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Jupiter, Florida, Jan. 13, 2025 (GLOBE NEWSWIRE) -- Jupiter Neurosciences, Inc. (NASDAQ: JUNS) (“Jupiter” or the “Company”), a clinical-stage pharmaceutical company developing JOTROL™, a patented resveratrol-based platform, today announced a strategic focus on targeting the NLRP3 inflammasome in all upcoming clinical trials. This shift aims to unlock new therapeutic potential for neurodegenerative diseases, longevity, and aging, positioning the Company at the forefront of innovation in neuroinflammation treatments. The NLRP3 inflammasome is a key inflammation driver linked to central nervous system (CNS) disorders, metabolic diseases, and aging-related conditions. JOTROL, Jupiter’s flagship product, overcomes resveratrol’s historical challenges of poor bioavailability and gastrointestinal side effects. With its ability to safely reach therapeutic levels in plasma and cross the blood-brain barrier, JOTROL represents a groundbreaking advance for targeting neuroinflammatory pathways like NLRP3. “By adding focus on NLRP3 evaluation, in addition to earlier established biomarkers, we expect to maximize JOTROL’s therapeutic potential in addressing unmet medical needs,” said Christer Rosén, Chairman and CEO of Jupiter Neurosciences. “We believe JOTROL’s ability to inhibit NLRP3, based on multiple published resveratrol trials, makes it an ideal candidate for diseases such as Parkinson’s and Alzheimer’s, and it positions Jupiter to pursue additional collaborations, particularly in the rapidly growing obesity treatment market.” Advancing Parkinson’s and Alzheimer’s Research Preclinical studies at the University of Miami have demonstrated JOTROL’s ability to mitigate key biomarkers of Parkinson’s disease, making this a primary target for Jupiter’s future trials. The company also continues to refine its strategy for Alzheimer’s research, leveraging its prior Phase I pharmacokinetics study funded by the National Institute on Aging. The U.S. Senate’s recent passage of the "National Plan to End Parkinson’s Act" highlights the growing urgency for effective treatments, and Jupiter is aligning its clinical focus to capitalize on this momentum. With a $50 billion market for Alzheimer’s treatments and a $500 million opportunity in Parkinson’s, Jupiter is well-positioned to address these high-value areas. Market Expansion and Strategic Partnerships In addition to its CNS focus, Jupiter is evaluating opportunities in longevity and metabolic health. Emerging data suggests that JOTROL’s inhibition of NLRP3, when combined with GLP-1 treatments, could enhance weight loss outcomes, opening doors to potential collaborations in the obesity market—a multibillion-dollar industry. The Company is also pursuing expansion in the Asia-Pacific region, driven by strong interest from regional partners. Recent agreements to accelerate clinical development and regulatory approval underscore Jupiter’s commitment to global growth. Why JOTROL is Different JOTROL’s patented micellar delivery system allows resveratrol to reach effective concentrations in the bloodstream without causing gastrointestinal side effects—a longstanding barrier for resveratrol-based treatments. This innovative approach has been validated in peer-reviewed studies and forms the basis of Jupiter’s strategy to pursue regulatory approval across multiple indications. About Jupiter Neurosciences, Inc. Jupiter Neurosciences is a clinical-stage pharmaceutical company focused on treating neuroinflammation, with a current focus on CNS disorders and rare diseases. The Company’s platform product, JOTROL™, is an enhanced orally administered resveratrol formulation designed and intended to deliver therapeutically relevant, safe levels of resveratrol. The Company’s pipeline is focused broadly on CNS disorder and includes indications such as Alzheimer’s Disease, Parkinson’s Disease, Mucopolysaccharidoses Type I, Friedreich’s Ataxia, and MELAS. More information may be found on the Company’s website www.jupiterneurosciences.com. About JOTROL Resveratrol is one of the world’s most extensively researched molecules. Thorough evaluation has shown that for the compound to be effective, it requires a high C-Max (~300 ng/ml of resveratrol in plasma), achievable only with doses exceeding 3 grams using earlier resveratrol products. Poor bioavailability has been a well-documented issue with resveratrol. Doses over 2 grams have been associated with severe gastrointestinal (GI) side effects, which have prevented the compound from receiving regulatory approval for any indication.