IGC Pharma highlights preclinical data on IGC-M3

IGC Pharma (IGC) announced preclinical results for IGC-M3, a novel small molecule designed to address multiple biological drivers of Alzheimer’s disease. IGC-M3 demonstrated activity in laboratory models against beta-amyloid aggregation, oxidative stress, mitochondrial dysfunction, and neuroinflammation, four key contributors to Alzheimer’s pathology. The findings underscore IGC Pharma’s dual-pronged strategy in Alzheimer’s disease, which includes: IGC-AD1 – A proprietary, cannabinoid-based formulation currently in Phase 2 clinical trials for agitation in Alzheimer’s disease, with potential disease-modifying effects under investigation. IGC-M3 – A multifunctional, next-generation small molecule with the potential to impact multiple disease mechanisms, currently in preclinical development. With natural-cannabinoid based IGC-AD1 approaching critical Phase 2 milestones and synthetic IGC-M3 progressing through preclinical development, IGC Pharma is positioned to deliver multiple data-driven catalysts in FY2026 that could create lasting value for patients, caregivers, and shareholders alike. Reducing Harmful Amyloid Clumps: In biochemical assays, IGC-M3 prevented over 90% of the formation of beta-amyloid fibrils – a type of protein buildup linked to Alzheimer’s – when tested at equal concentrations in the lab. It also helped break apart existing amyloid clumps in a dose-dependent way, with an effective concentration of about 7.9 micromolar. This suggests IGC-M3 may help keep these proteins in a safer, non-clumped form. Balancing Metal Ions: Parts of IGC-M3’s structure allow it to bind certain metal ions, like copper and zinc, which have been linked to Alzheimer’s disease. Lab tests confirmed that IGC-M3 can attach to these metals, which may help reduce metal-related oxidative stress and protein clumping in the brain. Powerful Antioxidant Properties: In antioxidant tests, IGC-M3 outperformed vitamin C in neutralizing harmful free radicals. It also helped protect human nerve cells from oxidative stress caused by hydrogen peroxide, improving their survival in the lab. Protecting Mitochondria and Preventing Cell Death: IGC-M3 reduced signs of mitochondrial damage caused by beta-amyloid, such as loss of membrane potential, increased oxidative molecules, and release of cytochrome c. It also lowered cell death rates without harming healthy cells. Reducing Brain Inflammation: In a model of brain immune cell activity, IGC-M3 lowered levels of a protein marker of inflammation, restored normal cell shape, and reduced stiffness and stickiness of the cells. It also decreased levels of inflammation-related molecules, including TNF-alpha, IL-6, and NF-B. Although these findings are in vitro models, the breadth of biological effects observed suggests that M3 has the potential to modulate multiple pathways in the Alzheimer’s disease cascade. The Company expects that M3 will advance to in vivo studies to evaluate potential efficacy and safety in animal models. If benefits are confirmed, M3 could represent a promising candidate for the development of disease-modifying treatments aimed at slowing or halting neurodegenerative progression in Alzheimer’s disease.