Allogeneic 4SCAR CAR T cells engineered to target CD38 on myeloma cells, delivering CD3ζ-based activation with co-stimulation to induce selective cytotoxicity and cytokine release.
Allogeneic donor T cells engineered to express a CD38-specific 4SCAR (CAR with CD3ζ activation and co-stimulatory domains) bind CD38 on myeloma cells, triggering T‑cell activation, cytokine release, proliferation, and targeted cytotoxic killing of malignant plasma cells as an off‑the‑shelf cellular immunotherapy.
CD38-targeted CAR T cells bind CD38, become activated via CD3zeta/co-stimulation, and kill CD38+ cells through T-cell cytotoxic pathways (perforin/granzyme release and death-receptor signaling).
Off-the-shelf allogeneic CAR T cells employing a 4SCAR construct specific for CD19 to eliminate CD19-expressing B-lineage cells, potentially addressing myeloma subpopulations and normal B cells.
Off-the-shelf allogeneic T cells are engineered to express a 4SCAR chimeric antigen receptor targeting CD19. Upon binding CD19 on B-lineage cells and relevant myeloma subpopulations, CAR signaling (CD3zeta with co-stimulation) activates the T cells to release cytotoxic molecules and cytokines, leading to selective killing and depletion of CD19-expressing malignant and normal B cells.
CAR T cells bind CD19 on target cells and kill them via T-cell cytotoxic pathways (perforin/granzyme-mediated lysis and death-receptor apoptosis, with cytokine-mediated effects).
A half-life–extended ImmTAC (TCR-based bispecific biologic) comprising a soluble, high-affinity TCR that binds PRAME peptide presented by HLA-A*02:01 on tumor cells fused to an anti-CD3 effector to recruit and activate T cells, redirecting cytotoxic T cells to PRAME-positive cancer cells and inducing tumor cell lysis.
A half-life–extended ImmTAC (TCR-based bispecific) that uses a soluble, high-affinity TCR to bind PRAME peptide presented by HLA-A*02:01 on tumor cells and an anti-CD3 effector to recruit and activate T cells, redirecting polyclonal T cells to PRAME-positive cells to form an immune synapse, trigger TCR–CD3 signaling and cytokine release, and induce tumor cell lysis (HLA-A*02:01-restricted).
The ImmTAC’s TCR binds the PRAME peptide–HLA-A*02:01 complex on tumor cells and its anti‑CD3 arm engages T cells, forming an immune synapse that activates T-cell cytotoxicity (perforin/granzyme and cytokine-mediated killing) of the bound target cell.
Autologous/allogeneic T cells engineered via lentiviral transduction to express a CAR targeting BCMA; IV infusion at 2×10^6–1×10^7 CAR-T/kg; designed to kill BCMA+ plasma cells/myeloma cells through CAR-triggered cytotoxicity and cytokine release.
Autologous or allogeneic T cells are lentivirally engineered to express an anti-BCMA chimeric antigen receptor that recognizes BCMA on malignant plasma cells; CAR engagement activates T cells to proliferate and kill target cells via perforin/granzyme release and cytokine-mediated immune effects, leading to elimination of BCMA-positive myeloma cells.
BCMA-directed CAR T cells bind BCMA on target cells and, upon engagement, kill them via T-cell cytotoxicity (perforin/granzyme-mediated lysis and apoptosis, with possible Fas–FasL signaling).
An autologous anti-BCMA chimeric antigen receptor T-cell (CAR T) therapy generated by ex vivo retroviral transduction and infused fresh; CAR T cells bind BCMA (TNFRSF17) on clonal plasma cells and mediate targeted cytotoxicity to reduce amyloidogenic free light chains.
Autologous T cells engineered ex vivo via retroviral transduction to express a BCMA (TNFRSF17)-targeted chimeric antigen receptor; upon binding BCMA on clonal plasma cells, the CAR activates T-cell effector functions to mediate targeted cytotoxicity, eliminating light chain–producing cells and reducing amyloidogenic free light chains.
BCMA-specific CAR T cells bind BCMA on target cells, activating T-cell effector functions (perforin/granzyme release and death receptor pathways) to lyse and induce apoptosis of BCMA-expressing cells.