Anti-CD20 chimeric IgG1 monoclonal antibody that mediates ADCC/ADCP, complement-dependent cytotoxicity, and direct apoptosis, leading to B-cell depletion.
Chimeric anti-CD20 IgG1 monoclonal antibody that depletes CD20+ B cells via Fc-mediated ADCC/ADCP, complement-dependent cytotoxicity, and direct induction of apoptosis.
Binds CD20 on B cells and induces killing via FcγR-mediated ADCC/ADCP, complement-dependent cytotoxicity (CDC), and can directly trigger apoptosis upon CD20 cross-linking.
Anti-CD19 humanized, Fc-engineered IgG1 monoclonal antibody that enhances ADCC/ADCP and induces apoptosis, depleting malignant and normal B cells.
Fc‑engineered, humanized anti‑CD19 IgG1 monoclonal antibody that binds CD19 on B cells and engages Fcγ receptors on NK cells and macrophages to enhance ADCC and ADCP, while also inducing apoptosis, leading to depletion of malignant and normal CD19+ B cells.
Binds CD19 on B cells and engages Fc gamma receptor–bearing effector cells (NK cells, macrophages) to trigger ADCC and ADCP, and can also induce apoptosis, leading to killing of CD19+ cells.
Gene-modified autologous macrophages expressing an anti-HER2 chimeric antigen receptor (CAR). Derived from patient PBMCs, differentiated to macrophages, transduced ex vivo via an adenoviral vector, and administered intraperitoneally to induce HER2-dependent tumor cell phagocytosis and cytotoxicity and remodel the tumor microenvironment.
Autologous macrophages engineered to express an anti-HER2 chimeric antigen receptor bind HER2 on tumor cells, activating macrophage phagocytosis and cytotoxicity and remodeling the tumor microenvironment to enhance anti-tumor immunity.
HER2-directed CAR macrophages bind HER2 on tumor cells and directly kill them via CAR-triggered phagocytosis and macrophage cytotoxic effector functions (phagolysosomal killing, ROS/cytotoxic mediators).
Anti-CD47 monoclonal antibody immunotherapy that blocks the CD47–SIRPα 'don't-eat-me' signal, enhancing macrophage-mediated phagocytosis of leukemia cells.
Anti-CD47 monoclonal antibody that blocks the CD47-SIRPa interaction, removing the 'don't eat me' signal and promoting macrophage-mediated phagocytosis of leukemia cells.
Blocks CD47–SIRPα to remove the “don’t‑eat‑me” signal and engages Fcγ receptors on macrophages, inducing antibody‑dependent cellular phagocytosis (ADCP) of CD47+ cells.
Small-molecule BH3-mimetic BCL-2 inhibitor that triggers intrinsic (mitochondrial) apoptosis in AML cells.
Selective BH3-mimetic that inhibits BCL-2 by binding its hydrophobic groove, blocking its anti-apoptotic function and restoring intrinsic (mitochondrial) apoptosis in tumor cells; spares BCL-XL.
Venetoclax directly inhibits BCL-2 as a BH3 mimetic, freeing BAX/BAK to induce mitochondrial outer membrane permeabilization, cytochrome c release, and caspase-mediated apoptosis in BCL-2–dependent cells.