16C11

16C11 is a murine monoclonal antibody (mAb) that specifically targets the C-terminal region of the amyloid-beta (Aβ) peptide, specifically residues 33–42. Developed by Elan Pharmaceuticals in collaboration with Wyeth, it was a foundational research tool in the landmark study by Bard et al. (2000) which demonstrated that passive immunization could reduce amyloid plaque burden in Alzheimer's disease mouse models. The antibody is capable of crossing the blood-brain barrier in small amounts, where it binds to existing amyloid deposits and triggers microglial cells to clear these plaques via Fc receptor-mediated phagocytosis. While 16C11 successfully demonstrated the potential of passive immunotherapy, it was primarily used as a tool compound to understand the mechanisms of amyloid clearance, while N-terminal directed antibodies like 3D6 (the precursor to bapineuzumab) were prioritized for clinical development.

Other names

mAb 16C11mAb16C11mAb-16C11anti-Abeta 16C11anti-Abeta16C11anti-Abeta-16C11