Oral small-molecule BCL-2 inhibitor that triggers mitochondrial apoptosis in leukemic cells.
Selective BH3-mimetic that inhibits BCL-2 by binding its hydrophobic groove, neutralizing its anti-apoptotic function and restoring mitochondrial apoptosis (MOMP and caspase activation) in BCL-2–dependent tumor cells; minimal BCL-XL inhibition reduces thrombocytopenia risk.
Venetoclax inhibits BCL-2 in BCL-2–dependent cells, enabling BAX/BAK activation and mitochondrial outer membrane permeabilization, leading to caspase-mediated apoptosis.
Autologous gene-modified T cells expressing dual CARs targeting CD19 and CD22 to recognize and kill B-ALL blasts, aiming to reduce antigen escape.
Autologous T cells are gene-modified to express dual chimeric antigen receptors that bind CD19 and CD22 on B‑cell leukemia cells. CAR engagement activates the T cell, leading to cytokine release, proliferation, and targeted cytotoxic killing of CD19+/CD22+ blasts, with dual targeting designed to reduce antigen escape.
CAR binding to CD19 on target cells activates the engineered T cell, forming an immune synapse and inducing perforin/granzyme release (and Fas/FasL signaling), causing apoptosis/lysis of the CD19+ cells.
Autologous gene-modified T cells expressing dual CARs targeting CD19 and CD22 to recognize and kill B-ALL blasts, aiming to reduce antigen escape.
Autologous T cells are gene-modified to express dual chimeric antigen receptors that bind CD19 and CD22 on B‑cell leukemia cells. CAR engagement activates the T cell, leading to cytokine release, proliferation, and targeted cytotoxic killing of CD19+/CD22+ blasts, with dual targeting designed to reduce antigen escape.
CAR-T cells bind CD22 on target cells, become activated, and kill them via perforin/granzyme-mediated apoptosis and death receptor pathways (e.g., Fas/FasL).
An autologous CD19-directed CAR T-cell therapy (also known as CNCT19) in which a patient’s T cells are genetically modified to express a chimeric antigen receptor targeting CD19 on B-lineage cells to eliminate residual leukemic cells.
Autologous T cells are genetically modified to express a CD19‑specific chimeric antigen receptor. Binding to CD19 on B‑lineage cells triggers T‑cell activation, expansion, cytokine release, and perforin/granzyme‑mediated cytotoxicity, eliminating CD19‑positive leukemic (and normal) B cells to clear residual disease.
CD19-directed CAR T cells bind CD19 on B cells and kill them via T-cell–mediated cytolysis (perforin/granzyme-induced apoptosis).
Autologous T lymphocytes genetically engineered to express a chimeric antigen receptor targeting CD19 on B cells for treatment of CD19+ B-cell non-Hodgkin lymphoma.
Autologous T cells are genetically engineered to express a chimeric antigen receptor that recognizes CD19 on B cells. CAR engagement activates CD3zeta and costimulatory domains (e.g., CD28 or 4-1BB), driving T-cell proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of CD19+ malignant B cells.
CD19 CAR T cells bind CD19 on target B cells, triggering CD3ζ/co-stimulatory signaling and forming a cytotoxic synapse that kills CD19+ cells via perforin/granzyme-mediated apoptosis (and Fas/FasL pathways).