Tillkännagivande • Aug 04
ProMIS Neurosciences, Inc. to Report Q2, 2026 Results on Aug 13, 2026 ProMIS Neurosciences, Inc. announced that they will report Q2, 2026 results on Aug 13, 2026 Tillkännagivande • Jul 28
ProMIS Neurosciences Inc. Reports Positive Blinded Six-Month Interim Safety and Biomarker Data for PMN310 in PRECISE-AD Phase 1b Alzheimer’s Disease Trial ProMIS Neurosciences Inc. announced positive blinded six-month interim safety and biomarker results from PRECISE-AD, the Phase 1b trial of its lead drug candidate, PMN310, in patients with mild cognitive impairment due to Alzheimer’s disease or mild Alzheimer’s disease. In the blinded interim analysis evaluating 136 Alzheimer’s disease patients, PMN310 was observed to have a favorable safety profile across all genotypes, with no cases of amyloid-related imaging abnormalities-edema (ARIA-E) reported as of the data cutoff date, and early, directionally consistent movement in disease-relevant biomarkers potentially reflective of the randomization pattern. The trial remains blinded and ongoing with topline 12-month results expected in the first quarter of 2027. No ARIA-E observed across all genotypes, including APOE4 homozygotes. ARIA-H tracking background rates. Early biomarker movement consistent with target engagement. 12-month topline results expected in the first quarter of 2027. Favorable safety profile across all genotypes: No ARIA-E and 4.4% total ARIA (all mild and asymptomatic, consisting of only amyloid-related imaging abnormalities-microhemorrhages (ARIA-H)), with no treatment-related serious adverse events and no drug-related discontinuations at the interim. Same profile in high-risk APOE4 carriers: No ARIA-E observed in any genotype in a population that included 61% APOE4 carriers, of which 11% were homozygotes. Early biomarker movement consistent with target engagement: On a blinded basis, a majority of patients showed reductions in disease-relevant biomarkers against expected increases in natural-history trajectories: 68.5% of patients had a decline from baseline (change = 0) in plasma pTau217 and 62.5% had a decline in CSF MTBR-tau243, consistent with a potential beneficial drug effect and potentially reflective of the trial’s 3:1 active-to-placebo randomization. These are blinded interim biomarker observations, meaning treatment allocations between drug and placebo groups are not known at this time. These observed biomarker trends are not a determination of efficacy, and trends in biomarkers may not ultimately be reflective of clinical effects. Differentiated, oligomer-selective mechanism: PMN310 is designed to selectively bind toxic amyloid-beta oligomers while avoiding plaque, a mechanism intended to decouple potential efficacy from ARIA risk. Clear path forward: Unblinded 12-month topline data expected in the first quarter of 2027, including efficacy data. PMN310, ProMIS’ lead product candidate for the treatment of Alzheimer’s disease, is a humanized IgG1 monoclonal antibody designed to selectively target only the toxic oligomers of amyloid-beta (AßOs), believed to be among the earliest and most damaging drivers of Alzheimer’s disease, while avoiding binding to amyloid plaques and vascular deposits. This selectivity may reduce or eliminate the risk of amyloid-related imaging abnormalities (ARIA), including brain swelling (ARIA-E) and microhemorrhages (ARIA-H), which are commonly associated with plaque-binding antibodies. PMN310 was granted Fast Track Designation by the U.S. Food and Drug Administration in July 2025. Based on encouraging results from a Phase 1a trial (NCT06105528) in healthy volunteers, ProMIS initiated the PRECISE-AD Phase 1b trial to evaluate PMN310 in patients with mild cognitive impairment due to Alzheimer’s disease or mild Alzheimer’s disease. PRECISE-AD (NCT06750432) is a randomized, double-blind, placebo-controlled study evaluating the safety, tolerability, and pharmacokinetics of multiple ascending doses (5, 10, and 20 mg/kg) of intravenous PMN310. The study has completed enrollment of 144 participants across the three dosing cohorts who are being treated for twelve months. It is designed to provide meaningful insight into the effects of PMN310 on biomarkers and clinical outcomes. Tillkännagivande • Jul 14
ProMIS Neurosciences Reports First Human Evidence Of Amyloid-Beta Oligomer Target Engagement By PMN310 At AAIC ProMIS Neurosciences Inc. announced the first human evidence of dose-dependent amyloid-beta oligomer (AßO) reduction by its lead Alzheimer’s drug candidate, PMN310, presented at AAIC 2026. The findings, drawn from analysis of samples collected during the Company's Phase 1a trial in healthy volunteers (NCT06105528), showed that individuals receiving PMN310 exhibited a dose-dependent reduction in detectable AßO in cerebrospinal fluid (CSF) at both three and 29 days after dosing. While healthy individuals carry lower oligomer burdens than Alzheimer's patients, amyloid-beta oligomers are detectable in CSF even in cognitively normal adults, making this a meaningful measure of target engagement. This represents one of the first quantitative demonstrations of treatment-related oligomer