InMed's INM-901 Demonstrates Favorable Pharmacological and Behavioral Effects in In Vivo Preclinical Alzheimer's Disease Studies
- Positive preclinical data for INM-901 in potential Alzheimer's disease treatment
- INM-901 demonstrates preferential signaling agonism for CB1/CB2 receptors and impacts the PPAR signaling pathway
- Reduction in neuroinflammation and improvement in neuronal function observed with INM-901
- INM-901 shows potential to target biological pathways associated with AD, including neuroprotection and improvement of neuronal function
- Promising results from preclinical studies with INM-901 in AD models
- None.
Insights
The announcement by InMed Pharmaceuticals Inc. regarding INM-901's preclinical data sheds light on the potential of cannabinoids in addressing neurodegenerative diseases, particularly Alzheimer's disease (AD). From a pharmaceutical research perspective, the multi-target approach of INM-901, engaging both CB1/CB2 receptors and the PPAR signaling pathway, is promising given the complex pathology of AD. The drug's preferential signaling agonism suggests specificity in its mechanism of action, which may translate to a therapeutic profile with fewer side effects compared to broad-spectrum agonists.
The impact of these findings on the pharmaceutical industry hinges on the successful transition from preclinical to clinical studies. It's important to note that while preclinical data are essential for understanding a drug's potential, the true test comes during human trials. The focus on neuroinflammation, neuroprotection and neuritogenesis aligns with current research suggesting these factors' roles in AD progression. If INM-901 maintains its efficacy and safety profile through clinical phases, it could position InMed as a notable player in the AD treatment market, potentially affecting the company's valuation and investor interest.
With Alzheimer's disease being a condition with limited effective treatments and a growing patient population, InMed's progress in developing INM-901 could have significant market implications. The biotech sector is highly sensitive to such preclinical study outcomes, as they can indicate a company's future revenue potential. Investors often look for breakthrough therapies that can fill unmet medical needs and INM-901's novel approach to targeting multiple pathways in AD could differentiate it from existing treatments that focus on amyloid plaque reduction.
Furthermore, the AD drug development space is competitive with major pharmaceutical companies investing heavily. InMed's success in advancing INM-901 through the pipeline could attract partnership opportunities or even make it a takeover target. While it's too early to predict market share, the long-term potential for InMed's stock hinges on the continued success of INM-901, including favorable data from upcoming long-term behavioral studies and the development of drug substance and oral drug product formulations.
Understanding the pharmacological effects of INM-901 in the context of Alzheimer's disease offers insights into potential treatment pathways that are currently underserved. The involvement of cannabinoid receptors in neuroprotection and the modulation of neuroinflammation is a relatively recent area of interest and INM-901's targeting of these receptors could represent a shift in how AD is treated. Moreover, the impact on the PPAR signaling pathway, which is associated with various metabolic processes, suggests a broader therapeutic potential that may benefit patients' overall health.
In the medical community, there is cautious optimism for treatments that show promise in preclinical models, yet the translation to human efficacy is notoriously challenging. The medical research community will be closely monitoring the progression of INM-901's clinical trials for both efficacy and safety outcomes. Positive results could lead to a paradigm shift in AD treatment and offer hope for patients and caregivers. However, it is important to remain objective and await robust clinical data before drawing conclusions about the drug's potential impact on patient care.
INM-901 receptor binding studies indicate preferential signaling agonism for CB1/CB2 and impacts the PPAR signaling pathway
In Vivo studies demonstrate INM-901 reduces neuroinflammation and improves neuronal function
Molecular analysis data further explains previously reported observations in behavioral studies on locomotion, memory and cognition
Vancouver, British Columbia--(Newsfile Corp. - April 4, 2024) - InMed Pharmaceuticals Inc. (NASDAQ: INM) ("InMed" or the "Company"), a leader in the manufacturing, development and commercialization of rare cannabinoids and proprietary cannabinoid analogs, today announced additional preclinical data demonstrating INM-901's positive pharmacological effects in the potential treatment of Alzheimer's disease ("AD").
Dr. Eric Hsu, Senior Vice President of Preclinical Research and Development at InMed, stated, "The recent results demonstrating pharmacological effects in in vivo disease models continue to validate INM-901 as a potential treatment of AD. We are particularly encouraged with indications that INM-901 has multiple potential mechanisms of action as a preferential signaling agonist for both cannabinoid 1 ("CB1") and cannabinoid 2 ("CB2") receptors, as well as impacting the peroxisome proliferator-activated receptor ("PPAR") signaling pathway. 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."
Several preclinical studies were conducted in well-characterized AD models. A summary of recent INM-901 preclinical study results includes:
INM-901 is a preferential signaling agonist of the CB1/CB2 receptors and impacts the PPAR signaling pathway,
INM-901 demonstrates reduced neuroinflammation and improved neuronal function,
INM-901 mRNA data supports the observations made in the previously released behavior studies in locomotor activity, cognition and memory.
Previous studies of INM-901 showed the potential to target several biological pathways associated with AD, including neuroprotection to the differentiated neuronal cells from beta-amyloid peptide-induced toxicity and improvement of neuronal function via extension of neurite length, a potential breakthrough in the treatment of AD.
