InMed's INM-901 Significantly Reduces Neuroinflammation in Alzheimer's Disease Ex Vivo Study
InMed Pharmaceuticals (NASDAQ: INM) has announced promising preclinical results for INM-901, their therapeutic candidate for Alzheimer's disease. In an ex vivo study, INM-901 demonstrated significant reduction of neuroinflammation in animal brain tissue.
The study revealed that INM-901 significantly reduced levels of key inflammatory markers, including NLRP3, IL-6, IL-1β, KC/Gro, and IL-2. Notably, these anti-inflammatory effects were achieved independently of amyloid beta or tau pathology, suggesting potential applications in various dementia-related diseases.
INM-901's key characteristics include oral administration capability, neuroprotective effects through CB1/CB2 receptor interaction, and demonstrated improvements in cognitive function and memory in preclinical studies. The company plans to advance INM-901 through additional preclinical studies, followed by IND-enabling studies.
InMed Pharmaceuticals (NASDAQ: INM) ha annunciato risultati preclinici promettenti per INM-901, il loro candidato terapeutico per la malattia di Alzheimer. In uno studio ex vivo, INM-901 ha mostrato una significativa riduzione della neuroinfiammazione nei tessuti cerebrali animali.
Lo studio ha evidenziato che INM-901 ha ridotto significativamente i livelli di importanti marcatori infiammatori, tra cui NLRP3, IL-6, IL-1β, KC/Gro e IL-2. È importante notare che questi effetti anti-infiammatori sono stati ottenuti indipendentemente dalla patologia dell'amiloide beta o della tau, suggerendo potenziali applicazioni in diverse malattie correlate alla demenza.
Le caratteristiche principali di INM-901 includono la possibilità di somministrazione orale, effetti neuroprotettivi tramite l'interazione con i recettori CB1/CB2 e miglioramenti dimostrati nella funzione cognitiva e nella memoria negli studi preclinici. L'azienda prevede di portare avanti INM-901 con ulteriori studi preclinici, seguiti da studi per l'abilitazione IND.
InMed Pharmaceuticals (NASDAQ: INM) ha anunciado resultados preclínicos prometedores para INM-901, su candidato terapéutico para la enfermedad de Alzheimer. En un estudio ex vivo, INM-901 demostró una reducción significativa de la neuroinflamación en tejido cerebral animal.
El estudio reveló que INM-901 redujo significativamente los niveles de marcadores inflamatorios clave, incluyendo NLRP3, IL-6, IL-1β, KC/Gro e IL-2. Cabe destacar que estos efectos antiinflamatorios se lograron independientemente de la patología de beta amiloide o tau, lo que sugiere aplicaciones potenciales en diversas enfermedades relacionadas con la demencia.
Las características principales de INM-901 incluyen la capacidad de administración oral, efectos neuroprotectores mediante la interacción con los receptores CB1/CB2 y mejoras demostradas en la función cognitiva y la memoria en estudios preclínicos. La compañía planea avanzar con INM-901 a través de estudios preclínicos adicionales, seguidos de estudios para habilitar el IND.
InMed Pharmaceuticals (NASDAQ: INM)는 알츠하이머병 치료 후보물질인 INM-901에 대한 유망한 전임상 결과를 발표했습니다. ex vivo 연구에서 INM-901은 동물 뇌 조직 내 신경염증을 크게 감소시키는 효과를 보였습니다.
연구 결과 INM-901은 NLRP3, IL-6, IL-1β, KC/Gro, IL-2 등 주요 염증 표지자들의 수치를 유의미하게 감소시켰습니다. 특히 이러한 항염 효과는 아밀로이드 베타나 타우 병리와 무관하게 나타나 다양한 치매 관련 질환에 적용 가능성을 시사합니다.
INM-901의 주요 특징은 경구 투여가 가능하며, CB1/CB2 수용체와의 상호작용을 통한 신경 보호 효과를 가지고 있고, 전임상 연구에서 인지 기능 및 기억력 개선이 입증되었다는 점입니다. 회사는 추가 전임상 연구를 진행한 후 IND 승인 연구를 계획하고 있습니다.
InMed Pharmaceuticals (NASDAQ : INM) a annoncé des résultats précliniques prometteurs pour INM-901, leur candidat thérapeutique contre la maladie d'Alzheimer. Dans une étude ex vivo, INM-901 a démontré une réduction significative de la neuroinflammation dans les tissus cérébraux animaux.
L'étude a révélé qu'INM-901 réduisait significativement les niveaux de marqueurs inflammatoires clés, notamment NLRP3, IL-6, IL-1β, KC/Gro et IL-2. Fait notable, ces effets anti-inflammatoires ont été obtenus indépendamment des pathologies amyloïde bêta ou tau, suggérant des applications potentielles dans diverses maladies liées à la démence.
