Autologous anti-CD19 chimeric antigen receptor T-cell (CAR T) therapy. Patient T cells are genetically modified to express a CD19-targeted CAR; upon CD19 engagement, CAR signaling activates and expands T cells to mediate cytotoxic killing and cytokine release, depleting CD19+ B cells and clearing tumors. Administered as a single IV infusion at 0.2–2.0 × 10^6 CAR T cells/kg. Indications include B-ALL, large B-cell lymphoma (DLBCL/PMBCL/transformed FL), and mantle cell lymphoma.
Autologous T cells are genetically engineered to express a CD19-specific chimeric antigen receptor. Upon binding CD19 on B-lineage tumor cells, CAR signaling activates and expands the T cells, inducing cytotoxic granule release and cytokine-mediated killing that depletes CD19+ B cells and clears tumors.
CD19-targeted CAR T cells bind CD19+ cells and, upon CAR activation, kill them via perforin/granzyme cytolysis and cytokine-mediated apoptosis.
An autologous NKG2D-based CAR T-cell therapy in which patient T cells are gene-engineered to express a chimeric antigen receptor using the NKG2D receptor ectodomain fused to intracellular activation/costimulatory domains (e.g., CD3ζ). The cells target stress-induced NKG2D ligands (MICA, MICB, ULBP1–6) on tumor cells to mediate cytotoxicity and cytokine release.
Autologous T cells are engineered to express an NKG2D-based CAR (NKG2D ectodomain fused to 4-1BB and CD3ζ signaling domains) that recognizes stress-induced NKG2D ligands (MICA, MICB, ULBP1–6) on tumors, activating T cells to release cytokines and mediate perforin/granzyme-dependent cytotoxicity against NKG2DL-positive cancer cells.
NKG2D-based CAR T cells bind ULBP3 on target cells, triggering 4-1BB/CD3zeta signaling and perforin/granzyme-dependent cytolysis (with cytokine release).
Autologous gene-modified T cells expressing a chimeric antigen receptor targeting CD19 on B cells to mediate targeted cytotoxicity.
Autologous T cells engineered to express a chimeric antigen receptor targeting CD19 on B cells. CAR engagement activates CD3zeta and costimulatory domains (e.g., CD28 or 4-1BB), driving T-cell activation, expansion, cytokine release, and perforin/granzyme-mediated cytotoxicity to eliminate CD19-positive malignant and normal B cells.
CAR T cells bind CD19 via the CAR, become activated, and kill CD19+ cells through perforin/granzyme-mediated cytolysis and apoptosis (with possible Fas–FasL and cytokine contributions).
Allogeneic “universal” CAR T-cell therapy engineered to target glypican-3 (GPC3); single-dose infusion following lymphodepleting chemotherapy for advanced HCC and NSCLC.
Allogeneic T cells engineered with a chimeric antigen receptor targeting glypican-3 (GPC3). Upon binding GPC3 on tumor cells, the CAR activates T-cell effector functions, leading to cytotoxic killing via perforin/granzyme release and cytokine-mediated responses of GPC3-positive cancer cells.
GPC3-targeted CAR T cells recognize GPC3 on tumor cells and kill them via T-cell effector functions, primarily perforin/granzyme-mediated cytolysis and cytokine-driven apoptosis.