Autologous CD19-directed CAR T-cell therapy (with CD28 costimulation) that targets and kills CD19-positive malignant B cells.
Autologous T cells are engineered with a CD19-directed chimeric antigen receptor containing a CD28 costimulatory domain and CD3ζ signaling domain. After infusion, the CAR T cells bind CD19 on malignant B cells, become activated, expand, release cytokines, and kill target cells via perforin/granzyme–mediated cytotoxicity, eliminating CD19-positive tumors.
CD19-directed CAR T cells bind CD19 on target cells, activate, and kill them via perforin/granzyme-mediated cytotoxicity.
An anti-HER2 IgG1 monoclonal antibody that binds domain IV of HER2, inhibits HER2 signaling, and mediates antibody-dependent cellular cytotoxicity (ADCC).
Humanized anti‑HER2 (ERBB2) IgG1 that binds domain IV of HER2, inhibits HER2 signaling and tumor cell proliferation, promotes receptor internalization/downregulation, and engages immune effector cells to mediate ADCC against HER2‑overexpressing tumor cells.
Trastuzumab binds HER2 on target cells and engages FcγR+ immune effectors (e.g., NK cells) to mediate ADCC, with possible complement-mediated lysis; it also blocks HER2 signaling.
Genetically engineered autologous T cells expressing a CD19 chimeric antigen receptor with 4-1BB costimulation (second-generation) to target CD19+ B-ALL blasts; adoptive cellular immunotherapy that enhances T-cell activation, proliferation, persistence, and cytotoxic killing to eliminate residual disease.
Autologous T cells genetically engineered to express a second-generation CD19-directed chimeric antigen receptor with 4-1BB costimulation. Upon binding CD19 on B-lineage blasts, CAR signaling (CD3 zeta with 4-1BB) activates the T cells, promoting expansion and persistence and mediating targeted cytotoxic killing of CD19-positive B-ALL cells.
CAR-T cells bind CD19 on target cells, activate via CD3ζ/4-1BB, form an immune synapse, and kill CD19+ cells primarily through perforin/granzyme-mediated cytolysis (and Fas–FasL apoptosis).
Oral small-molecule BH3 mimetic; selective BCL-2 inhibitor that restores mitochondrial apoptosis and sensitizes leukemic cells.
BH3-mimetic that selectively inhibits the anti-apoptotic protein BCL-2, freeing pro-apoptotic factors to induce mitochondrial outer membrane permeabilization, cytochrome c release, and caspase activation, leading to apoptosis of BCL-2–dependent tumor cells.
Venetoclax directly inhibits BCL-2, freeing pro‑apoptotic factors to activate BAX/BAK, induce mitochondrial outer membrane permeabilization, cytochrome c release, caspase activation, and intrinsic apoptosis in BCL-2–dependent cells.
Patient-derived T cells engineered with a chimeric antigen receptor targeting B-cell antigens; cellular immunotherapy administered sequentially after ASCT.
Autologous T lymphocytes are genetically engineered to express a chimeric antigen receptor that recognizes B-cell antigens in an HLA-independent manner. Upon antigen binding, CAR signaling domains activate the T cells, driving proliferation, cytokine release, and targeted cytotoxic killing of malignant B cells.
CAR-T cells bind the B-cell antigen, become activated, and kill the antigen-expressing cells via contact-dependent cytotoxicity (perforin/granzyme-mediated apoptosis and Fas–FasL pathways).