AGT‑160 is an investigational brain-penetrating anti-amyloid antibody (AAA) for the treatment of Alzheimer’s disease (AD).1 AD is caused by deposition of amyloid plaque in the brain, and administration of an AAA can break down plaque. However, the plaque in the brain is behind the BBB, and an AAA cannot penetrate the brain without disrupting the BBB. Additionally, the current class of AAA biologics can cause large and sustained elevations in blood concentrations of toxic molecules called amyloid peptides. AGT-160’s ability to cross the BBB allows AGT-160 to break down plaque without causing toxic side effects associated with high blood levels of amyloid peptide.1

In preclinical studies, AGT-m160 was rapidly removed from the blood.2 Additionally, in a mouse model of AD, IV injection of AGT-160 caused a 40-60% decrease in the brain concentration of ABeta amyloid peptide, but caused no elevation in ABeta amyloid peptide in the blood, and caused no cerebral micro-hemorrhage.3,4


1 Boado, RJ, Zhang, YF, Zhang, Y, Xia, C-F, Pardridge, WM (2007) Genetic engineering of a fusion antibody with bi-directional blood-brain barrier transport and Abeta fibril disaggregation. Bioconj. Chem. 18:447-455

2 Boado RJ, Zhou QH, Lu JZ, Hui EK, Pardridge WM (2010) Pharmacokinetics and brain uptake of a genetically engineered bifunctional fusion antibody targeting the mouse transferrin receptor. Mol Pharm. 7:237-44

3 Zhou QH, Fu A, Boado RJ, Hui EK, Lu JZ, Pardridge WM (2011) Receptor-Mediated Abeta Amyloid Antibody Targeting to Alzheimer’s Disease Mouse Brain. Mol Pharm. 8:280-5

4 Sumbria RK, Hui EK, Lu JZ, Boado RJ, Pardridge WM (2013) Disaggregation of amyloid plaque in brain of Alzheimer’s disease transgenic mice with daily subcutaneous administration of a tetravalent bispecific antibody that targets the transferrin receptor and the abeta amyloid Peptide. Mol Pharm. 10:3507-13