\ Jupiter Neurosciences (JUNS) conducted a Phase I study demonstrating that JOTROL achieves over nine times higher bioavailability compared to resveratrol used in earlier clinical trials (e.g., Turner et al., MCI/Early Alzheimer’s Disease trial, and Yui et al., Friedreich’s Ataxia trial). The results of this Phase I study, which will be cross-referenced in all upcoming JOTROL trials, were published in the Journal of Alzheimer’s Disease and AAPS Open in February 2022. About NLRP3 The NLRP3 inflammasome is a critical component of the innate immune system that mediates caspase-1 activation and the secretion of proinflammatory cytokines IL-1β/IL-18 in response to microbial infection and cellular damage. However, the aberrant activation of the NLRP3 inflammasome has been linked with several inflammatory disorders, which include cryopyrin-associated periodic syndromes, Alzheimer’s disease, diabetes, and atherosclerosis. The NLRP3 inflammasome is activated by diverse stimuli, and multiple molecular and cellular events, including ionic flux, mitochondrial dysfunction, and the production of reactive oxygen species, and lysosomal damage have been shown to trigger its activation. Kelley N, Jeltema D, Duan Y, He Y. The NLRP3 Inflammasome: An Overview of Mechanisms of Activation and Regulation. Int J Mol Sci. 2019 Jul 6;20(13):3328. doi: 10.3390/ijms20133328. PMID: 31284572; PMCID: PMC6651423. FORWARD-LOOKING STATEMENTS Certain statements in this announcement are forward-looking statements. These forward-looking statements involve known and unknown risks and uncertainties and are based on the Company’s current expectations, including the use of proceeds from the Offering. Investors can find many (but not all) of these statements by the use of words such as “approximates,” “believes,” “hopes,” “expects,” “anticipates,” “estimates,” “projects,” “intends,” “plans,” “will,” “would,” “should,” “could,” “may” or other similar expressions. Although the Company believes that the expectations expressed in these forward-looking statements are reasonable, it cannot assure you that such expectations will turn out to be correct. The Company cautions investors that actual results may differ materially from the anticipated results and encourages investors to read the risk factors contained in the Company’s final prospectus and other reports it files with the SEC before making any investment decisions regarding the Company’s securities. The Company undertakes no obligation to update or revise publicly any forward-looking statements to reflect subsequent occurring events or circumstances, or changes in its expectations, except as may be required by law. Contact: Dave GentryRedChip Companies, Inc.1-407-644-42561-800-RED-CHIP (733-2447)JUNS@redchip.com

The first patient with type 2 diabetes mellitus (T2D) and diabetes-related complications has been enrolled in a clinical trial called DAPAN-DIA in Basel, Switzerland, with Olatec's NLRP3 inhibitor, dapansutrile, which is sponsored by Principal Investigator, Marc Donath MD This Phase 2 randomized study is designed to evaluate dapansutrile's efficacy and safety in approximately 300 patients with elevated blood glucose, systemic inflammation and at risk for complications of diabetes, despite use of standard-of-care anti-diabetic therapy DAPAN-DIA represents the first T2D clinical trial of any selective NLRP3 inhibitor in the emerging class that will also assess cardiometabolic and other risk factors beyond anti-hyperglycemic effects including weight lowering efficacy in combination with GLP-1 therapy The trial is being funded by a consortium that includes Olatec, the European Union under the Horizon Europe Programme (GA No 101095433) and the Swiss Government as part of the INTERCEPT-T2D initiative NEW YORK, July 11, 2024 /PRNewswire/ -- Olatec Therapeutics, Inc. (Olatec), a leader in the emerging class of specific NLRP3 inhibitors, announced patients with type 2 diabetes mellitus (T2D) and diabetes-related complications (the DAPAN-DIA Study) are being enrolled in a Phase 2 clinical trial in Basel, Switzerland. Continue Reading The Phase 2 Type 2 Diabetes DAPAN-DIA study is being