Preclinical:
 The Research Powering IGC-AD1

IGC-AD1 springs from rigorous Preclinical testing and a people-first approach. In the lab, at low, non-toxic doses, its ingredient combination aimed to slow key Alzheimer’s Disease processes 
and showed encouraging signals.

Early Lab Discoveries
That Inspire Hope

Preclinical studies laid the groundwork for IGC-AD1 by testing its dual active ingredients in Alzheimer’s cell models and mouse models.

Preclinical Signals
in Mice

Mice treated with IGC-AD1 AP1 improved their spatial memory by about 50% and showed better mitochondrial function—crucial 

Reduces Key
Alzheimer’s Features

The therapy decreased the buildup of amyloid-beta (Aβ) plaques by 20% and maintained healthy APP levels in cell studies

Behavior-focused, with additional 
Preclinical signals
In preclinical models, IGC-AD1’s ingredients showed better spatial memory performance and improved mitochondrial markers, alongside effects on Aβs.

The science behind IGC-AD1: early indicators
that matter for Alzheimer’s Disease research

  • 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

Explore Our Development Path

Phase I:
Clinical trial

The study involved participants with mild-to-moderate Alzheimer’s Disease to evaluate the safety and tolerability of IGC-AD1.

Learn more
Phase II:
CALMA

CALMA is a multicenter Phase 2 clinical trial designed to evaluate the safety and efficacy of IGC-AD1 for treating agitation associated with Alzheimer’s dementia.

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