Our strategy
Vision
Alzheimer’s disease patients show two distinct types of lesion: amyloid plaques and neurofibrillary tangles. A certain consensus has established in the pharmaceutical industry about amyloid plaques and their potential toxicity. The major part of drug candidates in development targets this issue so far without success. In some cases, lack of significant results and/or serious side effects were observed and led to product abandon.
AlzProtect suggests a different hypothesis: Amyloid plaques would not cause neurons degeneration but could be a consequence. According to this hypothesis, Alzheimer’s disease would be linked to a default in APP’s metabolism. Therefore, Alzprotect develops products that favor the "good" metabolic pathway of APP instead of blocking bad pathway (amyloidogenic pathway) that generates Abeta aggregates and plaques. Moreover, favoring this non-amyloidogenic pathway could lead to the production of peptides with neuroprotective properties.
Therapeutic strategy
AlzProtect identified a library of compounds that restore the APP metabolism balance favoring the non amyloidogenic pathway to the non amyloidogenic pathway.
These compounds both :
• reduce the amyloidogenic pathway biomarkers:
o Amyloid beta peptide
o APP-CTFbeta
• increase non amyloidogenic pathway biomarkers :
o CTF alpha
o sAPPalpha
This last fragment is known for its neuroprotective properties.
Competitive advantages
Molecules developed by Alzprotect have interesting properties :
- An original mode of action
- Pharmacological studies were realized with wild type mice rather than transgenic mice.
- These products have the potential to modify disease evolution by opposition with current medication that are only able to reduce symptoms with more or less disappointing resutls.
- These compounds are small molecules
- These chemicals are proprietary