conducted as an investigator-sponsored study under Principal Investigator Marc Donath MD at the University Hospital of Basel in Switzerland, a long-time Olatec collaborator and advisor as well as a leading researcher-clinician in immuno-metabolism. The DAPAN-DIA Study is a randomized, double-blind, placebo-controlled multi-center trial of the efficacy and safety of dapansutrile in subjects with T2D and diabetes-related complications. Target enrollment is approximately 300 patients who, upon entry into the trial, present with low-grade inflammation, obesity and inadequately controlled glycemia (elevated HbA1c) despite use of standard anti-diabetic therapy. Patients will be treated with dapansutrile or placebo for six months. "We expect the data from this trial, including the combination with GLP-1 therapy, will be highly relevant for understanding the full potential of anti-inflammatory intervention with an NLRP3 inhibitor in this setting," shared Mustafa Noor MD, Chief Medical Officer, Olatec Therapeutics. The study is being conducted as an investigator-sponsored study under Principal Investigator Marc Donath MD at the University Hospital of Basel in Switzerland, a long-time Olatec collaborator and advisor as well as a leading researcher-clinician in immuno-metabolism. In addition to the Swiss sites, the trial is intended to be expanded at medical and scientific diabetes centers of excellence within Europe, including: Hôpital Lariboisière, Hôpital Bichat-Claude Bernard and Hôpital Cochin in Paris, France; German Diabetes Center, Düsseldorf, Germany; and University Hospital of Liège in Belgium. Funding is being provided through the INTERCEPT-T2D initiative by the European Union under the Horizon Europe Programme (GA No 101095433), in collaboration with the Swiss Government and Olatec. T2D is a chronic condition characterized by elevated levels of glucose in blood, resulting from insulin resistance and inadequate insulin secretion. The disease is often concurrent with obesity and associated with a range of complications, including cardiovascular disease, renal dysfunction, retinopathy, neuropathy, and non-alcoholic steatohepatitis, where chronic, elevated low-grade systemic inflammation and activation of NLRP3 and upregulation IL-1β are observed. Unlike existing diabetic treatments that primarily focus on glucose lowering, dapansutrile offers a novel approach to disease-course modification, by targeting the underlying NLRP3 inflammation pathway that is implicated in driving resistance to insulin action in T2D, promoting body weight gain and associated with higher cardiometabolic risks. Dr. Donath stated that, "there is a large unmet need for effective treatment of T2D that goes beyond glycemic control and addresses the underlying inflammatory component of the disease and its cardiometabolic complications. The ground-breaking DAPAN-DIA Study has the potential for dapansutrile to represent a significant step forward in the management of T2D." Olatec's Founder and CEO, Damaris Skouras, commented: "Building on our previous data in heart failure and gout, DAPAN-DIA Study represents a major milestone in the development of dapansutrile in the inter-related cardiometabolic diseases linked by chronic low-grade inflammation due to NLRP3/IL-1 activation." About Type 2 Diabetes Type 2 diabetes (T2D) is a serious, chronic condition that occurs when levels of glucose in blood are elevated because the body cannot produce any or enough of the hormone, insulin, or cannot effectively use the insulin it produces. Insufficient amount of insulin, or the inability of cells to respond to it (insulin resistance), leads to high levels of blood glucose, which is the clinical indicator of T2D and measured clinically as HbA1c. High blood sugar levels can cause damage to many of the body's organs, leading to disabling and life-threatening health complications. Life expectancy for typical patients with T2D has been estimated to be 8 years shorter and driven by 200% increased risk of all-cause mortality. Approximately 70% die from atherosclerotic cardiovascular disease, 40% develop chronic kidney disease (CKD) due to diabetic nephropathy, and almost one-third develop retinopathy. As the prevalence of T2D increases globally, the condition and its associated complications are generating considerable - - and growing - -economic burden on healthcare systems