Anti-CD19 monoclonal antibody that depletes B-lineage cells, including plasmablasts, to reduce autoantibody production.
Humanized, afucosylated anti-CD19 IgG1 monoclonal antibody that binds CD19 on B-lineage cells (including plasmablasts) and depletes them via enhanced Fc-mediated ADCC, thereby reducing pathogenic autoantibody production.
The anti-CD19 IgG1 binds CD19 on B-lineage cells and recruits FcγR-expressing effector cells to mediate antibody-dependent cellular cytotoxicity (and phagocytosis), depleting CD19+ cells; complement activation may also contribute.
A chimeric IgG1 anti–TNF-α monoclonal antibody biosimilar to infliximab. Binds soluble and transmembrane TNF-α to block TNFR1/2 signaling and downstream NF-κB/MAPK pathways, reducing proinflammatory cytokines (e.g., IL-1, IL-6) and adhesion molecules; can induce apoptosis and Fc-mediated cytotoxicity of TNF-expressing immune cells. Administered subcutaneously (120 mg every 2 weeks) or intravenously (5–10 mg/kg every 8 weeks) for maintenance therapy in Crohn’s disease.
Chimeric IgG1 anti–TNF-alpha monoclonal antibody (biosimilar to infliximab) that binds soluble and transmembrane TNF-alpha, neutralizing TNFR1/2 signaling and downstream NF-kB/MAPK pathways; reduces proinflammatory cytokines and adhesion molecules and can induce apoptosis and Fc-mediated cytotoxicity of TNF-expressing immune cells.
The IgG1 antibody binds transmembrane TNF on cells and can trigger apoptosis via reverse signaling and mediate Fc-dependent ADCC/CDC by effector cells/complement, killing TNF-expressing immune cells (neutralization of soluble TNF does not kill cells).
Anti-CD20 monoclonal antibody that depletes CD20+ B cells via antibody-dependent cellular cytotoxicity, complement activation, and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes them via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and induction of apoptosis.
Rituximab binds CD20 on B cells and eliminates them via Fc-mediated ADCC by effector cells, complement-dependent cytotoxicity (CDC), and direct apoptosis signaling.
Oral small-molecule BCL-2 inhibitor that promotes mitochondrial apoptosis in malignant B cells.
Selective oral BCL-2 inhibitor that mimics BH3-only proteins and binds the BCL-2 hydrophobic groove, blocking its anti-apoptotic function and restoring intrinsic (mitochondrial) apoptosis in BCL-2–dependent tumor cells; spares BCL-XL compared with navitoclax.
Venetoclax inhibits anti-apoptotic BCL-2, releasing BH3 activators to trigger BAX/BAK activation, mitochondrial outer membrane permeabilization, cytochrome c release, and caspase-dependent apoptosis in BCL-2–dependent cells.
A humanized IgG1 monoclonal antibody given subcutaneously that binds c-Kit (CD117) and blocks stem cell factor (SCF) signaling, leading to inhibition/depletion of c-Kit–positive cells, particularly airway mast cells, to reduce early and late allergic bronchoconstriction and airway hyperresponsiveness; may also impact c-Kit+ hematopoietic progenitors.
Humanized IgG1 monoclonal antibody targeting c‑Kit (CD117) that blocks stem cell factor (SCF) signaling, leading to functional inhibition and depletion of c‑Kit–positive cells—particularly airway mast cells—thereby reducing allergic activation/bronchoconstriction and airway hyperresponsiveness; may also affect c‑Kit+ hematopoietic progenitors.
Humanized IgG1 anti–c-Kit binds CD117 on target cells, blocks SCF survival signaling, and via its Fc engages immune effectors (NK cells/macrophages, complement) to mediate ADCC/ADCP/CDC, leading to depletion/apoptosis of c‑Kit–positive cells.