Engineered universal T-cell therapy expressing a chimeric NK receptor that enables NK-like recognition of stress-induced NK ligands on dysregulated/activated immune cells. Engagement triggers T-cell activation, perforin/granzyme-mediated cytotoxicity, and immunomodulation to eliminate pathogenic immune cells driving steroid-refractory/resistant or steroid-dependent GVHD. Administered IV in Phase 1 SAD/MAD dosing.
Engineered universal T cells expressing a chimeric NK receptor (NK-like CAR, e.g., NKG2D-based) that recognizes stress-induced NK ligands on activated/dysregulated immune cells; receptor engagement triggers T-cell activation with perforin/granzyme-mediated cytotoxicity and immunomodulation to eliminate pathogenic alloreactive T cells and antigen-presenting cells driving steroid-refractory/resistant GVHD.
An NKG2D-based chimeric receptor on the engineered T cells binds ULBP4 (RAET1E), activating the T cells to degranulate and kill the ligand-expressing cell via perforin/granzyme-mediated cytotoxicity.
Engineered universal T-cell therapy expressing a chimeric NK receptor that enables NK-like recognition of stress-induced NK ligands on dysregulated/activated immune cells. Engagement triggers T-cell activation, perforin/granzyme-mediated cytotoxicity, and immunomodulation to eliminate pathogenic immune cells driving steroid-refractory/resistant or steroid-dependent GVHD. Administered IV in Phase 1 SAD/MAD dosing.
Engineered universal T cells expressing a chimeric NK receptor (NK-like CAR, e.g., NKG2D-based) that recognizes stress-induced NK ligands on activated/dysregulated immune cells; receptor engagement triggers T-cell activation with perforin/granzyme-mediated cytotoxicity and immunomodulation to eliminate pathogenic alloreactive T cells and antigen-presenting cells driving steroid-refractory/resistant GVHD.
Engineered T cells express an NKG2D-based chimeric receptor that binds ULBP5 on target cells, triggering T-cell activation and perforin/granzyme-mediated cytolysis.
Engineered universal T-cell therapy expressing a chimeric NK receptor that enables NK-like recognition of stress-induced NK ligands on dysregulated/activated immune cells. Engagement triggers T-cell activation, perforin/granzyme-mediated cytotoxicity, and immunomodulation to eliminate pathogenic immune cells driving steroid-refractory/resistant or steroid-dependent GVHD. Administered IV in Phase 1 SAD/MAD dosing.
Engineered universal T cells expressing a chimeric NK receptor (NK-like CAR, e.g., NKG2D-based) that recognizes stress-induced NK ligands on activated/dysregulated immune cells; receptor engagement triggers T-cell activation with perforin/granzyme-mediated cytotoxicity and immunomodulation to eliminate pathogenic alloreactive T cells and antigen-presenting cells driving steroid-refractory/resistant GVHD.
Engineered T cells with an NKG2D-based chimeric receptor bind ULBP6 on target cells, activating the T cells to kill via perforin/granzyme-mediated cytotoxicity.
Chimeric anti-CD20 monoclonal antibody (brand: MabThera) given 1 g IV on days 1 and 15; depletes CD20+ B cells via ADCC, CDC, and apoptosis to reduce pathogenic IgM, including anti-MAG autoantibodies.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on pre-B and mature B cells and depletes them via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis, reducing pathogenic IgM and autoantibody production.
Rituximab binds CD20 on B cells and induces Fc-mediated ADCC (NK/macrophages), complement-dependent cytotoxicity, and apoptosis upon CD20 crosslinking.
An off-the-shelf, gene-engineered CD19-directed chimeric antigen receptor (CAR) T-cell product. Binding to CD19 on B-lineage cells triggers CAR signaling (CD3ζ with co-stimulation), T-cell activation, cytokine release, and perforin/granzyme-mediated cytotoxicity, leading to depletion of CD19+ malignant B cells (e.g., B-ALL, B-cell lymphomas).
Gene‑engineered T cells expressing a CD19‑specific chimeric antigen receptor bind CD19 on B‑lineage cells, activating CAR signaling (CD3ζ with co‑stimulation) to trigger T‑cell activation, cytokine release, and perforin/granzyme‑mediated cytotoxicity, resulting in depletion of CD19+ malignant B cells.
CD19-specific CAR T cells bind CD19 on target B cells, activate T-cell effector functions, and kill via perforin/granzyme-mediated cytotoxicity (and Fas–FasL apoptosis).