reduction in humans. Using CSF samples from our Phase 1a study, subjects receiving PMN310 showed a clear dose-dependent reduction in oligomer particles, which, we believe, represents direct evidence that PMN310 was able to reach the brain and engage its intended target. The company intends to deploy this assay in its ongoing PRECISE-AD Phase 1b trial to directly measure oligomer burden in Alzheimer's patients before and after treatment. A large body of evidence in Alzheimer's disease research indicates that disease pathogenesis is not directly driven by plaque burden, but rather by soluble toxic amyloid-beta oligomers. Selectively targeting oligomers while avoiding plaque could have a meaningful impact on both the efficacy and safety of treatment, reducing off-target binding that limits effective dosing and potentially limiting the ARIA side effects associated with plaque-binding antibodies. The data presented provide pharmacodynamic evidence supportive of PMN310's differentiated mechanism of action. The interim analysis will focus on blinded aggregate safety data and overall trends in selected biomarkers across study participants. Top line unblinded results are expected in early First Quarter 2027. Amyloid-beta oligomers in CSF were measured using surface-based fluorescence intensity distribution analysis (sFIDA) developed by attyloid GmbH, an assay which enables direct quantification of oligomer particles with unprecedented sensitivity. While the assay is currently exploratory, it provides pharmacodynamic evidence of target engagement by PMN310. Oligomer reduction: Placebo-treated healthy volunteers (N=40) in the Phase 1a trial exhibited low levels of AßO in CSF. PMN310 administration resulted in a dose-dependent reduction in detectable AßO particles in CSF. Strict oligomer selectivity: PMN310 demonstrated strong binding to AßO with no interaction with monomers by surface plasmon resonance (SPR), and no detectable reactivity with plaques or vascular deposits of Aß in AD brain tissue sections, representing the potential for a differentiated clinical profile. Favorable pharmacokinetics and tolerability: PMN310 was generally well-tolerated, with CSF concentrations linearly dose-dependent, reaching 100–600 times the estimated molar concentration of AßO, and a CSF half-life of approximately 27 days. Preclinical memory preservation: In a transgenic AD mouse model, PMN310 preserved memory and learning performance in the Morris Water Maze task. PMN310, ProMIS’ lead product candidate for the treatment of AD, is a humanized IgG1 monoclonal antibody designed to selectively target only the toxic oligomers of amyloid-beta (AßOs), believed to be among the earliest and most damaging drivers of Alzheimer's disease, while avoiding binding to amyloid plaques and vascular deposits. This selectivity may reduce or eliminate the risk of amyloid-related imaging abnormalities (ARIA), including brain swelling (ARIA-E) and microhemorrhages (ARIA-H), which are commonly associated with plaque-binding antibodies. PMN310 was granted Fast Track Designation by the U.S. Food and Drug Administration in July 2025. Based on encouraging results from a Phase 1a trial (NCT06105528) in healthy volunteers, ProMIS initiated the PRECISE-AD Phase 1b trial to evaluate PMN310 in patients with mild cognitive impairment due to AD or mild AD. PRECISE-AD (NCT06750432) is a randomized, double-blind, placebo-controlled study evaluating the safety, tolerability, and pharmacokinetics of multiple ascending doses (5, 10, and 20 mg/kg) of intravenous PMN310. The study has completed enrollment of 144 participants across the three dosing cohorts who are being treated for twelve months. It is designed to provide meaningful insight into the effects of PMN310 on biomarkers and clinical outcomes. Tillkännagivande • Apr 10
ProMIS Neurosciences, Inc., Annual General Meeting, May 20, 2026 ProMIS Neurosciences, Inc., Annual General Meeting, May 20, 2026. New Risk • Nov 28
New major risk - Market cap size The company's market capitalization is less than US$10m. Market cap: US$623.1k This is considered a major risk. Companies with a small market capitalization are most likely businesses that have not yet released a product to market or are simply a very small company without a wide reach. Either way, risk is elevated with these companies because there is a chance the product may not come to fruition or the company's addressable market or demand may not be as large as expected. In addition, if the company's size is the main factor, it is less likely to have many investors and analysts following it and scrutinizing its performance and outlook. Currently, the following risks have been identified for the company: Major Risks Less than 1 year of cash runway based on free cash flow trend (-US$28m free cash flow). Earnings are forecast to decline by an average of 15% per year for the foreseeable future. Shareholders have been substantially diluted in the past year (65% increase in shares outstanding). Revenue is less than US$1m. Market cap is less than US$10m (US$623.1k market cap). Minor Risks Currently unprofitable and not forecast to become profitable over next 3 years (US$51m net loss in 3 years). Share price has been volatile over the past 3 months (13% average weekly change). New Risk • Nov 15
