The promise of
IGC-AD1
To improve the quality of life of Alzheimer’s patients and their caregivers with a new oral formulation that has shown promising results in pre-clinical and clinical studies.
The FIRST natural cannabis-based formulation to treat Alzheimer’s Disease with low doses of THC (a psychoactive cannabinoid) as its main active ingredient
The ONLY natural THC-based drug candidate currently undergoing FDA trials
registered on clinicaltrials.gov
IGC-AD1 is a liquid oral solution
IGC-AD1 Timeline
2022
Phase II Clinical Trial to evaluate the efficacy of IGC-AD1 begins.
Patent IGC-507B is granted to IGC for Alzheimer’s Disease in the U.S.
2021
Phase I Clinical Trial for safety and tolerability in participants with Alzheimer’s Disease is completed successfully.
Patent IGC-507A is granted to IGC for Alzheimer’s Disease in the U.S.
2019
IGC-AD1 is approved as an Investigational New Drug (IND). Approval # 146069
2017
The development of IGC-AD1’s oral formulation begins.
2000
Pre-clinical trials begin on IGC-AD1’s active ingredient.
Ongoing
Phase II
Clinical Trial
“Trial of the Safety and Efficacy of IGC-AD1 on Agitation in Participants with Dementia due to Alzheimer’s Disease”
We are currently conducting a clinical trial at 5-7 sites in the U.S.
and Canada with a target number of 146 participants.
What is THC?
- D9-tetrahydrocannabinol (THC) is the most psychoactive compound found in the cannabis plant.
- It is in the cannabinoid class along with cannabidiol (CBD).
- THC and other phytocannabinoids are found on the trichome glands of cannabis flowers.
- D9-THC is the main active ingredient in IGC-AD1.
How is THC
obtained
from cannabis?
How is THC
obtained
from cannabis?
Why THC & Alzheimer’s
Disease?
THC promotes neurogenesis.
It also may protect the brain from inflammation and oxidative stress, which restores memory and cognitive function.
Low doses of THC have shown promising fibril content reduction in Alzheimer’s patients’ brains.
Results of our Pre-Clinical Studies
Pre-Clinical Studies
Based on pre-clinical data on Alzheimer’s cell lines and transgenic mice, we hypothesize that our formulation is a potential Disease Modifying Drug that could:
-
Reduce Aβ production and aggregation, while maintaining precursor (APP) levels.
-
Inhibit protein GSK3β, which is involved in protein tau expression.
-
Enhance mitochondrial function.
-
Improve spatial memory.
-
Achieve all the above with no neurotoxicity.
More detailed information
about pre-clinical studies’ results
The active THC in IGC-AD1 inhibits Aβ40 peptide production and Aβ42 aggregation in Alzheimer’s cell lines.
Representation of Cao et al., 2014
In Alzheimer’s cell line tests, the active THC in IGC-AD1 increased Aβ monomers in a dose dependent manner and decreased Aβ aggregation
Representation of Cao et al., 2014
The active ingredients in IGC-AD1 (THC and Melatonin) did not reduce APP levels in Alzheimer’s cell lines.
The Amyloid Precursor Protein (APP) modulates cell growth, motility, and survival; it is cleaved to create small fragments such as the Aβ peptide.
Representation of Cao et al., 2014
Memory Improved in Alzheimer’s Mice Model
In the Morris Water Maze test, mice treated with the active ingredient in IGC-AD1 significantly improved times and made less errors than those in the control group.
Nature Protocols. 2006; 1: 848-858; Int. J. Mol. Sci. 2022, 23, 2757
In a period of 48 hours, repeated low-dose exposure to the active THC in IGC-AD1 was not toxic to Alzheimer’s cells.
-
Aβ Production
& Aggregation -
The active THC in IGC-AD1 inhibits Aβ40 peptide production and Aβ42 aggregation in Alzheimer’s cell lines.
Representation of Cao et al., 2014 - Aβ Monomers
-
In Alzheimer’s cell line tests, the active THC in IGC-AD1 increased Aβ monomers in a dose dependent manner and decreased Aβ aggregation
Representation of Cao et al., 2014 - APP Levels
-
The active ingredients in IGC-AD1 (THC and Melatonin) did not reduce APP levels in Alzheimer’s cell lines.
