Anti-CD20 monoclonal antibody that depletes B cells via ADCC, complement-mediated cytotoxicity (CDC), and apoptosis.
Chimeric anti‑CD20 monoclonal antibody that binds CD20 on pre‑B and mature B lymphocytes and depletes CD20+ B cells primarily via Fc‑mediated antibody‑dependent cellular cytotoxicity (ADCC), complement‑dependent cytotoxicity (CDC), and induction of apoptosis.
Binds CD20 on B cells and induces killing via Fc-mediated antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and direct apoptosis signaling.
Anti–TNF-α chimeric IgG1 monoclonal antibody that neutralizes soluble and transmembrane TNF-α, blocking TNFR→NF-κB signaling, reducing inflammatory cytokines/adhesion molecules, and inducing apoptosis of activated T cells/macrophages to dampen Th1/Th17-driven gut inflammation.
Chimeric IgG1 monoclonal antibody against TNF-α that neutralizes soluble and transmembrane TNF-α, blocking TNFR→NF-κB signaling, decreasing proinflammatory cytokines and adhesion molecules, and inducing apoptosis of activated T cells and macrophages to suppress Th1/Th17-driven inflammation.
By binding transmembrane TNF-α on activated immune cells, infliximab’s IgG1 Fc triggers ADCC and complement-dependent cytotoxicity and can induce reverse-signaling apoptosis in tmTNF-α–expressing cells.
Oral small-molecule BCL-2 inhibitor that promotes apoptosis in BCL-2–dependent myeloid blasts.
Selective oral BH3-mimetic that binds the hydrophobic groove of the anti-apoptotic protein BCL-2, blocking its function and restoring mitochondrial apoptosis in BCL-2–dependent tumor cells; relatively spares BCL-XL to limit thrombocytopenia.
BH3-mimetic binds and inhibits BCL-2, releasing pro-apoptotic effectors (e.g., BAX/BAK) to trigger mitochondrial outer membrane permeabilization, cytochrome c release, caspase activation, and apoptosis in BCL-2–dependent cells.
Anti-CD52 monoclonal antibody for lymphodepletion to reduce rejection and graft-versus-host disease.
Humanized anti-CD52 IgG1 monoclonal antibody that binds CD52 on B and T lymphocytes (and some monocytes, macrophages, NK cells), inducing cell depletion via complement-dependent cytotoxicity and Fc-mediated ADCC, producing profound lymphodepletion to reduce rejection and graft-versus-host disease.
Alemtuzumab binds CD52 on target cells and induces complement-dependent cytotoxicity and Fc-mediated effector killing (ADCC/ADCP), leading to lysis and depletion of CD52+ cells.
Chimeric IgG1 monoclonal antibody against TNF-α; neutralizes soluble and transmembrane TNF-α, can induce apoptosis of activated effector T cells/monocytes, and suppresses NF-κB–driven cytokines.
Chimeric IgG1 monoclonal antibody that binds and neutralizes soluble and transmembrane TNF-alpha, blocking TNF signaling; can induce apoptosis of activated effector T cells/monocytes and suppress NF-kB–driven proinflammatory cytokines to reduce inflammation.
Infliximab binds transmembrane TNF on target cells; its IgG1 Fc mediates ADCC and complement-dependent cytotoxicity, and tmTNF reverse signaling can induce apoptosis of activated TNF+ T cells/monocytes.