Autologous anti-CD19 chimeric antigen receptor (CAR) T-cell therapy manufactured via SIN lentiviral transduction of CD4/CD8 T cells; single IV dose (1×10^6/kg). Designed to deplete CD19+ B cells and plasmablasts to reduce autoantibody-driven inflammation.
Autologous T cells are engineered via lentiviral transduction to express an anti-CD19 chimeric antigen receptor that recognizes CD19 on B-lineage cells. Upon engagement, CAR T cells mediate cytotoxic killing (e.g., perforin/granzyme) and depletion of CD19+ B cells and plasmablasts, leading to reduced autoantibody production and attenuation of B cell–driven inflammation.
Anti-CD19 CAR T cells recognize CD19 on B-lineage cells and directly kill them via T-cell cytotoxicity (perforin/granzyme-mediated apoptosis, with possible Fas–FasL contributions).
Subcutaneous bispecific T-cell–engaging IgG1 antibody (CD3×CD20) that redirects cytotoxic T cells to kill CD20+ B cells.
Bispecific IgG1 antibody that binds CD3 on T cells and CD20 on B cells, crosslinking them to activate cytotoxic T lymphocytes and induce perforin/granzyme-mediated lysis of CD20-positive B-cell malignancies.
Epcoritamab bridges CD3 on T cells to CD20 on target B cells, activating T cells to form an immunologic synapse and kill CD20+ cells via perforin/granzyme-mediated lysis.
Autologous T cells engineered to express a chimeric antigen receptor targeting cadherin‑17 (CDH17). CAR engagement triggers CD3ζ/costimulatory signaling, leading to T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of CDH17-positive tumor cells.
Autologous T cells engineered with a chimeric antigen receptor targeting CDH17. Upon CDH17 binding, the CAR delivers CD3-zeta and costimulatory signals that activate and expand T cells, leading to cytokine release and perforin/granzyme-mediated cytotoxic killing of CDH17-positive tumor cells.
CAR-T cells bind CDH17 on target cells; CAR signaling activates T cells to kill via perforin/granzyme release and death-receptor pathways (e.g., Fas-FasL).
Investigational intratumoral immunotherapy biologic administered as subtherapeutic microdoses to trigger local immune-mediated effector functions within the tumor microenvironment; specific molecular targets are undisclosed and the study focuses on pharmacodynamic biomarker changes rather than efficacy.
Engineered NK cell engager that binds ROR1 on tumor cells and CD16 (FcγRIII) on NK cells to bring them into proximity, activate NK cells, and induce antibody-dependent cellular cytotoxicity and NK-mediated lysis of ROR1-positive tumor cells.
The NK cell engager binds ROR1 on tumor cells and CD16 on NK cells, bridging and activating NK cells to induce ADCC and perforin–granzyme–mediated lysis of ROR1-positive cells.
Investigational bispecific T‑cell–engaging monoclonal antibody (IV) that binds HLA‑G on tumor cells and CD3 on T cells to redirect cytotoxicity and overcome HLA‑G–mediated immune suppression.
Bispecific antibody that binds HLA-G on tumor cells and CD3 on T cells, bringing them into proximity to activate and redirect cytotoxic T-cell killing of HLA-G-expressing tumor cells while counteracting HLA-G-mediated immune suppression.
The bispecific antibody binds HLA-G on target cells and CD3 on T cells, activating and redirecting cytotoxic T cells to kill HLA-G–expressing cells via perforin/granzyme (and Fas/FasL)–mediated apoptosis.