New major risk - Financial position The company has less than a year of cash runway based on its current free cash flow trend. Free cash flow: -US$28m This is considered a major risk. With less than a year's worth of cash, the company will need to raise capital or take on debt unless its cash flows improve. This would dilute existing shareholders or increase balance sheet risk. Currently, the following risks have been identified for the company: Major Risks Less than 1 year of cash runway based on free cash flow trend (-US$28m free cash flow). Earnings are forecast to decline by an average of 15% per year for the foreseeable future. Shareholders have been substantially diluted in the past year (65% increase in shares outstanding). Revenue is less than US$1m. Minor Risks Currently unprofitable and not forecast to become profitable over next 3 years (US$51m net loss in 3 years). Market cap is less than US$100m (US$21.0m market cap). Tillkännagivande • Oct 23
ProMIS Neurosciences, Inc. Appoints Slanix Paul Alex, Pharm.D as Board of Director ProMIS Neurosciences, Inc. announced that Slanix Paul Alex, Pharm.D., President and Portfolio Manager for Ally Bridge Groups Public Equity strategy, has joined the Companys Board of Directors. Dr. Alex has a highly distinguished Wall Street career spanning multiple leadership positions at public markets-focused healthcare investment firms and substantial sell-side biotechnology equity research experience. His deep understanding of capital markets, biopharma innovation and business development trends will provide valuable perspective to ProMIS. Dr. Alex joined Ally Bridge Group in 2023 and is the President and Portfolio Manager for the Public Equity
strategy. Before joining Ally Bridge Group, Slanix invested in life sciences companies as a founding Partner and Senior Analyst for Tri Locum Partners and previously as an Investment Analyst for Consonance Capital Management. Prior to the buy-side, Slanix worked in sell-side biotechnology equity research at RBC Capital Markets and Credit Suisse. Slanix began his career in strategy consulting at Bionest Partners, advising life sciences companies on business development and commercial strategy. Slanix is a licensed pharmacist and holds a PharmD from St Johns University. New Risk • Aug 15
New major risk - Shareholder dilution The company's shareholders have been substantially diluted in the past year. Increase in shares outstanding: 73% This is considered a major risk. Shareholder dilution occurs when there is an increase in the number of shares on issue that is not proportionally distributed between all shareholders. Often due to the company raising equity capital or some options being converted into stock. All else being equal, if there are more shares outstanding then each existing share will be entitled to a lower proportion of the company's total earnings, thus reducing earnings per share (EPS). While dilution might not always result in lower EPS (like if the company is using the capital to fund an EPS accretive acquisition) in a lot cases it does, along with lower dividends per share and less voting power at shareholder meetings. Currently, the following risks have been identified for the company: Major Risks Share price has been highly volatile over the past 3 months (47% average weekly change). Negative equity (-US$383k). Earnings are forecast to decline by an average of 25% per year for the foreseeable future. Shareholders have been substantially diluted in the past year (73% increase in shares outstanding). Revenue is less than US$1m. Minor Risks Currently unprofitable and not forecast to become profitable over next 3 years (US$50m net loss in 3 years). Market cap is less than US$100m (US$32.6m market cap). New Risk • Aug 14
New major risk - Negative shareholders equity The company has negative equity. Total equity: -US$383k This is considered a major risk. Being in negative equity means that the company's liabilities exceed its assets, meaning it owes more to creditors than it has in owned assets. While this doesn't mean the company is about to collapse, in the long-term, this is unsustainable. The company may have issues meeting financial obligations, is at risk of becoming insolvent and may have difficulty raising capital, especially more debt, if needed. Currently, the following risks have been identified for the company: Major Risks Share price has been highly volatile over the past 3 months (47% average weekly change). Negative equity (-US$383k). Earnings are forecast to decline by an average of 23% per year for the foreseeable future. Revenue is less than US$1m. Minor Risks Currently unprofitable and not forecast to become profitable over next 3 years (US$41m net loss in 3 years). Market cap is less than US$100m (US$22.9m market cap). Tillkännagivande • Aug 14
ProMIS Neurosciences, Inc. has filed a Follow-on Equity Offering in the amount of $17.988524 million. ProMIS Neurosciences, Inc. has filed a Follow-on Equity Offering in the amount of $17.988524 million.
