Autologous CD19-directed CAR T-cell therapy; patient T cells engineered to express a CAR targeting CD19, administered as a single IV dose to deplete CD19+ B-lineage cells and reset humoral immunity.
Autologous T cells engineered to express an anti-CD19 CAR with a 4-1BB costimulatory domain bind and kill CD19+ B-lineage cells (including B cells and plasmablasts), producing deep B-cell depletion and resetting humoral immunity.
Anti-CD19 CAR T cells bind CD19 on target cells and directly induce T-cell cytotoxicity via perforin/granzyme release and death-receptor–mediated apoptosis.
Intravenous T-cell–engaging bispecific antibody that binds CD20 on malignant B cells and CD3 on T cells to activate TCR/CD3 signaling and mediate T-cell cytotoxicity and cytokine release, depleting CD20+ B cells.
Intravenous 2:1 anti-CD20 × anti-CD3 bispecific antibody that bridges T cells to CD20+ B cells, activating TCR/CD3 signaling to trigger T‑cell cytotoxicity and cytokine release, leading to depletion of malignant CD20-expressing B cells; bivalent CD20 and monovalent CD3 binding enhances tumor targeting and may reduce off-target T‑cell activation.
Bispecific T‑cell engager links CD3 on T cells to CD20 on target cells, activating TCR signaling; engaged T cells kill CD20+ cells via perforin/granzyme-mediated cytotoxicity.
Anti-CD30 antibody–drug conjugate that delivers the microtubule-disrupting agent MMAE to CD30-positive cells, causing cell cycle arrest and apoptosis.
Anti-CD30 monoclonal antibody linked via a protease-cleavable valine‑citrulline linker to the microtubule-disrupting agent MMAE. After CD30 binding and internalization, MMAE is released to inhibit tubulin polymerization, inducing G2/M arrest and apoptosis in CD30-positive cells.
The anti-CD30 ADC binds CD30, is internalized, and releases MMAE via proteolytic linker cleavage; MMAE disrupts microtubules, causing G2/M arrest and apoptosis of CD30-positive cells.
Anti-CD20 monoclonal antibody used as optional pre-treatment to debulk CD20+ B cells and mitigate cytokine-release risk prior to MBS303.
MIL62 is a glyco-engineered humanized anti-CD20 monoclonal antibody that binds CD20 on B cells, triggering Fc-mediated antibody-dependent cell-mediated cytotoxicity (ADCC) and B-cell apoptosis, with additional inhibition of CD20-mediated signaling. This depletes CD20+ B cells to reduce tumor burden and is used as optional pre-treatment to mitigate cytokine-release risk before MBS303.
MIL62 binds CD20 on B cells and its Fc engages FcγR on effector cells to induce ADCC; it can also trigger apoptosis (and complement-mediated lysis), directly depleting CD20+ cells.
Autologous, fully human anti-CD19 CAR T-cell therapy administered as a single IV dose; engineered T cells recognize CD19 on B-lineage cells and mediate targeted cytotoxic depletion, inducing deep B-cell aplasia and immune reset to reduce ACPA autoantibodies.
Autologous CD4/CD8 T cells engineered with a fully human anti‑CD19 chimeric antigen receptor (CD8α hinge/transmembrane, CD28 costimulatory, CD3ζ signaling). After infusion, the CAR T cells bind CD19 on B-lineage cells and mediate targeted cytotoxic depletion, inducing deep B‑cell aplasia and immune reset, thereby reducing pathogenic ACPA autoantibodies.
Anti-CD19 CAR T cells recognize CD19 on B cells and directly kill them via T-cell cytotoxic mechanisms (perforin/granzyme-mediated lysis and apoptosis, and Fas–FasL signaling).