The promise of
IGC-AD1
Pre-clinical and Phase 1 studies indicate that IGC-AD1 could safely reduce the debilitating symptoms that impact millions of Alzheimer’s patients.
Low doses of THC, a natural component of cannabis, can provide medical benefits.
The Phase 1 and Phase 2 trials are registered on clinicaltrials.gov
Our Phase II
clinical trial brings hope
As millions of Alzheimer’s patients present agitation, our ongoing Phase 2 trial brings hope for a treatment.
Clinical trial includes up to 10 sites in the U.S. and Canada with a target of 146 participants.
Why IGC-AD1 & Alzheimer’s?
IGC-AD1 contains two Active Pharmaceutical Ingredients (APIs),
one of them is THC.
The APIs in IGC-AD1 have been shown to reduce the plaque build-up associated with Alzheimer’s.
The API have been shown to promote mitochondrial functioning and the regeneration of neurons.
The API have been shown to restore spatial memory in a mouse model of Alzheimer’s.
Pre-clinical study results
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
that lead to memory loss. -
Inhibit the formation of plaques.
-
Enhance mitochondrial functioning.
-
Improve spatial memory.
Phase 1 clinical trial
results
The Phase 1 Clinical trial included patients with mild to severe Alzheimer’s. The trial showed that:
- IGC-AD1 is safe and tolerable at three different dosage levels.
- Caregiver distress, and Neuropsychiatric Symptoms (NPS), including agitation, anxiety, and depression improved.
- The impact of IGC-AD1 on the Neuropsychiatric Inventory (NPI) score for agitation was improved at all three dosage levels.
- IGC-AD1 also decreased the NPI score for both anxiety and depression.
As an oral liquid solution, IGC-AD1 could be an effective, simpler treatment option for patients
IGC-AD1 Timeline
2017
IGC Pharma begins development of the IGC-AD1 oral formulation
2019
IGC-AD1 is approved by the FDA as an investigational new drug
2021
Phase 1 clinical trial testing safety and tolerability in humans with Alzheimer’s successfully completed
IGC-AD1 is awarded patent protection in the U.S.
2022
Phase 2 clinical trial to evaluate the efficacy of IGC-AD1 begins
Additional patent awarded protecting IGC-AD1 formulation
Learn more about THC and Cannabis
- THC (∆9-tetrahydrocannabinol) is a psychoactive compound in the cannabis plant that is commonly associated with a euphoric high at high doses
- A low dose of THC is an active pharmaceutical ingredient in IGC-AD1
- The FDA has approved synthetic THC-based formulations for treating nausea and vomiting caused by chemotherapy
How is THC obtained from cannabis? IGC Pharma has production capabilities to safely
and legally procure THC from cannabis at scale
How is THC
obtained
from cannabis?
IGC Pharma has production capabilities to safely and legally procure THC from cannabis at scale.
Pre-clinical studies:
Detailed scientific results
IGC-AD1 reduces Aβ40 peptide production and Aβ42 aggregation in Alzheimer’s cell lines.
Representation of Cao et al., 2014
In Alzheimer’s cell line tests, IGC-AD1 increased Aβ monomers and decreased Aβ aggregation in a dose–dependent manner and decreased Aβ aggregation.
Representation of Cao et al., 2014
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. Representation of Cao et al., 2014
Memory Improved in Alzheimer’s Mice Model
In a Morris Water Maze test, mice dosed with the active agent 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 with IGC-AD1. group.
Nature Protocols. 2006; 1: 848-858; Int. J. Mol. Sci. 2022, 23, 2757
Over 48 hours, repeated low-dose exposure to IGC-AD1 was not toxic to Alzheimer’s cells.
-
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 ModelIn 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.
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
Phase1
Clinical Trial
Overall Study Design:
Participants with mild to severe Alzheimer’s disease
Participants were sequentially administered three doses over 14 days: once a day (QD), twice a day (BID), and three times a day (TID)
Double-blind
Objectives
Primary
Evaluate safety and tolerability of IGC-AD1 measured by patient-reported and observed Adverse Events.
Secondary
Measure any changes to neuropsychiatric symptoms (NPS) as measured by the neuropsychiatric inventory (NPI-12).
Demographics
Female
69.2%
Male
30.8%
Age
80.46 ± 5.71 y.o.
Weight
147.66 ± 31.62 lb.
Height
5.28 ± 0.46 ft.
BMI
41.77 ± 8.86
Phase 1 Clinical Study Results
- Results on NPS
-
Results on NPS: Neuropsychiatric Symptoms Measured by NPI Scores
Patients taking IGC-AD1 intervention showed an overall improvement in NPS, and specifically in agitation, anxiety, and depression domains. Caregiver distress improved as well.
- Results on Agitation
-
Results on Agitation
At all three dosages, agitation improved both clinically and statistically (p <05).
- Results on Anxiety and Depression
-
IGC-AD1 decreased the NPI scores for the anxiety and depression domains.
Results on NPS: Neuropsychiatric Symptoms Measured by NPI Scores
Patients taking IGC-AD1 intervention showed an overall improvement in NPS, and specifically in agitation, anxiety, and depression domains. Caregiver distress improved as well.
Results on Agitation
At all three dosages, agitation improved both clinically and statistically (p <05).
IGC-AD1 decreased the NPI scores for the anxiety and depression domains.
Results on NPS:
Patients taking IGC-AD1 intervention showed an overall improvement in NPS, including
agitation, anxiety, depression, and caregiver distress.
Agitation Results
At all three dosages, agitation improved both clinically and statistically (p <05).
IGC-AD1 decreased the NPI score for both the anxiety and depression.
IGC-AD1 decreased the NPI score in both the Anxiety and Depression domains.