and societies. In 2021, USD $966 billion in global health expenditures were due to T2D, which represents 316% increase over the last 15 years. There are an estimated 537 million adults living with diabetes worldwide, with the total number predicted to rise to 643 million by 2030 and 784 million by 2045. (Source: IDF Atlas 2021) About Scientific Rationale for NLRP3 in Type-2 Diabetes Low-grade chronic inflammatory response is one mechanism leading to the development of insulin resistance, T2D, and associated comorbidities, including liver and kidney damage. In particular, the NLRP3 inflammasome has been shown to play a central role in orchestrating inflammation and immune responses as it is activated in response to several altered metabolic signals in T2D, leading not only to the activation of caspase-1 and production of IL-1β, but also to insulin resistance and pancreatic β cell failure. Furthermore, activation of the NLRP3 inflammasome has been shown to promote vascular inflammation, endothelial dysfunction, and plaque destabilization, contributing to the pathogenesis of atherosclerosis and cardiovascular events. Antagonism of IL-1 pathways has been shown to prevent β-cell dysfunction and to improve glycaemia, cardiovascular complications and heart failure and it may counteract other complications of diabetes. Therefore, targeting this pathway in patients with T2D may have numerous therapeutic advantages over current treatments. (Reviewed by Donath and Dinarello Nature Reviews 2019). About Dr. Marc Donath, Principal Investigator Prof. Dr. Marc Donath is the Chief Physician, Clinic of Endocrinology, Diabetes & Metabolism, University of Basel. Dr. Donath's research aims at the understanding of the pathogenesis of type 2 diabetes, specifically to identify the inflammatory process underlying failure of insulin production in type 2 diabetes. Dr. Donath's work has contributed to the concept that the innate immune system is an integral component in the regulation of metabolism and shows that modulation of the immune system with anti-inflammatory intervention may improve the overall metabolic health and reduce cardiovascular risk in patients with type 2 diabetes. About the INTERCEPT-T2D Consortium INTERCEPT-T2D, which stands for Early Interception of Inflammatory-mediated Type 2 diabetes, coordinated by Nicolas Venteclef U1151 at INSERM (French National Institute of Health and Medical Research) represents a consortium of entities including Olatec, and several established European diabetes centers in addition to the Hôpital Lariboisière, Hôpital Bichat-Claude Bernard and Hôpital Cochin in Paris, France; German Diabetes Center, Düsseldorf, Germany; and University Hospital of Liège in Belgium. Funding is being provided from both (i) European Union under the Horizon Europe Programme (GA 101095433) and (ii) the Swiss Government as part of the Horizon Europe Programme and State Secretariat for Education Research and Innovation, respectively. About Olatec Therapeutics, Inc. Olatec is a leading, clinical-stage biopharmaceutical company developing a platform of oral NLRP3 inhibitors to treat and prevent a broad spectrum of acute and chronic inflammatory diseases. The lead drug candidate, dapansutrile (lab code: OLT1177®) is a small molecule, specific NLRP3 inhibitor, currently in Phase 2/3 clinical development has demonstrated to date that it is well tolerated and shown to improve clinical outcomes in patients with acute gout flare (see The Lancet Rheumatology) and heart failure (see Journal of Cardiovascular Pharmacology). In the heart failure trial, treatment with dapansutrile in subset of subjects with diabetes led to clinically meaningful reductions in fasting glucose levels relative to placebo. Ongoing clinical trials are evaluating dapansutrile in Gout, Parkinson's and Melanoma. For a complete list of Olatec's original publications on dapansutrile in various preclinical and clinical disease areas, please refer to Olatec's publications page, here. For more information, please visit Disclaimer & Forward-looking Statement This press release is not an offer to sell and is not soliciting an offer to buy any equity interests in the Company. The information contained herein is being provided for information purposes only. The Company makes no express or implied representation or warranty as to the completeness of this information. Any