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Small Molecules: Hit identification
Small Molecules: Hit-to-Lead optimization
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Small Molecules: ADME
Small Molecules: Toxicity
Small Molecules: Selectivity
Antibodies: Humanization and Optimization
Protein Modeling. Discovery
Protein Modeling: HERG binding
Protein Modeling: Albumin binding
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Beta Secretase
It is estimated that 3 percent of people aged 65 to 74 have Alzheimer's, a prevalence that may reach nearly 50 percent among those 85 and older. By 2020, 30 million people will be affected by this devastating disorder worldwide and by 2050, the number could increase to 45 million.
Alzheimer's disease is a progressive, irreversible brain disorder with no known cause or cure. Symptoms of the disease include memory loss, confusion, impaired judgment, personality changes, disorientation, and loss of language skills. Always fatal, Alzheimer's disease is the most common form of irreversible dementia. Current therapy, though offering modest cognitive benefits to many patients with mild to moderate disease, does not halt or even slow the underlying neurodegeneration.
Many researchers believe that amyloid plaques play a central role in Alzheimer’s disease. They believe that these plaques disturb neural communication and elicit an inflammatory response leading to neuronal degeneration. Although it is still under debate, if the "amyloid hypothesis"—the thesis that amyloid plaques are the cause of Alzheimer’s, is correct, then a medicine that blocks formation of plaques should lead to a better therapy.
Beta-secretase cleaves the amyloid precursor protein into toxic fragments. It is these fragments, known as beta-amyloid peptides, which aggregate to form amyloid plaques. By inhibiting beta-secretase, it should be possible to stop the production of the amyloid plaques and create an effective medicine for Alzheimer’s disease.