Les caractéristiques principales d'INM-901 comprennent la possibilité d'administration orale, des effets neuroprotecteurs via l'interaction avec les récepteurs CB1/CB2, ainsi que des améliorations démontrées des fonctions cognitives et de la mémoire lors d'études précliniques. L'entreprise prévoit de poursuivre le développement d'INM-901 avec des études précliniques supplémentaires, suivies d'études permettant l'autorisation IND.
InMed Pharmaceuticals (NASDAQ: INM) hat vielversprechende präklinische Ergebnisse für INM-901, ihren therapeutischen Kandidaten gegen Alzheimer, bekanntgegeben. In einer ex vivo Studie zeigte INM-901 eine signifikante Reduktion der Neuroinflammation im Gehirngewebe von Tieren.
Die Studie ergab, dass INM-901 die Spiegel wichtiger Entzündungsmarker wie NLRP3, IL-6, IL-1β, KC/Gro und IL-2 signifikant senkte. Bemerkenswert ist, dass diese entzündungshemmenden Effekte unabhängig von Amyloid-Beta- oder Tau-Pathologien erzielt wurden, was auf mögliche Anwendungen bei verschiedenen demenzbezogenen Erkrankungen hinweist.
Zu den Hauptmerkmalen von INM-901 zählen die orale Verabreichungsmöglichkeit, neuroprotektive Effekte durch Interaktion mit CB1/CB2-Rezeptoren sowie nachgewiesene Verbesserungen der kognitiven Funktion und des Gedächtnisses in präklinischen Studien. Das Unternehmen plant, INM-901 durch weitere präklinische Studien und anschließend durch IND-freigabefähige Studien voranzutreiben.
- Significant reduction in multiple pro-inflammatory markers including NLRP3, IL-6, IL-1β, KC/Gro, and IL-2
- Drug can be administered orally and achieve therapeutic brain levels
- Demonstrates improved cognitive function, memory, and behavioral improvements in preclinical studies
- Multiple mechanisms of action targeting both CB1/CB2 receptors and PPARs
- Still in early preclinical stage, requiring additional studies before IND
- Results limited to ex vivo studies in animal tissue
- No human trial data available yet
Insights
InMed's INM-901 shows promising anti-inflammatory effects in Alzheimer's preclinical model, targeting NLRP3 inflammasome pathway independent of amyloid/tau pathology.
The ex vivo results for INM-901 represent a mechanistically significant advancement in Alzheimer's disease research. The compound's ability to reduce multiple pro-inflammatory cytokines (IL-6, IL-1β, IL-2, KC/Gro) and decrease NLRP3 inflammasome activity addresses a fundamental pathological process in neurodegeneration that has been underexplored in drug development.
What makes these findings particularly valuable is the demonstration of anti-inflammatory effects independent of amyloid beta or tau pathology. This represents a paradigm shift from traditional approaches that have predominantly targeted protein aggregates with limited clinical success. The NLRP3 inflammasome has emerged as a central mediator in neuroinflammation, activating inflammatory cascades that contribute to neuronal damage across multiple neurodegenerative conditions.
The compound's reported CB1/CB2 receptor agonist properties combined with PPAR modulation suggests a multi-modal mechanism that could provide comprehensive neuroprotection. The endocannabinoid system has established roles in neuroinflammatory regulation, while PPAR activation has shown promise in metabolic and inflammatory aspects of neurodegeneration.
The claimed oral bioavailability with effective brain penetration would offer significant advantages over current treatment modalities if confirmed in further studies. However, these remain early-stage findings using an LPS-induced inflammatory model - a useful but simplified representation of Alzheimer's complex pathophysiology. The transition from ex vivo models to human efficacy involves substantial challenges, with most preclinical candidates failing to demonstrate clinical benefit.
These results position INM-901 as a novel approach focusing on neuroinflammation as a primary driver rather than a consequence of protein aggregation in Alzheimer's disease, with potential applications in other neuroinflammatory conditions.
- Demonstrates statistically significant reduction of pro-inflammatory cytokines, including IL-6, IL-1β, IL-2, and KC/Gro
- Significantly reduces levels of inflammasome marker, NLRP3, a key contributor to neurodegeneration
- Reduces key pro-inflammatory markers, independent of amyloid beta or tau pathology
Vancouver, British Columbia--(Newsfile Corp. - June 24, 2025) - InMed Pharmaceuticals Inc. (NASDAQ: INM) ("InMed" or the "Company"), a pharmaceutical company focused on developing a pipeline of proprietary small molecule drug candidates for diseases with high unmet medical needs, today announced new preclinical data demonstrating that INM-901 significantly reduces inflammation in ex vivo models of neuroinflammation, further supporting its potential as a therapeutic candidate in Alzheimer's disease.