forward-looking statements contained in this release are based on assumptions made by Olatec at the time this Press Release was prepared. Any forward-looking statement contained in this Press Release is subject to known and unknown risks, uncertainties and other factors that may be materially different from those contemplated in such forward-looking statements. All information with respect to industry data has been obtained from sources believed to be reliable and current, but the accuracy thereof cannot be guaranteed by the Company. Olatec does not undertake any obligation to update or revise the forward-looking statements contained in this Press Release to reflect events or circumstances occurring after the date this Press Release was prepared, or to reflect the occurrence of unanticipated events. SOURCE Olatec Therapeutics, Inc.

This publication, authored by leading experts in inflammasome-mediated inflammation and neurology at University of Miami Miller School of Medicine, demonstrates that multiple inflammasome triggers (NLRP1 and pyrin) govern the inflammatory response in Alzheimer’s Disease (AD), and that release of inflammasome laden extracellular vesicles (EV) into the blood induce significant inflammation in cardiovascular cells.ZyVersa is developing Inflammasome ASC Inhibitor IC 100 to inhibit multiple types of inflammasomes, including NLRP1 and pyrin, and their associated ASC specks that trigger damaging inflammation and its spread to surrounding tissues.AD, a progressive neurodegenerative disease affecting 6.7 million people in the US, is associated with many comorbidities, especially heart disease and stroke, resulting in increased morbidity and mortality. WESTON, Fla., April 29, 2024 (GLOBE NEWSWIRE) -- ZyVersa Therapeutics, Inc. (Nasdaq: ZVSA, or “ZyVersa”), a clinical stage specialty biopharmaceutical company developing first-in-class drugs for treatment of inflammatory and renal diseases, announces that acclaimed inflammasome researchers from the University of Miami Miller School of Medicine and inventors of Inflammasome ASC Inhibitor IC 100, have published a scientific paper in the peer-reviewed journal, Frontiers in Molecular Neuroscience, highlighting how inflammasome-mediated inflammation in Alzheimer’s disease can trigger inflammation in the heart. The paper titled, “Extracellular vesicles mediate inflammasome signaling in the brain and heart of Alzheimer’s disease mice,” summarizes research evaluating serum and tissue cultures from an AD mouse model, and experiments of adoptive transfer of EV from AD patients into cardiovascular cells. Following is a summary of key findings: NLRP1, pyrin, caspase-1, and ASC were significantly elevated in the cortex of AD mice.In AD mice, there was a heightened level of inflammatory proteins circulating in the body via EVs containing an inflammasome protein cargo.Inflammasome activation was demonstrated in the heart of AD mice, associated with an increase in ASC oligomerization into specks.In adoptive transfer experiments, EVs released from AD patients induced significant inflammation in cardiovascular cells when compared to EVs from healthy individuals. “Our data provide evidence that there is a neural-cardiac axis mediated by EVs in AD. Therefore, inflammasomes may provide a novel therapeutic target for the treatment of cardiac comorbidities in AD and beyond,” said Juan Pablo de Rivero Vaccari, Associated Professor of Neurological Surgery and The Miami Project to Cure Paralysis at the University of Miami. “This research reinforces the importance of attenuating activation of multiple types of inflammasomes that govern the inflammatory response in AD and mediating systemic inflammatory signals in EVs to control the spread of damaging inflammation to cardiovascular and other cells,” commented Stephen C. Glover, ZyVersa’s Co-founder, Chairman, CEO, and President. “ZyVersa’s Inflammasome ASC inhibitor IC 100 is designed to inhibit formation of multiple types of inflammasomes to attenuate initiation of the inflammatory cascade and to inhibit their associated ASC specks to reduce spread and perpetuation of damaging inflammation.” To review a white paper summarizing the mechanism of action and preclinical data for IC 100, Click Here. About Inflammasome ASC Inhibitor IC 100 IC 100 is a novel humanized IgG4 monoclonal antibody that inhibits the inflammasome