The Amyloid Precursor Protein (APP) modulates cell growth, motility, and survival; it is cleaved to create small fragments such as the Aβ peptide.Representation of Cao et al., 2014
- Spatial Memory
-
Memory Improved
in Alzheimer’s Mice ModelIn the Morris Water Maze test, mice treated with the active ingredient in IGC-AD1 significantly improved times and made less errors than those in the control group.
Nature Protocols. 2006; 1: 848-858; Int. J. Mol. Sci. 2022, 23, 2757 - Neurotoxicity
-
Over a 48-hour period, repeated exposure to low doses of active THC in IGC-AD1 resulted in no toxicity to Alzheimer’s cells.
Representation of Cao et al., 2014
Representation of Cao et al., 2014
In Alzheimer’s cell line tests, the active THC in IGC-AD1 increased Aβ monomers in a dose dependent manner and decreased Aβ aggregation
Representation of Cao et al., 2014
The active ingredients in IGC-AD1 (THC and Melatonin) did not reduce APP levels in Alzheimer’s cell lines.
The Amyloid Precursor Protein (APP) modulates cell growth, motility, and survival; it is cleaved to create small fragments such as the Aβ peptide.
Representation of Cao et al., 2014
Memory Improved
in Alzheimer’s Mice Model
In the Morris Water Maze test, mice treated with the active ingredient in IGC-AD1 significantly improved times and made less errors than those in the control group.
Over a 48-hour period, repeated exposure to low doses of active THC in IGC-AD1 resulted in no toxicity to Alzheimer’s cells.
Representation of Cao et al., 2014
Our Phase1
Clinical Trial showed that IGC-AD1 is safe and tolerable at different doses.
Phase 1, Clinical Trial
In 2021, IGC completed a Phase 1 medical trial to evaluate the safety and tolerability of IGC-AD1 at three different daily doses.
This is the first such clinical study of its kind completed on Alzheimer’s patients
Overall Study Design
- Participants with mild to severe Alzheimer’s disease
- Multiple Ascending Dose (MAD)
- Three dosage cohorts: once a day (QD), twice a day (BID), and three times a day (TID)
- Double Blind
Objectives
Primary
Evaluate safety & tolerability of IGC-AD1
measured by solicited and non-solicited Adverse Events.
Secondary
Compare pre and post intervention neuropsychiatric symptoms (NPS) scores 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
Neuropsychiatric
Symptoms Results
- Results on NPS
-
Results on NPS: Neuropsychiatric Symptoms Measured by NPI Scores
GC-AD1 intervention showed an overall improvement in NPS measured by the (NPI) score.
Specific domains such as Agitation, Anxiety, Depression, and Caregiver Distress improved.
- Results on Agitation
-
Agitation Results
The NPI domain score for agitation was measured at baseline and remeasured on day 15.
At three different doses, agitation improved both clinically and statistically (p <05).
- Results on Anxiety and Drepression
-
IGC-AD1 decreased the NPI score in both the Anxiety and Depression domains.
Results on NPS: Neuropsychiatric Symptoms Measured by NPI Scores
GC-AD1 intervention showed an overall improvement in NPS measured by the (NPI) score.
Specific domains such as Agitation, Anxiety, Depression, and Caregiver Distress improved.
Agitation Results
The NPI domain score for agitation was measured at baseline and remeasured on day 15.
At three different doses, agitation improved both clinically and statistically (p <05).
IGC-AD1 decreased the NPI score in both the Anxiety and Depression domains.
Results on NPS: Neuropsychiatric Symptoms Measured by NPI Scores
IGC-AD1 intervention showed an overall improvement in NPS measured by the (NPI) score.
Specific domains such as Agitation, Anxiety, Depression, and Caregiver Distress improved.
Agitation Results
The NPI domain score for agitation was measured at baseline and remeasured on day 15.
At three different doses, agitation improved both clinically and statistically (p <05).
IGC-AD1 decreased the NPI score in both the Anxiety and Depression domains.
