Autologous BCMA-directed CAR T-cell therapy; a single infusion of gene-modified T cells that recognize BCMA and trigger T-cell activation and cytotoxic elimination of myeloma cells.
Autologous T cells are transduced with a lentiviral vector to express a BCMA-specific chimeric antigen receptor. Binding to BCMA on malignant plasma cells triggers T-cell activation, expansion, cytokine release, and perforin/granzyme-mediated cytotoxic elimination of BCMA-expressing myeloma cells.
BCMA-targeted CAR T cells bind BCMA on target cells, activate, and kill them via perforin/granzyme-mediated cytolysis (apoptosis) after immunologic synapse formation.
Anti-CD38 monoclonal antibody that mediates ADCC, CDC, direct apoptosis, and immune modulation.
Human IgG1k anti‑CD38 monoclonal antibody that binds CD38 on malignant plasma cells and other CD38+ cells, inducing direct apoptosis and immune‑mediated killing via ADCC, ADCP, and CDC; additionally depletes CD38+ immunosuppressive cells (Tregs, Bregs, MDSCs), thereby modulating the tumor immune microenvironment.
Daratumumab binds CD38 on target cells and triggers Fc-mediated killing (ADCC by NK cells, ADCP by macrophages, complement-dependent cytotoxicity) and can induce direct apoptosis.
Autologous chimeric antigen receptor T-cell therapy: patient T cells are lentivirally transduced to express an anti-CD4 scFv derived from the humanized mAb ibalizumab, with third-generation signaling domains (CD28 and 4-1BB co-stimulation plus CD3ζ activation). Administered as a single IV infusion after lymphodepleting chemotherapy. Targets CD4 on malignant cells with expected on-target depletion of normal CD4+ T cells; risks include cytokine release syndrome.
Autologous T cells are lentivirally transduced to express an anti-CD4 chimeric antigen receptor (scFv from ibalizumab) with CD28 and 4-1BB costimulatory domains and CD3zeta activation. Upon binding CD4 on malignant cells, CAR signaling drives T-cell activation, proliferation, cytokine release, and cytotoxic killing of CD4+ tumor cells, with expected on-target depletion of normal CD4+ T cells. Administered after lymphodepleting chemotherapy.
Anti-CD4 CAR T cells bind CD4 on target cells and induce T-cell effector killing via perforin/granzyme-mediated cytolysis and apoptosis (and potentially Fas–FasL signaling).
Bispecific T-cell engager (BiTE) biologic that binds CD19 on B-lineage cells and CD3 on T cells, redirecting cytotoxic T cells to eliminate CD19+ leukemia/minimal residual disease.
Blinatumomab is a bispecific CD19×CD3 antibody (BiTE) that bridges CD19+ B-lineage cells and CD3+ T cells, forming an immunologic synapse that activates and redirects cytotoxic T cells to lyse CD19-expressing leukemia cells and clear minimal residual disease, independently of MHC.
Blinatumomab bridges CD19 on target cells to CD3 on T cells, forming an immunologic synapse; activated T cells kill CD19+ cells via perforin/granzyme-mediated cytolysis (MHC-independent).
Antibody–drug conjugate targeting CD79b on B cells; delivers MMAE to disrupt microtubules and induce apoptosis.
Monoclonal antibody targets CD79b on B cells; after internalization, a protease-cleavable linker releases MMAE, which inhibits microtubule polymerization, causing G2/M arrest and apoptosis in malignant B cells.
An anti-CD79b antibody–drug conjugate binds CD79b on B cells, is internalized, and releases MMAE, which inhibits microtubule polymerization, causing G2/M arrest and apoptosis of CD79b-expressing cells.