Security Name: Common Shares
Security Type: Common Stock
Transaction Features: At the Market Offering Tillkännagivande • Jul 28
ProMIS Neurosciences, Inc. announced that it expects to receive CAD 3 million in funding from Ally Bridge Group ProMIS Neurosciences, Inc announced a private placement and entered into a purchase agreement to issue 16,000,000 warrants at a price of CAD 0.1875 for aggregate gross proceeds of CAD 3,000,000 on July 28, 2025. The Warrants have an exercise price of CAD 1.25 per Warrant, are immediately exercisable and will expire five years from the date of initial issuance. The transaction will include participation from existing institutional investors, including Ally Bridge Group. The transaction is expected to close on July 29, 2025. New Risk • Jul 14
New minor risk - Share price stability The company's share price has been volatile over the past 3 months. It is more volatile than 75% of American stocks, typically moving 14% a week. This is considered a minor risk. Share price volatility indicates the stock is highly sensitive to market conditions or economic conditions rather than being sensitive to its own business performance, which may also be inconsistent. It also increases the risk of potential losses in the short term as the stock tends to have larger drops in price more frequently than other stocks. Currently, the following risks have been identified for the company: Major Risks Less than 1 year of cash runway based on free cash flow trend (-US$22m free cash flow). Earnings are forecast to decline by an average of 44% per year for the foreseeable future. Shareholders have been substantially diluted in the past year (72% increase in shares outstanding). Revenue is less than US$1m. Minor Risks Currently unprofitable and not forecast to become profitable over next 3 years (US$59m net loss in 3 years). Share price has been volatile over the past 3 months (14% average weekly change). Market cap is less than US$100m (US$12.8m market cap). Board Change • Jul 10
Insufficient new directors No new directors have joined the board in the last 3 years. The company's board is composed of: No new directors. 7 experienced directors. 5 highly experienced directors. Member of Scientific Advisory Board Carsten Korth was the last director to join the board, commencing their role in 2022. The following issues are considered to be risks according to the Simply Wall St Risk Model: Insufficient board refreshment. Tillkännagivande • Apr 30
ProMIS Neurosciences, Inc., Annual General Meeting, Jun 12, 2025 ProMIS Neurosciences, Inc., Annual General Meeting, Jun 12, 2025. Tillkännagivande • Mar 25
ProMIS Neurosciences Showcases Preclinical Data on Platform-Derived Antibody and Vaccines for Neurodegenerative Diseases at Alzheimer's Disease/Parkinson's Disease 2025 International Conference ProMIS Neurosciences Inc. announced plans to deliver virtual oral presentations at the 2025 Alzheimer's and Parkison's Disease (AD/PD) International Conference taking place in Vienna, Austria from April 1 - 4, 2025. The oral presentations are available on demand starting on Tuesday, April 1, 2025 at 7:00am C.E.T (2:00am E.T). A novel approach was utilized to select an optimal vaccine composition amongst 15 possible combinations of one to four epitopes to provide maximal binding to a toxic oligomer-enriched low molecular weight fraction of soluble AD brain extract. Results from the preclinical study showed that immunization with a single conformational epitope, peptide 301, the target of the PMN310 antibody, was sufficient to produce maximal reactivity against AD brain oligomers. Vaccination against pathogenic species of alpha-synuclein (ASyn; toxic oligomers, small soluble seeding fibrils), has the potential to protect against synucleinopathies, which include Parkinson's disease, dementia with Lewy bodies and multiple system atrophy. Vaccine constructs containing computationally-derived conformational B cell epitopes of misfolded pathogenic ASyn were tested in mice. The potential advantage of this approach, as opposed to inducing pan-ASyn reactivity, lies in preserving normal ASyn function and minimizing the diversion of active antibody by the more abundant non-toxic forms of the protein in the blood and central nervous system. Results from the pre clinical study showed that vaccination with conformational B cell epitopes produced highinity antibodies with the desired selectivity for pathogenic ASyn and identified optimal vaccine configurations for further development. TAR DNA-binding protein 43 (TDP-43) is associated with the pathogenesis of ALS, frontotemporal dementia, and AD. The study's objective was to generate and evaluate the activity of monoclonal antibodies and intrabodies against an N-terminal domain epitope only exposed when the protein is misfolded in disease. Results of the preclinical study provided proof-of-concept evidence that supports selective targeting of misfolded toxic aggregates of TDP-43 as a potentially safe and effective avenue to treat neurodegenerative diseases associated with TDP-43 proteinopathy. By selectively targeting toxic soluble AbOs, PMN310 aims to directly address the growing body of evidence indicating they may be the primary underlying cause of the neurodegenerative process in Alzheimer's disease. PMN310 has successfully completed a Phase 1a clinical study (NCT06105528), a double-blind, placebo-controlled, single ascending dose study of the safety, tolerability and pharmacokinetics of PMN310 infusions in healthy volunteers. Tillkännagivande • Feb 25
