An autologous, genetically modified BCMA-targeting chimeric antigen receptor (CAR) T-cell therapy engineered to express a high-affinity BCMA-directed CAR with CD3ζ signaling and costimulation; administered as a single IV infusion after lymphodepleting chemotherapy.
Autologous T cells are genetically modified to express a high‑affinity BCMA‑directed chimeric antigen receptor with CD3ζ signaling and costimulatory domains. Upon binding BCMA on malignant plasma/B‑lineage cells, the CAR activates T‑cell effector functions, leading to proliferation, cytokine release, and cytotoxic killing of BCMA‑expressing tumor cells. Administered after lymphodepleting chemotherapy to promote in vivo expansion and persistence.
BCMA-directed CAR T cells bind BCMA on target cells and kill them via T-cell effector functions, primarily perforin/granzyme-mediated cytolysis and Fas–FasL apoptosis, after CAR signaling (CD3ζ with costimulation).
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-CAR T cells bind ULBP2 on target cells, become activated via 4-1BB/CD3ζ signaling, and kill the bound cells through perforin/granzyme-mediated cytotoxicity with cytokine release.
Ex vivo–expanded, patient-derived T cells recognizing tumor neoantigens via TCRs; administered via hepatic arterial infusion to kill melanoma cells through perforin/granzyme and cytokine release and establish durable anti-tumor immunity.
Autologous, ex vivo-expanded tumor-infiltrating T cells that recognize patient-specific tumor neoantigens via native TCRs; after hepatic arterial infusion they home to liver metastases and kill melanoma cells through perforin/granzyme-mediated cytolysis and cytokine release, with expansion/persistence to provide durable anti-tumor immunity.
Transferred TILs recognize the patient-specific neoantigen peptide–HLA class I complex via their native TCRs and directly kill the presenting cells through perforin/granzyme-mediated cytolysis (and Fas–FasL/apoptotic pathways).
Ex vivo–expanded, patient-derived T cells recognizing tumor neoantigens via TCRs; administered via hepatic arterial infusion to kill melanoma cells through perforin/granzyme and cytokine release and establish durable anti-tumor immunity.
Autologous, ex vivo-expanded tumor-infiltrating T cells that recognize patient-specific tumor neoantigens via native TCRs; after hepatic arterial infusion they home to liver metastases and kill melanoma cells through perforin/granzyme-mediated cytolysis and cytokine release, with expansion/persistence to provide durable anti-tumor immunity.
TILs recognizing the neoantigen–HLA class II complex via their native TCRs directly kill target-expressing tumor cells through perforin/granzyme cytolysis and can also trigger apoptosis via death receptor signaling and proinflammatory cytokines.
Anti-CD38 IgG1 monoclonal antibody that depletes CD38+ plasma cells/plasmablasts via ADCC/CDC/apoptosis and inhibits CD38 ectoenzyme activity to reduce donor-specific antibody production.
Isatuximab is a humanized IgG1 anti-CD38 monoclonal antibody that binds CD38 on plasma cells/plasmablasts and other CD38+ cells, inducing antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis; it also inhibits CD38 ectoenzyme activity, resulting in depletion of CD38+ cells and reduced pathogenic antibody production.
Isatuximab binds CD38 on target cells and triggers Fc-mediated ADCC and complement-dependent cytotoxicity, and can directly induce apoptosis, leading to killing of CD38+ cells.