An autologous, gene-modified anti-CD19 chimeric antigen receptor (CAR) T-cell therapy administered as a single IV infusion. Patient T cells are engineered to express a CD19-directed CAR that, upon target engagement, activates cytotoxic effector functions to deplete CD19+ B-lineage cells and plasmablasts, aiming to reduce pathogenic B-cell activity and CNS inflammation in progressive multiple sclerosis.
Autologous T cells are gene-modified to express a CD19-directed chimeric antigen receptor. Upon binding CD19 on B-lineage cells (including naive/memory B cells and plasmablasts), the CAR triggers T-cell activation and cytotoxic effector functions (e.g., perforin/granzyme), leading to targeted depletion of CD19+ cells. This reduces pathogenic B-cell activity and associated CNS inflammation implicated in progressive multiple sclerosis.
YES
DIRECT
CD19-directed CAR T cells bind CD19 on target B-lineage cells and kill them via T-cell cytotoxic effector functions—primarily perforin/granzyme-mediated apoptosis (and death-receptor pathways such as Fas/FasL).
Fc-engineered anti-CD19 IgG1 monoclonal antibody (tafasitamab-cxix) that depletes B cells via ADCC, phagocytosis, and apoptosis.
Fc-engineered humanized IgG1 anti-CD19 monoclonal antibody that binds CD19 on B cells and, via enhanced Fc-gamma receptor engagement, promotes antibody-dependent cellular cytotoxicity and antibody-dependent cellular phagocytosis and can induce apoptosis, leading to depletion of CD19-positive B cells.
YES
DIRECT
Binds CD19 on B cells and, via enhanced FcγR engagement, triggers ADCC and ADCP by effector cells; binding can also induce apoptosis, leading to depletion of CD19+ cells.
Off-the-shelf allogeneic engineered natural killer (NK) cell therapy designed to augment antibody-directed killing; combined with tafasitamab to eliminate CD19+ B cells.
Allogeneic engineered NK cells equipped with an enhanced Fc receptor (PluReceptor) to increase binding to therapeutic IgG1 antibodies and amplify antibody-dependent cellular cytotoxicity. In combination with tafasitamab (anti-CD19), the NK cells recognize antibody-opsonized CD19+ B cells and kill them via perforin/granzyme-mediated cytotoxicity and innate pathways, leading to depletion of pathogenic B cells.
NO
INDIRECT
Engineered NK cells bind the IgG1 Fc of therapeutic antibodies (e.g., tafasitamab) and mediate ADCC against antibody-opsonized CD19+ B cells via perforin/granzyme; the IgG1 Fc itself is not a cell-expressed target.
Gene-modified autologous T lymphocytes expressing a chimeric antigen receptor targeting CD70; upon binding CD70 on tumor cells, they activate cytotoxic effector functions and proliferate to eradicate CD70-positive disease.
Autologous T lymphocytes genetically engineered to express a chimeric antigen receptor that binds CD70 on tumor cells; antigen engagement activates CAR signaling (CD3ζ with costimulatory domains), driving T-cell proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of CD70-positive malignant cells.
YES
DIRECT
CD70-CAR T cells bind CD70 on target cells, triggering CAR signaling and T-cell effector functions that kill via perforin/granzyme-mediated cytolysis (and Fas/FasL apoptosis).
Anti-CD3 monoclonal antibody used to activate T cells during CIK cell expansion.
Muromonab-CD3 (OKT3) is a monoclonal antibody that binds the CD3ε chain of the T-cell receptor complex. Cross-linking triggers TCR signaling, causing rapid T-cell activation and proliferation; prolonged engagement can lead to activation-induced cell death and Fc-mediated depletion. In this study it is used ex vivo to polyclonally activate T cells during CIK expansion.
YES
DIRECT
Muromonab-CD3 binds CD3ε on T cells, causing TCR cross-linking and activation-induced apoptosis, and its Fc mediates ADCC/CDC, depleting CD3+ cells.