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Pre-clinical

Preclinical studies have allowed us to identify the potential of IGC-AD1 to be an AD-modifying drug. The combination of the active ingredients at low, non-toxic concentrations was shown to reduce Aβ aggregation in N2aAβPPswe cells, maintain APP levels, and enhance mitochondrial function in a dose-dependent manner.

Pre-clinical
Study results

pre-clinical studies
The pre-clinical studies tested the API in IGC-AD1 on Alzheimer’s cell lines and Alzheimer’s mouse models  and found that it had the potential to be a disease modifying drug that could: 
  • Inhibit the formation of neurofibrillary tangles
  • Inhibit the formation of plaques.
  • Enhance mitochondrial functioning.
  • Improve spatial memory.

Pre-clinical studies:
Detailed scientific results

  • Aβ Production
    & Aggregation

  • The API in IGC-AD1 reduces Aβ40 peptide production and Aβ42 aggregation in Alzheimer’s cell lines.
    Representation of Cao et al., 2014
  • Aβ Monomers

  • In Alzheimer’s cell lines, IGC-AD1 increased Aβ monomers and decreased Aβ aggregation in a dose-dependent manner.

    Representation of Cao et al., 2014

  • APP Levels

  • The APIs in IGC-AD1 did not reduce Amyloid Precursor Protein (APP) levels in Alzheimer’s cell lines. APP modulates cell growth, motility, and survival; it is cut to create small fragments such as the Aβ peptide that eventually deposit as plaque. 
    Representation of Cao et al., 2014
  • Spatial Memory

  • Memory Improved
    in Alzheimer’s Mice Model

    In a Morris Water Maze test, mice dosed with the API in IGC-AD1 had significantly improved times and less errors than those in the control group demonstrating that memory improved in transgenic (APP/PS1) mice.

    Nature Protocols. 2006; 1: 848-858; Int. J. Mol. Sci. 2022, 23, 2757
  • Neurotoxicity

  • Over 48 hours, repeated low-dose exposure to the API in IGC-AD1 was not toxic to Alzheimer’s cells (N2a/AßPPsWe cells). 
    Representation of Cao et al., 2014
The API in IGC-AD1 reduces Aβ40 peptide production and Aβ42 aggregation in Alzheimer’s cell lines.
Representation of Cao et al., 2014
In Alzheimer’s cell lines, IGC-AD1 increased Aβ monomers and decreased Aβ aggregation in a dose-dependent manner.

Representation of Cao et al., 2014

The APIs in IGC-AD1 did not reduce Amyloid Precursor Protein (APP) levels in Alzheimer’s cell lines. APP modulates cell growth, motility, and survival; it is cut to create small fragments such as the Aβ peptide that eventually deposit as plaque. 
Representation of Cao et al., 2014

Memory Improved
in Alzheimer’s Mice Model

In a Morris Water Maze test, mice dosed with the API in IGC-AD1 had significantly improved times and less errors than those in the control group demonstrating that memory improved in transgenic (APP/PS1) mice.

Nature Protocols. 2006; 1: 848-858; Int. J. Mol. Sci. 2022, 23, 2757
Over 48 hours, repeated low-dose exposure to the API in IGC-AD1 was not toxic to Alzheimer’s cells (N2a/AßPPsWe cells). 
Representation of Cao et al., 2014