B cells, causing depletion of malignant B cells. A truncated EGFR (EGFRt) tag enables in vivo tracking and on‑demand ablation of the CAR T cells with cetuximab via ADCC.
CD19-directed CAR T cells bind CD19 on target cells and, upon CD28/CD3ζ signaling, directly kill CD19+ cells via T-cell cytotoxic mechanisms (perforin/granzyme release and Fas–FasL–mediated apoptosis).
Chimeric anti-EGFR IgG1 monoclonal antibody used here to ablate EGFRt-tagged CAR T cells as a safety switch.
Chimeric IgG1 monoclonal antibody that binds the extracellular domain of EGFR, blocking ligand binding and receptor dimerization to inhibit downstream signaling and tumor cell proliferation; can elicit immune effector functions (e.g., ADCC). In this study, used to target the EGFRt safety tag to ablate EGFRt-tagged CAR T cells on demand.
Cetuximab binds EGFR/EGFRt on target cells and its IgG1 Fc engages FcγR-bearing effector cells to mediate ADCC (and complement activation), depleting EGFRt-expressing cells.
Investigational intravenous antibody-drug conjugate targeting a tumor-associated surface antigen; upon binding and internalization, it releases a cytotoxic payload to kill antigen-expressing tumor cells. Being evaluated in a first-in-human Phase 1 dose escalation/expansion study in advanced solid tumors.
An intravenous antibody–drug conjugate whose monoclonal antibody binds a tumor-associated surface antigen, is internalized, and releases a linked cytotoxic payload inside the cell to kill antigen-expressing tumor cells.
An ADC binds the tumor-associated surface antigen, is internalized, and releases a cytotoxic payload inside the cell (after linker cleavage), causing cell death (e.g., via microtubule disruption or DNA damage).
Lentivirally transduced T cells expressing an anti-CD33 chimeric antigen receptor with CD3ζ signaling and 4-1BB costimulation to recognize and kill CD33-positive AML cells.
Lentivirally transduced T cells engineered to express an anti‑CD33 chimeric antigen receptor with CD3ζ signaling and 4‑1BB costimulation. Upon binding CD33 on AML cells, the CAR activates T‑cell cytotoxicity and cytokine release, leading to targeted lysis of CD33‑positive leukemia cells.
Anti-CD33 CAR T cells bind CD33 and induce T-cell–mediated killing via perforin/granzyme release and death-receptor signaling.