Promis Neurosciences Doses First Patients in Phase 1B Precise-Ad Trial of Pmn310 for Alzheimer's Disease ProMIS Neurosciences Inc. announced important progress in the PRECISE-AD Phase 1b clinical trial with the dosing of multiple patients with its lead drug candidate, PMN310, designed for the treatment of Alzheimer's disease (AD). The dosing of several patients marks an important milestone in assessing the safety, tolerability, and pharmacokinetics of PMN310 and underscores ProMIS's commitment to addressing the urgent need for targeted therapies in AD by selectively targeting toxic oligomers, which believe to be a key driver of disease progression. The company believe PMN310's selective binding to toxic Ab oligomers and not to plaque or monomers differentiates it from other drugs currently on the market or in development and the company have the potential to deliver a more effective and well-tolerated treatment for patients suffering from Alzheimer's disease. Tillkännagivande • Jan 09
ProMIS Neurosciences Receives Nasdaq Non-Compliance Notice Regarding Minimum Bid Price Rule On January 3, 2025, ProMIS Neurosciences Inc. (Company") received written notice (the Notice") from the Listing Qualifications Department of The Nasdaq Stock Market LLC (Nasdaq") stating that the Company's common shares, no par value (the Common Shares") failed to comply with the $1 minimum bid price required for continued listing on The Nasdaq Capital Market under Nasdaq Listing Rule 5550(a)(2) (the Minimum Bid Price Rule") based upon the closing bid price of the Common Shares for the 30 consecutive trading days prior to the date of the Minimum Bid Price Notice from Nasdaq. The Notice has no effect on the listing of the Company's Common Shares at this time, and the Company's Common Shares will continue to trade on the The Nasdaq Capital Market under the symbol PMN." The Company has been provided an initial compliance period of 180 calendar days, or until July 2, 2025, to regain compliance with the Minimum Bid Price Rule which requires that the closing bid price of the Common Shares meet or exceed $1.00 per share for a minimum of ten consecutive trading days. If the Company is unable to regain compliance with the Minimum Bid Price Rule, the Company may be eligible for an additional 180-day compliance 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 Minimum Bid Price Rule, and will need to provide written notice to Nasdaq of its intention to cure the deficiency during the second compliance period. If the Company does not qualify for the second compliance period or fails to regain compliance during the second 180-day period, Nasdaq will notify the Company of its determination to delist the Common Shares, at which point the Company would have an opportunity to appeal the delisting determination to a Hearings Panel. The Company will continue to monitor the bid price of the Common Shares and consider its available options to regain compliance with the Minimum Bid Price Rule. However, there can be no assurance that the Company will be able to regain compliance with the Minimum Bid Price Rule. Tillkännagivande • Aug 07
ProMIS Neurosciences Announces Data on the Pathogenic Role of Toxic Misfolded SOD1 Aggregates in ALS Published in Acta Neuropathologica and Open Biology ProMIS Neurosciences Inc. announced the publication of two papers highlighting the role of toxic misfolded superoxide dismutase-1 (SOD1) aggregates in the pathogenesis of ALS. One paper published in Acta Neuropathologica is titled, “Seeding activity of human superoxide dismutase 1 aggregates in familial and sporadic amyotrophic lateral sclerosis postmortem neural tissues by real-time quaking-induced conversion,” and the other publication in the online journal Open Biology is titled, “Amyloidogenic regions in beta-strands II and III modulate the aggregation and toxicity of SOD1 in living cells.” ALS is a fatal neurodegenerative disease of motor neurons. Toxic aggregates of SOD1 and TAR DNA-binding protein 43 (TDP-43) in motor neurons are characteristic of ALS. As recently reported by ProMIS, these two proteins interact such that misfolding of TDP-43 leads to misfolding and aggregation of SOD1. ProMIS is currently developing PMN267, a humanized IgG1 antibody directed against toxic misfolded TDP-43 as a potential therapeutic for ALS. The newly published research in Acta Neuropathologica reports on the seminal finding that aggregated SOD1 seeds are present in ALS neural tissues, not only in patients with SOD1 mutations, but also in patients with the most common sporadic form of the disease, which supports the relevance of misfolded SOD1 as a therapeutic target and as a potential biomarker of disease. The OpenBiology publication highlights the importance of a previously underappreciated SOD1 amyloidogenic region in ß-strand II and III to the aggregation and toxicity of SOD1 in ALS mutants, suggesting that ß-strands II and III are potential targets for the development of SOD1-associated ALS therapies. As described in Acta Neuropathologica, the seeding activity of misfolded SOD1 aggregates in ALS neural tissues was measured using a real-time quaking-induced conversion (RT-QuIC) seed amplification assay system newly adapted to SOD1. Confirmation of the existence of measurable SOD1 seeds across different forms of ALS is an impactful contribution to the fundamental understanding of the disease. In addition, the observation that seeding activity was reduced after removal of misfolded SOD1from ALS tissue preparations with antibodies supports targeting SOD1 aggregates as a therapeutic approach. The ProMIS platform is designed to identify target epitopes restricted to pathogenic forms of proteins including SOD1 and, as reported in Open Biology, in silico tools used to predict amyloidogenic regions in the ALS-associated SOD1-G85R mutant led to the identification of seven regions throughout the structure. Modifying the structure of these regions showed a reduction in the aggregation propensity and toxicity of SOD1-G85R, which supports their potential as a target for therapeutic intervention. Tillkännagivande • Aug 01