The study evaluated INM-901 in an ex vivo model of lipopolysaccharide (LPS)-induced inflammation in animal brain tissue, which is designed to induce a strong expression of pro-inflammatory cytokines IL-6, IL-1β, IL-2, and KC/Gro and inflammasome marker NLRP3. Results demonstrated that INM-901 treatment can reduce pro-inflammatory cytokines and may have a direct impact on neuroinflammation independent of the influence of amyloid beta or tau aggregation. This study model offers insight into INM-901's potential therapeutic impact on brain inflammation that may underlie a broad range of neurodegenerative diseases, including Alzheimer's disease.
Key Findings from the Study:
- INM-901 significantly reduced levels of NLRP3 and IL-1β, two inflammasome markers increasingly implicated in the pathogenesis of Alzheimer's disease and other neuroinflammatory diseases.
- INM-901 treatment resulted in a dose-dependent and statistically significant reduction in several key pro-inflammatory markers, including IL-6, IL-1β, KC/Gro, and IL-2.
- INM-901 reduced key pro-inflammatory markers, independent of amyloid-beta or tau pathology, signifying potential to treat other dementia-related diseases.
"NLRP3-driven inflammation is recognized as a key contributor to neurodegenerative disease progression," said Dr. Eric Hsu, SVP of Preclinical Research & Development. "The data derived from this LPS-induced inflammation study further support our previous findings in the amyloid beta animal model following INM-901 treatment, which demonstrated a significant reduction in inflammatory markers. Notably, the results from the LPS study suggest that INM-901 exerts a direct effect on neuroinflammation, independent of the contributions from amyloid beta plaques or tau aggregation."
NLRP3 has been implicated in the pathogenesis of several inflammatory, autoimmune, metabolic and neurodegenerative conditions such as Alzheimer's disease, Parkinson's, type 2 diabetes and others. In these diseases, overactivation of NLRP3 can result in chronic inflammation in the brain, which may contribute to neurodegeneration and cognitive decline.
This most recent study represents a key advancement for the program, highlighting INM-901 as a distinctive and promising therapeutic candidate for the treatment of Alzheimer's disease and supports continued development toward a lead indication in Alzheimer's disease. The Company plans to advance INM-901 through additional preclinical studies, with IND-enabling studies to follow.
INM-901: Program Summary to date:
INM-901 is a proprietary small molecule drug candidate for Alzheimer's disease with potentially multiple mechanisms of action. Key characteristics of INM-901 include:
- demonstrates reduced neuroinflammation and improved neurite growth and neuronal function, indicating the potential to restore damage caused by Alzheimer's disease;
- is a preferential signaling agonist of the CB1/CB2 receptors and has been shown to have neuroprotective effects, helping protect the neurons in the brain from damage and cell death;
- impacts the peroxisome proliferator-activated receptors ("PPARs"), which have been shown to play an important role in diabetes and are also considered as one of the potential therapeutic targets for neurodegenerative disorders such as Alzheimer's disease;
- can be administered orally and achieve therapeutic levels in the brain comparable to those obtained through intraperitoneal injection, offering many potential advantages over routes of administration of the currently approved products; and
- demonstrates significant improvement in cognitive function, memory, locomotor activity, anxiety-based behavior and sound awareness in long-term preclinical behavioural studies.
To learn more about INM-901, please visit the website at: https://www.inmedpharma.com/pharmaceutical/inm-901-for-alzheimers-disease/.
About InMed:
InMed Pharmaceuticals is a pharmaceutical company focused on developing a pipeline of proprietary small molecule drug candidates targeting the CB1/CB2 receptors. InMed's pipeline consists of three separate programs in the treatment of Alzheimer's, ocular and dermatological indications. For more information, visit www.inmedpharma.com.
Investor Contact:
Colin Clancy
Vice President, Investor Relations
and Corporate Communications
T: +1 604 416 0999
E: ir@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. Without limiting the foregoing, forward-looking information in this news release includes, but is not limited to, statements about: the efficacy of INM-901, INM-901's potential impact on inflammation, INM-901's impact on neuroinflammation independent of amyloid beta or tau pathology, the role of NLRP3 in the pathogenesis of several neurodegenerative conditions, INM-901's ability to treat Alzheimer's, marketability and uses for INM-901, the results of further studies into INM-901 and continued development of InMed's Alzheimer's 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, in Item 1A. of the Quarterly Report for the period ended March 31, 2025, 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.
To view the source version of this press release, please visit https://www.newsfilecorp.com/release/256573
FAQ
What are the key findings of InMed's INM-901 ex vivo study for Alzheimer's disease?
How does INM-901 differ from other Alzheimer's treatments?
What is the current development stage of INM-901?
How does INM-901 impact NLRP3 and why is this significant?
What behavioral improvements has INM-901 shown in preclinical studies?
