Our Science

Leveraging our deep understanding of amyloid beta oligomers to usher in a medical breakthrough for Alzheimer’s disease.

Amyloid Beta (Aβ) Species in Alzheimer’s Disease

In Alzheimer’s patients, five dominant pools of Aβ species have been identified: Aβ monomers, Aβ oligomers (AβOs), protofibrils, fibrils, and amyloid plaques.1

Historically, the primary focus of Alzheimer’s drug development efforts has been on Aβ monomers and amyloid plaques.2,3

Focusing on Toxic AβOs

Acumen’s therapeutic target for Alzheimer’s disease is different from historical approaches.
Decades of research support the hypothesis that soluble AβOs are the most toxic form of Aβ. AβOs are an early trigger and persistent driver of Alzheimer’s-associated pathology and neurodegeneration.1,2,4

The accumulation of AβOs disrupts brain circuitry, preventing neurons from signaling properly, and is associated with synapse deterioration, tau hyper-phosphorylation, and inflammation.1,4

Targeting Toxic AβOs with ACU193

Recent studies suggest that eliminating the toxic soluble species from the neuronal system may enable damaged circuits to regain some of their function.3

Enter ACU193, an anti-AβO monoclonal antibody (mAb) developed to selectively target and inhibit toxic soluble AβOs, preventing them from binding to synapses, and thereby preserving or restoring neuronal function. This mechanism of action gives ACU193 the potential to be the best-in-class treatment, providing superior efficacy and safety.1,3

ACU193: The First Immunotherapy Drug Candidate Targeting Toxic Soluble AβOs

ACU193 is a monoclonal antibody that is distinguished from other anti-Aβ mAbs for several reasons:

  • Highly selective for soluble oligomers, the toxic Aβ species; other anti-Aβ mAbs are less selective and/or target different amyloid species, such as monomers, fibrils, or plaques1,2,4
  • Designed to provide improved clinical efficacy with lower rate of ARIA (amyloid-related imaging abnormalities) as compared to anti-plaque mAbs1,2
  • Potential for cognitive improvement in addition to slowing of disease progression2
  • Prevents toxic soluble AβOs from binding to synapses, thereby preserving or resorting neuronal function2