ProMIS Neurosciences, Inc. Showcases Novel Vaccine Approach for Maximal Targeting of Toxic Amyloid-Beta Oligomers at the 2024 Alzheimer's Association International Conference ProMIS Neurosciences Inc. presented preclinical data at the 2024 Alzheimer’s Association International Conference (AAIC) that further supports the potential therapeutic advantage of the Company’s novel approach to optimization of an Alzheimer’s disease (AD) vaccine for maximum targeting of toxic amyloid-beta oligomers (AßO). A large body of evidence indicates that the most pathogenic species of amyloid-beta (Aß) in AD consist of soluble toxic oligomers as opposed to insoluble fibrils and monomers. ProMIS’ proprietary computational platform identified four different AßO-restricted conformational B cell epitopes as vaccine candidates. Additionally, the Company’s novel ex vivo approach selected an optimal vaccine configuration to provide maximal binding to a toxic oligomer-enriched low molecular weight fraction of soluble AD brain extracts. The results from the study showed that vaccination with AßO-restricted conformational B cell epitopes produced strong antibody responses with no measurable pro-inflammatory T cell responses against Aß. Importantly, immunization with epitope 301, the target of PMN310, alone was sufficient to produce maximal reactivity against brain AßO. Tillkännagivande • Jul 27
ProMIS Neurosciences, Inc. announced that it expects to receive CAD 30.3 million in funding from Great Point Partners, LLC, Armistice Capital LLC, Ally Bridge Group, Sphera Funds Management Ltd and other investors ProMIS Neurosciences Inc announced entered into a unit purchase agreement of common share units at issue price CAD 2.15 per Unit and pre-funded units at issue price CAD 2.14 per pre funded unit for gross proceeds CAD 30,300,000 on July 26, 2024. The transaction included participation from new and existing healthcare specialist investors such as Great Point Partners, LLC, Armistice Capital, Ally Bridge Group, Sphera Healthcare, and other institutional and individual accredited investors. The Pre-Funded Warrants have an exercise price of CAD 0.01 per Warrant Share, are immediately exercisable and will expire when exercised in full. The Tranche A Common Share purchase warrants have an exercise price of CAD 2.02, are exercisable immediately upon Shareholder Approval (as defined below) and will expire upon the earlier of 18 months or within 60 days of the public announcement via press release or the filing of a Current Report on Form 8-K of 6-month data from the cohorts treated with multiple ascending doses of PMN310. The financing is expected to close on July 31, 2024, subject to customary closing conditions. Tillkännagivande • Jul 26
ProMIS Neurosciences, Inc. Reports Positive Top-Line Data from its Phase 1a Alzheimer's Trial ProMIS Neurosciences, Inc. announced positive top-line data from the first four cohorts of its first-in-human Phase 1a clinical trial of PMN310 in healthy volunteers. The Phase 1a clinical data, which has been collected and analyzed from the first four of five cohorts, indicated that PMN310 demonstrated a favorable safety profile, was well tolerated and, importantly, crossed the blood brain barrier in healthy volunteers, in a dose dependent manner and at concentrations that suggest sufficient target engagement in the planned follow-on clinical trial in Alzheimer’s patients. PMN310 builds on a large body of scientific evidence that points to the role of soluble amyloid-beta oligomers (AbO) as a primary driver of Alzheimer’s pathology. By selectively targeting toxic oligomers, ProMIS seeks to expand therapeutic options beyond those treatments that target amyloid plaques, which it believes could provide a differentiated treatment for AD patients. PMN310 Appears Well-Tolerated Across Four Dose Cohorts: PMN310 was generally well-tolerated through the first four single-ascending (SAD) dose cohorts (2.5, 5, 10, 20 mg/kg), with no treatment-emergent serious adverse events (SAEs) observed after administration of PMN310. Cerebrospinal fluid (CSF) collection was done on days 3 and 29 after PMN310 administration. Measurement of PMN310 levels in CSF showed dose proportionality at both days 3 and 29, with the lowest dose reaching a greater than 100-fold molar excess compared to expected levels of oligomers in the CSF. The half-life of PMN310 in CSF was approximately 25 days, which is supportive of once per month dosing. The Phase 1a clinical trial was a randomized, double-blind, placebo-controlled study evaluating the safety and tolerability of PMN310 in healthy volunteers (NCT06105528). The study consisted of five SAD cohorts and was designed to evaluate the safety, tolerability, and pharmacokinetics (PK), of intravenous doses of PMN310. The study completed enrollment of all 40 subjects across 2 active sites in the United States. The Company has completed its analysis of the first four cohorts with the fifth and final cohort undergoing final analysis; we anticipate the fifth cohort will yield similar encouraging results. The trial was initiated based on encouraging nonclinical studies of PMN310 that support the selective targeting of AßOs. ProMIS expects to present the full dataset at an upcoming medical meeting in the second half of 2024. Tillkännagivande • Jul 06
