News Release
InMed (NASDAQ: INM) Developing Cannabinoids Analogs To Treat Alzheimer's – New Studies Showcase INM-901's Therapeutic Abilities
Benzinga
By Meg Flippin, Benzinga Whether due to an aging population or overall population growth, cases of Alzheimer's are increasing. As it stands, nearly seven million Americans suffer from this disease that attacks memory and cognitive functions. By 2050, that’s forecast to reach close to 13 million people. The costs associated with treating Alzheimer's and dementia are projected to swell to $1 trillion by 2050 from $360 billion today. Alzheimer’s is the fifth leading cause of death for people 65 and older. There are several treatments on the market, but they focus on addressing the symptoms rather than repairing and regenerating the damaged neurons. Some drugs and treatments may slow the progression of cognitive decline, but none can reverse the effects of Alzheimer’s. That may change thanks to companies like InMed Pharmaceuticals Inc. (NASDAQ: INM). The leader in cannabinoid and cannabinoid analogs pharmaceutical research, development, manufacturing and commercialization has identified a rare cannabinoid to treat Alzheimer’s. Named INM-901 and based on early preclinical research, the cannabinoid analog showed potential to target several biological pathways associated with Alzheimer’s, providing neuroprotection to the brain neurons and improving neuronal function. Fighting Alzheimer’s With Cannabinoids Recent in vivo studies have shown that INM-901 can improve cognitive function and memory, locomotor activity, anxiety-based behavior, sound awareness and neuronal function. INM-901 also displayed neuroprotective effects by reducing cell death in an amyloid-beta-induced cytotoxicity study. Most recently, the company announced additional preclinical data demonstrating INM-901’s positive pharmacological effects. Several preclinical studies that were conducted in well-characterized Alzheimer’s models demonstrated that INM-901 was able to reduce neuroinflammation and improve neuronal function. The company said the studies also supported the observations made in previously released behavior studies in which locomotor activity, cognition and memory were improved. As a result of these studies, InMed said it plans to accelerate the development of its Alzheimer’s program. Currently, long-term behavioral and mechanism of action / receptor interaction studies are underway with data read-out expected in the third quarter. Meanwhile, InMed said the development of the chemistry, manufacturing and controls (CMC) for drug substance and oral drug product formulation are on-going. “The recent results demonstrating pharmacological effects in in vivo disease models continue to validate INM-901 as a potential treatment of AD,” said Dr. Eric Hsu, Senior Vice President of Preclinical Research and Development at InMed. “There continues to be a major unmet medical need for this multi-factorial disease and differentiated therapeutic mechanisms may play an important role. We believe the development of INM-901 may address several pathological factors including neuroinflammation, neuroprotection and neuritogenesis.” Multiple Mechanisms Of Action InMed said it is particularly encouraged that INM-901 has multiple potential ways of impacting the cannabinoid 1 (CB1) and cannabinoid 2 (CB2) receptors and the peroxisome proliferator-activated receptor (PPAR) signaling pathway. CB1 and CB2 receptors are part of the endocannabinoid system and are found throughout the body, including in the brain. CB1 receptors are primarily located in the central nervous system, particularly in areas involved in memory, cognition and motor function. CB2 receptors are involved in modulating neuroinflammation and immune responses. Activation of CB1 and CB2 receptors has been shown to help protect brain cells from damage and death. In Alzheimer’s where neuronal death is a hallmark feature, enhancing the activity of these receptors may help to slow down the progression of the disease, reports InMed. Activation of these receptors and other cellular receptors has also been shown to have an impact on neuroinflammation, which is believed to contribute to the progression of Alzheimer’s. As a result, InMed believes INM-901 could offer novel therapeutic strategies for the treatment of this devastating condition. Adding To Its Expertise To further develop INM-901, InMed is deepening its pedigree, and it recently added Dr. David G. Morgan, a renowned leader in neurodegenerative disease, to its Scientific Advisory Board. This reinforces InMed’s commitment to advancing its INM-901 program for the treatment of Alzheimer’s disease. Morgan is the director of the Alzheimer’s Alliance and MSU Foundation Professor of Translational Neuroscience at Michigan State University. His research interests are Alzheimer’s disease, aging and brain function. He is internationally recognized for his work on immunotherapy and gene therapy to treat Alzheimer-related pathologies. “We are privileged to welcome someone of Dr. Morgan’s stature to our SAB, which underscores the recent progress we’ve achieved in the INM-901 program. Dr. Morgan’s significant contributions and pioneering breakthroughs have made him a leading authority in Alzheimer’s research. His guidance and expertise will be invaluable as we advance to the next stages of development of our INM-901 program in the treatment of Alzheimer’s,” said Hsu. The number of Alzheimer’s cases is set to soar in the years to come as the population ages. InMed wants to slow that, and is betting INM-901 can help. So far studies are backing that up, with more data to come this year. Featured photo by Natasha Connell on Unsplash. Benzinga is a leading financial media and data provider, known for delivering accurate, timely, and actionable financial information to empower investors and traders. This post contains sponsored content. This content is for informational purposes only and not intended to be investing advice. Contact Details Benzinga +1 877-440-9464 info@benzinga.com Company Website http://www.benzinga.com
May 07, 2024 09:00 AM Eastern Daylight Time
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