An autologous anti-BCMA chimeric antigen receptor (CAR) T-cell therapy.
Autologous T cells are genetically engineered to express a chimeric antigen receptor targeting BCMA on malignant plasma cells. Upon BCMA binding, the CAR delivers activation and costimulatory signals, driving T‑cell activation, expansion, cytokine release, and perforin/granzyme‑mediated cytotoxicity to eliminate BCMA‑expressing myeloma cells.
Anti-BCMA CAR T cells bind BCMA on target cells and kill them via T-cell cytotoxicity (perforin/granzyme release and death receptor pathways).
Allogeneic anti-CD19 chimeric antigen receptor (CAR) T-cell therapy. Donor T cells are engineered to express a CAR that binds CD19 on B cells; CAR signaling (CD3ζ with co-stimulatory domains) activates T-cell cytotoxicity and cytokine release to eliminate malignant CD19+ B cells.
Allogeneic donor T cells engineered with an anti-CD19 chimeric antigen receptor (CAR) engage CD19 on B cells. CAR signaling (CD3z plus co-stimulatory domains) activates T-cell cytotoxicity and cytokine release to lyse CD19+ malignant B cells; disruption of endogenous TCR/CD3 minimizes graft-versus-host disease risk.
Anti-CD19 CAR T cells bind CD19 and, upon CAR signaling, kill CD19+ cells via perforin/granzyme-mediated cytolysis and apoptosis (with additional death receptor/cytokine effects).
Autologous chimeric antigen receptor T-cell therapy targeting CD19-expressing large B-cell lymphomas; administered prior to golcadomide.
Autologous T cells are genetically engineered to express a chimeric antigen receptor that recognizes CD19 on B cells. CAR engagement of CD19 triggers CD3ζ and costimulatory signaling (e.g., CD28 or 4-1BB), leading to T‑cell activation, proliferation, cytokine release, and cytotoxic killing of CD19‑positive malignant B cells via perforin/granzyme and apoptosis pathways, resulting in depletion of CD19+ tumor cells (and on-target B‑cell aplasia).
Anti-CD19 CAR T cells bind CD19 and, via CD3z and costimulatory signaling, activate cytotoxic T-cell effector functions to kill CD19+ cells through perforin/granzyme-mediated cytolysis and death receptor-mediated apoptosis.
Autologous gene-engineered CAR T-cell product expressing a CD70-specific CAR with co-expression of CXCR2 (IL-8 receptor) to enhance trafficking to IL-8–rich glioblastoma, administered as a single IV infusion in dose escalation.
Autologous T cells are gene-engineered to express a CD70-specific chimeric antigen receptor and the IL-8 receptor CXCR2. CXCR2 enhances chemotaxis toward IL-8–rich glioblastoma, improving tumor homing and infiltration. CAR engagement of CD70 on tumor cells activates T-cell effector functions, leading to targeted cytotoxic killing (perforin/granzyme) and cytokine release against CD70-positive glioblastoma cells.
CD70-specific CAR T cells bind CD70 on target cells and kill them via T-cell cytotoxicity, primarily perforin/granzyme-mediated lysis after CAR engagement.
Autologous adoptive T-cell therapy in which patient-derived tumor-reactive T cells are expanded ex vivo and reinfused to recognize peptide-HLA complexes via native T-cell receptors, activating cytotoxic effector functions (perforin/granzyme and cytokines) to kill tumor cells.
Autologous tumor-infiltrating T cells are expanded ex vivo and reinfused to recognize tumor peptide–HLA complexes via their native T‑cell receptors, triggering TCR signaling and cytotoxic effector functions (perforin/granzyme release and cytokine secretion) to kill tumor cells.
TCR recognition of the tumor peptide–HLA-A class I complex activates the reinfused T cells, which kill target cells via perforin/granzyme-mediated lysis and Fas–FasL–induced apoptosis.