BAN2401 is an experimental drug, an engineered monoclonal (cell derived or formed from a single clone) antibody for Alzheimer's disease that is the result of a strategic research alliance between Eisai, a Japanese pharmaceutical company, and BioArtic, a Swedish research intensive biopharma company.
BAN2401 is in the clinical development stage as a possible treatment for people with mild cognitive impairment or mild Alzheimer's disease as it aims to target the hallmark amyloid plaques that are central in the Alzheimer's disease progression and in the destruction of brain cells.
BAN2401 was licensed to Eisai, and in March 2014, Eisai entered into a collaboration agreement with Biogen, a Boston biotechnology company, for joint development of this therapeutic antibody.
At the Alzheimer's Association International Conference in July, Eisai and Biogen announced results of an 18-month, Phase II clinical trial of BAN2401. The findings lent hope to Alzheimer's sufferers and their caregivers.
Alzheimer’s is the only cause of death among the top 10 diseases that cannot be prevented, cured or even slowed, according to the the association.
With the BAN2401 study, researchers endeavored to find a drug that would be able to reverse, stop or even slow the progression of this devastating disorder. The study targeted the amyloid deposits in the brain.
In Alzheimer's disease, neurons deteriorate and eventually die by two types of normal proteins that begin to accumulate in large quantities in the cerebral cortex of the brain. The first type of proteins are the beta-amyloid proteins, which, if not cleared from the brain, begin to surround brain cells massively, causing inflammation and the clogging of synapses, which interrupts neurotransmission, and eventually brain cells die.
The second types of protein are the twisted protein fibers known as "tangles" or "tau." These tau proteins form inside the neuron, which leads to degeneration.
Skeptics of this research study understand that BAN2401 does a good job of clearing out or reducing these beta-amyloid plaques from the brain, which in turn has a significant slowing in clinical decline of the affected person.
However, according to a July article at Fortune.com by Clifton Leaf, “this approach doesn't seem to flip the Alzheimer's switch, causing many in the field to doubt whether the ancient and vaunted 'amyloid hypothesis' is the right one (to target)."
At the beginning of the year, there were no less than 32 investigative research studies targeting the amyloid plaques in mid- to late-clinical trials, according to Jeffrey Cummings and his colleagues at the Cleveland Clinic Lou Ruvo Center for Brain Health.
Leaf said in his article that the failure rate for Alzheimer's drugs is 99.6 percent and that virtually every time the strategy of attacking or reducing amyloid plaques is researched in studies, it has failed.
BAN2401 continues to be in investigational research, but it will be many more years before clinical development is completed and approval from the Food and Drug Administration is attained.