adaptor protein ASC. IC 100 was designed to attenuate both initiation and perpetuation of the inflammatory response. It does so by binding to a specific region of the ASC component of multiple types of inflammasomes, including NLRP1, NLRP2, NLRP3, NLRC4, AIM2, and Pyrin. Intracellularly, IC 100 binds to ASC monomers, inhibiting inflammasome formation, thereby blocking activation of IL-1β early in the inflammatory cascade. IC 100 also binds to ASC in ASC Specks, both intracellularly and extracellularly, further blocking activation of IL-1β and the perpetuation of the inflammatory response that is pathogenic in inflammatory diseases. Because active cytokines amplify adaptive immunity through various mechanisms, IC 100, by attenuating cytokine activation, also attenuates the adaptive immune response. About ZyVersa Therapeutics, Inc. ZyVersa (Nasdaq: ZVSA) is a clinical stage specialty biopharmaceutical company leveraging advanced, proprietary technologies to develop first-in-class drugs for patients with renal and inflammatory diseases who have significant unmet medical needs. The Company is currently advancing a therapeutic development pipeline with multiple programs built around its two proprietary technologies – Cholesterol Efflux Mediator™ VAR 200 for treatment of kidney diseases, and Inflammasome ASC Inhibitor IC 100, targeting damaging inflammation associated with numerous CNS and other inflammatory diseases. For more information, please visit www.zyversa.com. Cautionary Statement Regarding Forward-Looking Statements Certain statements contained in this press release regarding matters that are not historical facts, are forward-looking statements within the meaning of Section 21E of the Securities Exchange Act of 1934, as amended, and the Private Securities Litigation Reform Act of 1995. These include statements regarding management’s intentions, plans, beliefs, expectations, or forecasts for the future, and, therefore, you are cautioned not to place undue reliance on them. No forward-looking statement can be guaranteed, and actual results may differ materially from those projected. ZyVersa Therapeutics, Inc (“ZyVersa”) uses words such as “anticipates,” “believes,” “plans,” “expects,” “projects,” “future,” “intends,” “may,” “will,” “should,” “could,” “estimates,” “predicts,” “potential,” “continue,” “guidance,” and similar expressions to identify these forward-looking statements that are intended to be covered by the safe-harbor provisions. Such forward-looking statements are based on ZyVersa’s expectations and involve risks and uncertainties; consequently, actual results may differ materially from those expressed or implied in the statements due to a number of factors, including ZyVersa’s plans to develop and commercialize its product candidates, the timing of initiation of ZyVersa’s planned preclinical and clinical trials; the timing of the availability of data from ZyVersa’s preclinical and clinical trials; the timing of any planned investigational new drug application or new drug application; ZyVersa’s plans to research, develop, and commercialize its current and future product candidates; the clinical utility, potential benefits and market acceptance of ZyVersa’s product candidates; ZyVersa’s commercialization, marketing and manufacturing capabilities and strategy; ZyVersa’s ability to protect its intellectual property position; and ZyVersa’s estimates regarding future revenue, expenses, capital requirements and need for additional financing. New factors emerge from time-to-time, and it is not possible for ZyVersa to predict all such factors, nor can ZyVersa assess the impact of each such factor on the business or the extent to which any factor, or combination of factors, may cause actual results to differ materially from those contained in any forward-looking statements. Forward-looking statements included in this press release are based on information available to ZyVersa as of the date of this press release. ZyVersa disclaims any obligation to update such forward-looking statements to reflect events or circumstances after the date of this press release, except as required by applicable law. This press release does not constitute an offer to sell, or the solicitation of an offer to buy, any securities. Corporate, Media, and IR Contact:Karen CashmereChief Commercial Officerkcashmere@zyversa.com786-251-9641