The Role of CB1, CB2 and PPAR in the treatment of Alzheimer's
CB1 and CB2 receptors are both 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, while CB2 receptors are involved in modulating neuroinflammation and immune responses.
Activation of CB1 and CB2 receptors has been shown to have neuroprotective effects, meaning they can help protect brain cells from damage and death. In AD, where neuronal death is a hallmark feature, enhancing the activity of these receptors may help to slow down the progression of the disease. Activation of these receptors and other cellular receptors has also been shown to have an impact on neuroinflammation. As neuroinflammation is also believed to contribute to the progression of AD, targeting these receptors could help alleviate this inflammatory response. While further research is needed to fully understand the role of CB1 and CB2 receptors in AD, INM-901 could offer novel therapeutic strategies for the treatment of this devastating condition. (1)(2)
Peroxisome proliferator-activated receptors ("PPARs") are also considered potential therapeutic targets for neurodegenerative disorders such as AD. PPAR's are ligand-activated transcription factors of nuclear hormone receptor superfamily comprising of the following three subtypes: alpha ("PPAR-α"), gamma ("PPAR-γ"), and beta/delta ("PPAR-β/δ"). Activation of PPAR-α reduces triglyceride level and is involved in regulation of energy homeostasis. Activation of PPAR-γ causes insulin sensitization and enhances glucose metabolism, whereas activation of PPAR-β/δ enhances fatty acids metabolism. (3)(4)
Next steps advancing preclinical studies
InMed intends to accelerate the development of its AD program. Long-term behavioural and mechanism of action / receptor interaction studies are underway with data read-out expected in calendar 3Q 2024. Development of the chemistry, manufacturing and controls ("CMC") for drug substance and oral drug product formulation are on-going.
Limited treatment options for Alzheimer's disease - a major unmet medical need
Approved AD medications primarily address symptoms related to memory and cognitive function via the reduction of beta-amyloid plaques. These medications are aimed at removing amyloid plaque build-up between the neurons in the brain; however, they do not actively restore or rebuild deteriorating neurons and, thus, do not reverse AD progression. In addition, use of these treatments can be limited due to significant side effects, including inflammation and bleeding in the brain. Several large pharmaceutical companies such as Eli Lilly, Roche, AbbVie, Eisai and Biogen lead research and commercialization efforts in AD drug development.
References:
(1) Cannabinoid Receptors in the Central Nervous System: Their Signaling and Roles in Disease
(2) Cannabinoid CB2 Receptors in Neurodegenerative Proteinopathies: New Insights and Therapeutic Potential
(3) The peroxisome proliferator-activated receptor: A family of nuclear receptors role in various diseases
(4) PPARs in the central nervous system: roles in neurodegeneration and neuroinflammation
Learn more about InMed's INM-901 program:
https://www.inmedpharma.com/pharmaceutical/inm-901-for-alzheimers-disease/
About InMed:
InMed Pharmaceuticals is a global leader in the manufacturing, development and commercialization of rare cannabinoids and proprietary cannabinoid analogs. Together with our subsidiary, BayMedica LLC, we have unparalleled cannabinoid manufacturing capabilities to serve a spectrum of consumer markets, including pharmaceutical and health and wellness. We are a clinical-stage company developing a pipeline of rare cannabinoid therapeutics with programs in Alzheimer's disease, age-related macular degeneration, glaucoma, and epidermolysis bullosa. For more information, visit www.inmedpharma.com.
Investor Contact:
Colin Clancy
Vice President, Investor Relations and Corporate Communications
T: +1 604 416 0999
E: cclancy@inmedpharma.com
Cautionary Note Regarding Forward-Looking Information:
This news release contains "forward-looking information" and "forward-looking statements" (collectively, "forward-looking information") within the meaning of applicable securities laws. Forward-looking statements are frequently, but not always, identified by words such as "expects", "anticipates", "believes", "intends", "potential", "possible", "would" and similar expressions. Such statements, based as they are on current expectations of management, inherently involve numerous risks, uncertainties and assumptions, known and unknown, many of which are beyond our control. Forward-looking information is based on management's current expectations and beliefs and is subject to a number of risks and uncertainties that could cause actual results to differ materially from those described in the forward-looking statements. Forward-looking information in this news release includes statements about: the efficacy of INM-901, INM-901's ability to treat AD, marketability and uses for INM-901, the results of further studies into INM-901 and acceleration of the development of Inmed's AD program.
Additionally, there are known and unknown risk factors which could cause InMed's actual results, performance or achievements to be materially different from any future results, performance or achievements expressed or implied by the forward-looking information contained herein. A complete discussion of the risks and uncertainties facing InMed's stand-alone business is disclosed in InMed's Annual Report on Form 10-K and other filings with the Securities and Exchange Commission on www.sec.gov.
All forward-looking information herein is qualified in its entirety by this cautionary statement, and InMed disclaims any obligation to revise or update any such forward-looking information or to publicly announce the result of any revisions to any of the forward-looking information contained herein to reflect future results, events or developments, except as required by law.
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FAQ
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