BACE is a cleaving enzyme of aspartyl protease with beta-secretase activity. It acts as a precursor of beta-amyloid (Aβ) protein. In Alzheimer’s disease, the Aβ protein fragments get accumulated in plaques in the brain. BACE initiates Aβ production by cleaving amyloid precursor protein (APP) to generate APPβ and C99, which is critical for the subsequent cleavage of C99 by gamma-secretase to release Aβ1-40 and Aβ1-42. Inhibition of BACE enzyme disrupts the production of toxic Aβ and forms plaque and new soluble oligomers.
Alzheimer’s disease is a common type of dementia and a fatal illness. It includes memory loss and loss of other intellectual abilities, which results in serious interference with daily life. Around 60% to 80% of dementia cases turn out to be Alzheimer’s disease. It causes problems with behavior, thinking and memory. Symptoms usually develop at a slow rate and become worse with time, causing severe interference with daily routine. The efficient inhibition of BACE is expected to stop the progression of Alzheimer’s disease. BACE inhibitors as drug candidates will block Aβ enzyme, which would prevent the buildup of beta-amyloid and may also help to reduce or halt Alzheimer’s disease.
Although significant progress has been witnessed in BACE inhibitor development, studies are still focused on BACE inhibitors with high potential, and reduced or no side effects. Also, even after promising growth in the development of BACE inhibitors, BACE therapeutics for Alzheimer’s disease treatment are still not available in the market due to the difficulty in the designing of BACE1 inhibitor drugs that can pass the blood–brain barrier.
As of February 2017, the BACE inhibitors pipeline comprised 15 product candidates in different stages of development.
Some of the key players developing BACE inhibitors pipeline are AstraZeneca plc, Eli Lilly & Company and Merck & Co and others.
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