Type II anti-CD20 glycoengineered monoclonal antibody that depletes CD20+ B cells via enhanced ADCC, CDC, and direct apoptosis.
Glycoengineered type II humanized anti-CD20 IgG1 that binds CD20 on B cells; afucosylated Fc enhances FcγRIIIa engagement, driving potent antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and direct (caspase-independent) apoptosis to deplete CD20+ B cells.
Obinutuzumab binds CD20 on B cells; its afucosylated Fc engages Fc gamma RIIIa on effector cells to trigger ADCC, activates complement for CDC, and also induces direct caspase-independent apoptosis of CD20+ cells.
Oral small-molecule BH3-mimetic BCL-2 inhibitor that triggers apoptosis of CLL B cells.
Selective oral BH3-mimetic that inhibits BCL-2 by binding its hydrophobic groove, blocking anti-apoptotic function and restoring mitochondrial apoptosis in BCL-2-dependent tumor cells (e.g., CLL), with minimal BCL-XL inhibition.
Venetoclax binds and inhibits BCL-2, restoring mitochondrial apoptosis (BAX/BAK activation, MOMP, cytochrome c release, caspase activation) in BCL-2–dependent cells.
Intravenous humanized type II anti-CD20 monoclonal antibody that depletes B cells via enhanced ADCC/ADCP and direct cell death.
Glycoengineered humanized type II anti‑CD20 IgG1 that binds CD20 on B cells and promotes potent FcγRIIIa‑mediated ADCC/ADCP and direct, caspase‑independent cell death, leading to depletion of CD20+ malignant B lymphocytes.
Binds CD20 on B cells, recruits effector cells via FcgammaRIIIa to mediate ADCC/ADCP, and also induces direct caspase-independent cell death of CD20+ cells.
Autologous T cells engineered ex vivo with synthetic mRNA to transiently express an HBV-specific T-cell receptor, redirecting cytotoxic CD8+ T cells to HBV peptide–HLA complexes on infected hepatocytes for targeted killing.
Autologous T cells are ex vivo transfected with synthetic mRNA encoding an HBV-specific T-cell receptor, leading to transient TCR expression that recognizes HBV peptide–HLA complexes on infected hepatocytes and triggers TCR signaling–mediated cytotoxicity (perforin/granzyme) for targeted elimination of HBV-infected cells.
Engineered HBV-specific TCR-T cells recognize HBV peptide–HLA class I on infected hepatocytes and induce cytolysis via TCR-triggered perforin/granzyme-mediated apoptosis (and Fas/FasL).
Chimeric anti-CD20 IgG1 monoclonal antibody that depletes CD20+ B cells via ADCC, complement-dependent cytotoxicity, and apoptosis; brand name MabThera.
Chimeric anti‑CD20 IgG1 monoclonal antibody that binds CD20 on pre‑B and mature B cells and depletes them via antibody‑dependent cellular cytotoxicity, complement‑dependent cytotoxicity, and induction of apoptosis, thereby reducing pathogenic B‑cell and autoantibody activity.
Rituximab binds CD20 on B cells and induces killing via Fc-mediated ADCC by NK/macrophages, complement-dependent cytotoxicity (CDC), and can trigger apoptosis.