Reported Earnings • May 11
Third quarter 2026 earnings released: US$0.69 loss per share (vs US$1.94 loss in 3Q 2025) Third quarter 2026 results: US$0.69 loss per share. Net loss: US$2.79m (loss widened 32% from 3Q 2025). Announcement • Mar 28
InMed Pharmaceuticals Inc. Receives Nasdaq Notification Regarding Minimum Bid Price Compliance InMed Pharmaceuticals Inc. received a written notice from the Listing Qualifications Department of The Nasdaq Stock Market LLC dated March 27, 2026, notifying it that the closing bid price of the Company's common shares over a period of 30 consecutive trading days was below the minimum $1.00 per share requirement for continued listing on The Nasdaq Capital Market under Nasdaq Listing Rule 5550(a)(2) during the February 11, 2026 to March 26, 2026 period. The notice has no immediate impact on the listing of the Company's common shares, which will continue to trade on The Nasdaq Capital Market subject to the Company's continued compliance with the other listing requirements of The Nasdaq Capital Market. In accordance with applicable Nasdaq procedures, the Company has a period of 180 calendar days following the receipt of the written notice mentioned above to cure the deficiency and regain compliance. To regain compliance, the closing bid price of the common shares of the Company must meet or exceed $1.00 per share for at least 10 consecutive business days during the 180-calendar day compliance period. The common shares of the Company will continue to trade under the symbol "INM". The Company intends to monitor the closing share price for its common shares and explore available options to regain compliance. In the event the Company does not evidence compliance with the minimum bid price requirement during the 180-day grace period, the Company may be eligible for an additional 180 calendar day grace period. To qualify, the Company will be required to meet the continued listing requirement for market value of publicly held shares and all other initial listing standards for The Nasdaq Capital Market, with the exception of the bid price requirement, and will need to provide written notice of its intention to cure the deficiency during the second compliance period, by effecting a reverse stock split, if necessary, to Nasdaq. If it appears to the staff of Nasdaq that the Company will not be able to cure the deficiency, or if the Company is otherwise not eligible, the Company will not be entitled to an additional 180 calendar days grace period and Nasdaq will provide notice to the Company that its securities will be subject to delisting. If the Company does not regain compliance within the allotted compliance period(s), including any extensions that may be granted by Nasdaq, it is expected that Nasdaq would notify the Company that its common shares are subject to delisting. If the Company is notified by Nasdaq that its securities are subject to delisting, the Company may appeal such determination to a Nasdaq Hearings Panel but the Company's securities would be automatically suspended from trading on Nasdaq pending the completion of the appeal process. There can be no assurance that any such appeal would be successful or that the Company would be able to evidence compliance with the terms of any extension that may be granted by the Panel. Announcement • Mar 23
InMed Pharmaceuticals Announces Positive Data From Human Brain Organoid Neuroinflammation Models Supporting The INM-901 Alzheimer'S Disease Program InMed Pharmaceuticals Inc. announced new preclinical data demonstrating the effects of INM-901 in reducing neuroinflammation in 3D human brain organoid models of Alzheimer's disease. These studies, conducted in collaboration with Stem Pharm Inc. using their proprietary platform of human neuro-immune organoids, represent a key step in translating prior animal model results for INM-901 into a human-relevant system, helping to de-risk the INM-901 program ahead of a first-in-human clinical trial. The in vitro human organoid models represent some of the closest approximations to human brain tissue currently available, incorporating a complex cellular environment relevant to neurodegenerative disease. The organoids are composed of neurons, astrocytes, vascular cells and feature microglia, the brain's resident immune cells, and can be used to bridge the gap between traditional animal models and human clinical trials. INM-901 was evaluated in two distinct human 3D organoid models: a general model of neuroinflammation induced with lipopolysaccharide and interferon-gamma; and, Stem Pharm's proprietary neuroinflammation Alzheimer's disease model with specific features observed in Alzheimer's disease patients. INM-901 demonstrated significant reduction in neuroinflammation in Stem Pharm's lipopolysaccharide-induced model and in their Alzheimer's disease model. A dose-dependent reduction of key pro-inflammatory markers such as IL-6 and IL-8 was seen in both neuroinflammation models. Effects align with prior findings from an in vivo Alzheimer's model and an ex vivo lipopolysaccharide-induced neuroinflammation model. Provides supportive evidence of mechanistic translation from animal models to human tissue systems. The consistency of INM-901's anti-inflammatory effects across in vivo animal models, ex vivo systems and now human 3D brain organoids provide increasing confidence in the compound's potential to translate into clinical benefit in humans with neuroinflammatory conditions. Key datasets impacting anti-neuroinflammation to date: In a long-term mouse model mimicking Alzheimer's disease, INM-901 significantly reduced inflammatory biomarkers interferon-gamma, TNF-alpha, IL-1beta, KC-GRO, IL-2 and neurodegenerative marker neurofilament light chain. INM-901 significantly reduced inflammasome activation and multiple pro-inflammatory cytokines, including NLRP3, IL-1beta, IL-6, IL-2 and KC-GRO in an lipopolysaccharide-induced neuroinflammation ex vivo model, demonstrated anti-inflammatory effects independent of amyloid-beta or tau pathology. Reduction of neuroinflammation in 3D human brain organoid models of Alzheimer's disease. Next steps for the INM-901 program for Alzheimer's disease: Conduct a pre-IND meeting with the U.S. Food and Drug Administration in Third Quarter 2026. Continue to execute on IND-enabling pharmacology and toxicology studies. Continued development and scale-up of drug substance and product manufacturing activities to support IND enabling studies and submission. Engage regulatory/clinical experts in neurodegenerative diseases to map out topline clinical design for first-in-human clinical trials for the INM-901. Subject to regulatory feedback and completion of IND-enabling activities, the company targets submission of an IND and initiation of a Phase 1 clinical trial in 2027. Recent drug development efforts in Alzheimer's disease have largely focused on amyloid plaque and tau pathology, leading to the first disease-modifying therapies in recent years. However, increasing attention is being directed toward neuroinflammation as a key underlying driver of disease progression. Studies presented at the recent global Alzheimer's conferences highlighted the relationship between inflammatory biomarkers and the risk of Alzheimer's disease and other dementias, underscoring the growing importance of targeting inflammation. Current research has demonstrated significant progress in understanding disease mechanisms and clinical interventions, with inflammation emerging as a critical factor influencing long-term patient outcomes. As such, neuroinflammation is increasingly recognized as a strategic therapeutic target for next-generation Alzheimer's treatments. 
