Approximately 99.6% of potential Alzheimer’s drugs fail, thus developing successful drugs is a high priority. Therapeutic strategies aimed at treating two key hallmarks of AD, amyloid plaques and tau tangles, have so far been unsuccessful at halting or reversing disease progression. Thus, there are no known current therapeutics for AD that can prevent the progression of the disease. Research points towards the pathology of neuroinflammation as an important target for treatment of AD. We expect BT-11 to halt or mitigate neuroinflammation by activating the LANCL2 signaling, which is an important modulator of inflammation acting as an anti-inflammatory pathway. Thus, we expect BT-11 to reduce AD pathology, including neuroinflammation, neuronal loss and memory deficits.
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