Repurposing BT-11 to Treat Alzheimer’s Disease: Exploring the Glutathione-s-transferase LANCL2 as a Target
type: CreativeWork
description: Approximately 99.6% of potential Alzheimer’s drugs fail, thus developing successful drugs is a high priority. The failure at developing successful drugs relates to the complex nature of the disease itself. Many components act together to trigger a cascade that ultimately results in neurodegeneration and cognitive dysfunction associated with the disease. In building a multiplex model of Alzheimer’s it is important to understand its specific biological mechanisms. One of these key pathological mechanisms is neuroinflammation. Understanding the pathways involved in neuroinflammation in Alzheimer’s is an urgent need, as it poses a promising avenue for future effective therapeutics. Specifically, as many investigational and FDA approved drugs targeting inflammation already exist, repurposing drugs is a useful approach, and this avenue provides for a less expensive and quicker process than developing new pharmaceuticals. One of such drugs is BT-11, which is an orally active lanthionine synthetase C-like 2 (LANCL2) binding compound, shown to reduce inflammation in the gut and improve cognitive function. Additionally, LANCL2 was identified as a glutathione-s-transferase, suggesting a role in removing toxins and reducing oxidative stress. BT-11 was predicted to have potential to treat Alzheimer’s, based on in silico studies for drug repurposing. The overall GOAL of my studies was to explore the potential of the investigational drug BT-11 and its mechanisms to treat Alzheimer’s. My central hypothesis was that activation of the LANCL2 pathway with BT-11 prevents or diminishes the progression of Alzheimer’s. The RATIONALE of my studies was that understanding the effects and mechanisms by which BT-11 potentially prevents or diminishes disease progression, will advance the development of novel therapeutics and their target, LANCL2, to treat Alzheimer’s. The results of my studies to test the central hypothesis are addressed in the following chapters: 1. BT-11 treatment alleviates …
abstract: Approximately 99.6% of potential Alzheimer’s drugs fail, thus developing successful drugs is a high priority. The failure at developing successful drugs relates to the complex nature of the disease itself. Many components act together to trigger a cascade that ultimately results in neurodegeneration and cognitive dysfunction associated with the disease. In building a multiplex model of Alzheimer’s it is important to understand its specific biological mechanisms. One of these key pathological mechanisms is neuroinflammation. Understanding the pathways involved in neuroinflammation in Alzheimer’s is an urgent need, as it poses a promising avenue for future effective therapeutics. Specifically, as many investigational and FDA approved drugs targeting inflammation already exist, repurposing drugs is a useful approach, and this avenue provides for a less expensive and quicker process than developing new pharmaceuticals. One of such drugs is BT-11, which is an orally active lanthionine synthetase C-like 2 (LANCL2) binding compound, shown to reduce inflammation in the gut and improve cognitive function. Additionally, LANCL2 was identified as a glutathione-s-transferase, suggesting a role in removing toxins and reducing oxidative stress. BT-11 was predicted to have potential to treat Alzheimer’s, based on in silico studies for drug repurposing. The overall GOAL of my studies was to explore the potential of the investigational drug BT-11 and its mechanisms to treat Alzheimer’s. My central hypothesis was that activation of the LANCL2 pathway with BT-11 prevents or diminishes the progression of Alzheimer’s. The RATIONALE of my studies was that understanding the effects and mechanisms by which BT-11 potentially prevents or diminishes disease progression, will advance the development of novel therapeutics and their target, LANCL2, to treat Alzheimer’s. The results of my studies to test the central hypothesis are addressed in the following chapters: 1. BT-11 treatment alleviates …
author: Birnbaum, Emily
keywords: Biology, Disease Modeling, Molecular and Cellular Neuroscience, LANCL2, BT-11
date published: 2024-09-01T07:00:00Z
date modified: 2026-07-24T01:59:38Z
provider: City University of New York - Graduate Center
publisher: Networked Digital Library of Theses and Dissertations
type: WebPage
source organization: The Graduate School and University Center of The City University of New York