Autologous, gene-modified CAR T-cell therapy; patient T cells engineered to express a chimeric antigen receptor targeting B-lineage antigens (e.g., CD19 and CD20) to induce targeted cytotoxicity.
Autologous T cells are gene-modified to express a chimeric antigen receptor recognizing B-lineage antigens (e.g., CD19/CD20). Upon antigen binding, CAR signaling (CD3ζ with costimulatory domains) activates the T cells independently of MHC, inducing proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of malignant B cells.
CAR T cells bind CD20 on target cells, activating CAR signaling (CD3z with costimulation) and directly killing CD20+ cells via perforin/granzyme-mediated cytolysis (and Fas/FasL apoptosis).
Autologous, gene-modified CAR T-cell therapy; patient T cells engineered to express a chimeric antigen receptor targeting CD19 to induce targeted cytotoxicity.
Autologous T cells are genetically engineered to express an anti‑CD19 chimeric antigen receptor. Binding to CD19 on B‑lineage cells triggers MHC‑independent T‑cell activation (CD3ζ with costimulation), resulting in proliferation, cytokine release, and perforin/granzyme‑mediated cytotoxic killing of CD19+ malignant B cells, with on‑target depletion of CD19+ cells.
Anti-CD19 CAR T cells bind CD19 on target cells and trigger MHC-independent T-cell activation, leading to perforin/granzyme-mediated cytolysis (and death-receptor signaling) of CD19+ cells.
Oral small-molecule, highly selective BCL-2 inhibitor (BH3 mimetic) that restores mitochondrial apoptosis in CLL cells (also known as BGB-11417).
Oral BH3‑mimetic that selectively binds and inhibits the anti‑apoptotic protein BCL‑2, displacing pro‑apoptotic factors to trigger mitochondrial outer membrane permeabilization, caspase activation, and apoptosis in BCL‑2–dependent tumor cells (e.g., CLL).
BH3-mimetic inhibition of BCL-2 displaces pro-apoptotic factors, activates BAX/BAK, triggers mitochondrial outer membrane permeabilization, caspase activation, and intrinsic apoptosis in BCL-2–dependent cells.
Oral BCL-2 inhibitor (BH3 mimetic) that induces apoptosis in CLL cells.
Selective oral BCL-2 inhibitor (BH3 mimetic) that binds the BCL-2 hydrophobic groove, neutralizes its anti-apoptotic function, and restores mitochondrial apoptosis in malignant B cells; relatively spares BCL-XL, reducing thrombocytopenia risk.
Venetoclax is a BH3-mimetic that binds and inhibits BCL-2, releasing pro-apoptotic effectors (BAX/BAK) to trigger mitochondrial outer membrane permeabilization, caspase activation, and apoptosis in BCL-2–dependent cells.