Anti‑CD79b antibody–drug conjugate that delivers MMAE (vedotin), a microtubule inhibitor, to induce apoptosis in CD79b+ B cells.
Anti-CD79b monoclonal antibody–drug conjugate; binds CD79b on B cells, is internalized, and a protease-cleavable linker releases MMAE (vedotin), which inhibits tubulin polymerization, causing G2/M arrest and apoptosis of CD79b+ malignant B cells.
YES
DIRECT
The ADC binds CD79b on B cells, is internalized, and releases MMAE intracellularly; MMAE inhibits tubulin polymerization, causing G2/M arrest and apoptosis of CD79b+ cells.
Anti‑CD79b antibody–drug conjugate that delivers MMAE (vedotin), a microtubule inhibitor, to induce apoptosis in CD79b+ B cells.
Anti-CD79b monoclonal antibody–drug conjugate; binds CD79b on B cells, is internalized, and a protease-cleavable linker releases MMAE (vedotin), which inhibits tubulin polymerization, causing G2/M arrest and apoptosis of CD79b+ malignant B cells.
NO
INDIRECT
Polatuzumab vedotin targets CD79b on B cells; after internalization, the linker is cleaved to release MMAE, which inhibits tubulin polymerization causing G2/M arrest and apoptosis. Tubulin is the intracellular payload target, not the antigen recognized by the drug, so cells expressing tubulin alone are not selectively killed.
An allogeneic, off-the-shelf CAR T-cell therapy enriched for T stem cell memory (Tscm) cells. These engineered T cells express a dual CAR targeting CD19 and CD20 on B cells to drive activation, proliferation, and cytotoxic killing of malignant B cells. Administered as a single IV dose after lymphodepletion; the Tscm phenotype is intended to enhance persistence and self-renewal.
Allogeneic T cells enriched for T stem cell memory are engineered to express dual CARs targeting CD19 and CD20 on B cells. Antigen binding activates T-cell signaling leading to proliferation and cytotoxic killing of malignant B cells; dual targeting aims to limit antigen escape, while the Tscm phenotype supports persistence and self-renewal. Given after lymphodepletion; an optional rimiducid safety switch can induce rapid ablation of the cells if required.
YES
DIRECT
Anti-CD19 CAR T cells bind CD19 on target cells; CAR signaling activates cytotoxic T-cell effector functions, leading to perforin/granzyme-mediated apoptosis (and Fas/FasL killing) of CD19+ cells.
An allogeneic, off-the-shelf CAR T-cell therapy enriched for T stem cell memory (Tscm) cells. These engineered T cells express a dual CAR targeting CD19 and CD20 on B cells to drive activation, proliferation, and cytotoxic killing of malignant B cells. Administered as a single IV dose after lymphodepletion; the Tscm phenotype is intended to enhance persistence and self-renewal.
Allogeneic T cells enriched for T stem cell memory are engineered to express dual CARs targeting CD19 and CD20 on B cells. Antigen binding activates T-cell signaling leading to proliferation and cytotoxic killing of malignant B cells; dual targeting aims to limit antigen escape, while the Tscm phenotype supports persistence and self-renewal. Given after lymphodepletion; an optional rimiducid safety switch can induce rapid ablation of the cells if required.
YES
DIRECT
Dual CAR T cells recognize CD20 on target cells, activate, and kill via cytotoxic T-cell mechanisms (perforin/granzyme release and death-receptor–mediated apoptosis).
A community-type tumor neoantigen mRNA cancer vaccine designed to induce tumor-specific CD4+ and CD8+ T-cell responses to recognize and kill cancer cells.
Self-replicating mRNA encoding patient-specific tumor neoantigens is taken up by antigen-presenting cells (primarily dendritic cells), translated into neoantigen proteins, and presented on MHC class I and II. This primes and expands neoantigen-specific CD8+ cytotoxic and CD4+ helper T cells, leading to immune-mediated killing of neoantigen-expressing cancer cells.
YES
INDIRECT
The vaccine primes and expands neoantigen-specific CD8+ T cells; these CTLs recognize the neoantigen-HLA class I complex on tumor cells and kill them via perforin/granzyme-mediated cytolysis and Fas-FasL apoptosis.