ProMIS Neurosciences Receives Written Notice from Nasdaq Due to Non-Compliance with Nasdaq Listing Rule 5550(b)(2) On July 2, 2024, ProMIS Neurosciences Inc. (‘Company’) received written notice (the ‘Notice’) from the Listing Qualifications Department of The Nasdaq Stock Market LLC (‘Nasdaq’) stating that the Company is not in compliance with Nasdaq Listing Rule 5550(b)(2) (the ‘Rule’) because the Company has not maintained a minimum Market Value of Listed Securities (‘MVLS’) of at least $35 million for the last 30 consecutive business days. The Notice has no immediate effect on the listing or trading of the Company’s securities. The Company has 180 calendar days from the date of the Notice, or until December 29, 2024, to regain compliance. If the Company does not regain compliance with the MVLS requirement within the compliance period, or qualify under an alternative listing standard, the Company’s common stock will be subject to delisting. To regain compliance, during the 180 day period the MVLS must be at least $35 million for a minimum of ten consecutive business days (or such longer period of time as the Nasdaq staff may require in some circumstances, but generally not more than 20 consecutive business days). In the event the Company receives notice that the Company’s common stock is being delisted, Nasdaq’s rules permit the Company to appeal the delisting determination by the Nasdaq staff to a hearings panel. The Company intends to monitor the market value of the Company’s listed securities and may, if appropriate, consider available options to regain compliance with the MVLS requirement. The Company, by filing this Form 8-K, discloses its receipt of the notification from Nasdaq in accordance with Listing Rule 5810(b). There can be no assurance that the Company will be able to regain compliance with the MVLS requirement. Tillkännagivande • May 03
ProMIS Neurosciences, Inc. Publishes Study Highlighting Oligomer Selectivity and Benefit of Amyloid-Beta-Directed Antibodies ProMIS Neurosciences Inc. announced the publication of a paper titled, “Relationship between therapeutic activity and preferential targeting of toxic soluble aggregates by amyloid-beta-directed antibodies," in the online journal, bioRxiv. The study characterized and compared the binding profile of various amyloid-beta (Ab)-directed antibodies to monomers, soluble oligomers and insoluble Ab fibrils. The results indicate that selectivity for soluble toxic Aß oligomers may be a driver of clinical efficacy and indicated that PMN310 displayed the greatest degree of oligomer selectivity. PMN310, the Company’s novel monoclonal antibody being evaluated as a treatment for Alzheimer’s disease (AD), is currently undergoing Phase 1a clinical studies in healthy volunteers, with initial safety and pharmacokinetic data expected in mid-2024. Aß-directed antibodies tested clinically for therapeutic activity against AD have shown varying degrees of efficacy. A side-by-side comparison of antibody binding to different molecular species of Aß conducted by ProMIS provided insight into the observed variability in clinical outcomes. A correlation was observed between reported clinical efficacy and the ability of an antibody to retain binding to soluble oligomers from AD brains when faced with monomer competition. PMN310 showed a high degree of resistance to monomer competition. Importantly, unlike all other antibodies tested, PMN310 also avoided binding to plaque and vascular deposits of Ab. Consequently, PMN310, may reduce the risk of brain edema (ARIA-E) and microhemorrhages (ARIA-H) often associated with plaque-binding antibodies. This premise is supported by the results showing that weekly dosing of a murine version of PMN310 at very high doses (800 mg/kg) for 26 weeks in a mouse model of AD did not cause any detectable brain hemorrhages upon microscopic examination. Tillkännagivande • Apr 10
ProMIS Neurosciences Inc. Publishes in the Journal of Biological Chemistry on the Interaction Between Pathogenic Proteins as A Treatment Target for ALS ProMIS Neurosciences Inc. announced the publication of supportive preclinical data in the Journal of Biological Chemistry in an article titled, "Tryptophan residues in TDP-43 and SOD1 modulate the cross-seeding and toxicity of SOD1. ALS is a fatal neurodegenerative disease of motor neurons.oxic aggregates of superoxide dismutase-1 (SOD1) and TAR DNA-binding protein 43 (TDP-43) in motor neurons are characteristic of ALS. The study showed that these two proteins interact such that misfolding of TDP-43 leads to misfolding and aggregation of SOD1 in a cell system and promotes motor neuron damage in zebrafish. The study demonstrated a pathologic synergy between SOD1 and TDP-43 in cell culture and in zebra fish. The interaction between these 2 proteins was characterized at the molecular level. The results indicated that the misfolding TDP-43 epitope previously identified by ProMIS and targeted by PMN267 contains a tryptophan amino acid critical to the pathogenic interaction with SOD1 thereby providing further biological support for the potential of therapeutic intervention with PMN267. Tillkännagivande • Mar 22
ProMIS Neurosciences, Inc., Annual General Meeting, Jun 13, 2024 ProMIS Neurosciences, Inc., Annual General Meeting, Jun 13, 2024. Tillkännagivande • Jan 07
ProMIS Neurosciences, Inc. has filed a Follow-on Equity Offering in the amount of $25 million. ProMIS Neurosciences, Inc. has filed a Follow-on Equity Offering in the amount of $25 million.
Security Name: Common Shares
Security Type: Common Stock
Transaction Features: At the Market Offering Tillkännagivande • Dec 21
ProMIS Neurosciences Announces Publication on Novel Target for ALS ProMIS Neurosciences Inc. announced a publication identifying Receptor for Activated C-Kinase 1 (RACK1) as a novel misfolded protein target for ALS and frontotemporal lobar degeneration (FTLD). The article published in the online edition of Acta Neuropathologica Communications is titled, "Targeting RACK1 to alleviate TDP-43 and FUS proteinopathy-mediated suppression of protein translation and neurodegeneration." TAR DNA-binding protein 43 (TDP-43) and Fused in Sarcoma/Translocated in Sarcoma (FUS) are ribonucleoproteins associated with pathogenesis of ALS and FTLD. Under normal conditions, TDP-43 and FUS are predominantly localized in the nucleus of cells, where they participate in the regulation of protein expression. In disease, however, they typically become mislocalized in the cytoplasm of neurons where they form aggregates. The study authors reported that pathological FUS and TDP-43 both co-aggregate with RACK1 resulting in suppression of protein synthesis. Importantly, they showed that removal (knock-down) of RACK1 can restore protein synthesis in a cell system and alleviate neurodegeneration in a fruit fly model of disease. Tillkännagivande • Nov 21
Promis Neurosciences Inc. Doses First Subjects in Phase 1A Clinical Trial of PMN310 to Treat Alzheimer's Disease ProMIS Neurosciences Inc. announced that the Company dosed the first subjects in a first-in-human Phase 1a clinical trial of PMN310 as a potential treatment for Alzheimer's disease (AD). PMN310 is the Company's novel monoclonal antibody that is designed to be highly selective for toxic oligomers of amyloid-beta (Ab), which are believed to be a major driver of AD. In this Phase 1a clinical trial, will enroll up to five cohorts of eight adult healthy volunteers, each receiving a single dose of PMN310. The company expects to have initial safety and pharmacokinetic (PK) data to share in the first half of 2024. The company remain committed to investigating the hypothesis that selective targeting of toxic oligomers while avoiding monomer distraction and plaque binding will potentially provide differentiation on both safety and efficacy in AD treatment response. Results from the Phase 1a study will facilitate dose selection for subsequent Phase 1b study in patients with mild Cognitive Impairment (MCI) due to AD and patients with mild AD. This study will leverage recent results from a third-party clinical study, which demonstrated that plasma and cerebrospinal fluid (CSF) efficacy biomarkers can show a treatment response in as little as three months with oligomer-focused therapy. In addition, Phase 1b study will provide important insights into the safety profile of PMN310, which anticipate may differentiate PMN310 from other available and potentially disease-modifying treatments. The study titled, "A Phase 1a, Double-Blind, Placebo-Controlled, Single Ascending Dose Study of the Safety, tolerability and Pharmacokinetics of PMN310 Infusions in Healthy volunteers," is a randomized, double-blind, placebo-controlled study to evaluate the safety, tolerability and PK of single ascending doses of intravenous PMN310 in healthy adult volunteers. Eligible subjects will participate in the 85-day study with one optional follow up assessment at Day 120. Primary PK data will be obtained from day 1 to day 29. Tillkännagivande • Jul 11
ProMIS Neurosciences to Delist from TSX ProMIS Neurosciences Inc. announced that it intends to consolidate trading of its shares on the Nasdaq exchange and as such has applied and received approval for a voluntary delisting of its common shares from the Toronto Stock Exchange ("TSX"). The last trading day on TSX will be July 21, 2023. The delisting from the TSX will not affect the Company’s listing on the Nasdaq and common shares will continue to trade uninterrupted on the Nasdaq under the symbol “PMN”. ProMIS joined the Nasdaq Capital Market LLC on July 7, 2022, and it has since become the primary market based on trading volume. The Company believes that this consolidation to the Nasdaq will facilitate the opportunity to undertake transactions in accordance with the rules of Nasdaq as its primary market while creating a central marketplace for common shares and providing sufficient liquidity. The Company also believes that delisting from the TSX will lower the expenses of a dual listing and provide savings in time and effort of management, which can be redirected to initiatives intended to generate shareholder value. In accordance with the requirements of the TSX Company Manual, shareholder approval is not required in respect of the voluntary delisting from the TSX as the Company’s common shares are listed on Nasdaq, which is an acceptable alternative market for the listed securities. Tillkännagivande • May 09
ProMIS Neurosciences Inc. Announces FDA Clearance of Investigational New Drug Application for PMN310 in Alzheimer’s Disease ProMIS Neurosciences Inc. announced that it has received clearance from the U.S. Food and Drug Administration (FDA) for its Investigational New Drug (IND) application for PMN310 for the treatment of AD. PMN310 is a novel monoclonal antibody which is designed to be highly selective for toxic oligomers of amyloid-beta (Aß) that are believed to be a major driver of AD. In preclinical studies, PMN310 showed strong ex vivo target engagement of toxic oligomers in brain samples from patients with AD, with little or no diversion by Aß monomers or plaque. In a recent presentation of in vitro data at the AD/PD 2023 conference, PMN310 was the least impacted by monomer competition, compared to other Aß-directed antibodies, resulting in an overall greater ability to target toxic oligomers. In addition, PMN310 was not observed to bind to plaque, potentially reducing the risk of Aß-related imaging abnormalities (ARIA) observed with plaque-binding antibodies. The Company believes these data support a potentially differentiated clinical profile when compared to other antibody therapeutic candidates in AD. With the IND clearance for PMN310, the Company plans to initiate a Phase 1a clinical trial designed to evaluate the pharmacokinetics, safety and tolerability of a range of PMN310 doses in healthy adult volunteers.