HADHA

Paper reports that obesity exacerbates scarring of the heart’s muscular tissue (myocardial fibrosis) through recruitment of inflammasome ASC to the heart’s mitochondria, facilitating NLRP3 inflammasome assembly and activation leading to damaging inflammationObesity, which affects over 650 million adults, is a known risk factor for myocardial fibrosis which is associated with almost all heart diseasesZyVersa is developing Inflammasome ASC Inhibitor IC 100, designed to inhibit formation of multiple types of inflammasomes and their associated ASC specks to attenuate initiation and perpetuation of damaging inflammation WESTON, Fla., Oct. 25, 2023 (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 a publication in the peer-reviewed journal, Diabetes, demonstrating the role of ASC in myocardial fibrosis induced by obesity. ASC is an inflammasome adaptor protein that has a critical role in inflammasome activation. In the paper titled, “Obesity enables NLRP3 activation and induces myocardial fibrosis via hyperacetylation of HADHa,” the authors performed MRIs on obese and lean people and evaluated their plasma. They also studied an animal model of obesity, with and without induced myocardial injury. Data indicate that: Activated NLRP3 inflammasomes leading to increased levels of proinflammatory IL-1β and IL-18 contribute to obesity-related myocardial fibrosis in obese humans and mice.Inflammasome ASC localized in the heart’s mitochondria participates in NLRP3 inflammasome formation and activation based on mouse data.Inhibition of NLRP3 activation or removal of IL-1β and IL-18 abated the adverse effects on cardiac fibrosis and function in mice. The authors concluded that these results provide new evidence for the involvement of mitochondria-localized ASC in obesity-induced cardiac fibrosis. To read the article, Click Here. “Obesity, a well-established risk factor for cardiovascular disease, has reached pandemic proportions, and may affect up to two-thirds of the adult population in developed countries,” stated Stephen C. Glover, ZyVersa’s Co-founder, Chairman, CEO and President. “The research published in Diabetes demonstrates that ASC in the heart’s mitochondria facilitates NLRP3 inflammasome assembly and activation leading to damaging inflammation and myocardial fibrosis associated with obesity. This provides support for Inflammasome ASC Inhibitor IC 100 as a potential therapeutic option. By inhibiting ASC, IC 100 blocks formation of NLRP3 and other types of inflammasomes to block initiation of the inflammatory cascade. Likewise, IC 100 uniquely inhibits ASC specks to attenuate 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, 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 and IR Contact:Karen CashmereChief Commercial Officerkcashmere@zyversa.com786-251-9641 Media ContactsTiberend Strategic Advisors, Inc.Casey McDonaldcmcdonald@tiberend.com646-577-8520 Dave Schemeliadschemelia@tiberend.com609-468-9325

IRVINE, Calif., Jan. 31, 2023 (GLOBE NEWSWIRE) -- Reneo Pharmaceuticals, Inc. (Nasdaq: RPHM), a clinical-stage pharmaceutical company focused on the development and commercialization of therapies for patients with rare genetic mitochondrial diseases, today announced that the U.S. Food and Drug Administration (FDA) has granted mavodelpar (REN001) Fast Track designation for long-chain 3-hydroxyacyl-CoA dehydrogenase (LCHAD) deficiency, one of the predominant genotypes in patients with long-chain fatty acid oxidation disorder (LC-FAOD). “Receiving this Fast Track designation for a second indication continues to solidify mavodelpar as a potential therapeutic option for patients with rare mitochondrial disease,” said Gregory J. Flesher, President and Chief Executive Officer of Reneo Pharmaceuticals. “We appreciate the continued collaboration with the FDA and look forward to their partnership in advancing the LC-FAOD program which will include patients with LCHAD as well as other genotypes.” The FDA’s Fast Track regulatory process is designed to facilitate and expedite the development of investigational treatments that demonstrate a potential to address unmet medical needs in serious or life-threatening conditions. Programs with FDA Fast Track designation can benefit from early and frequent communication with the FDA in addition to a rolling submission of the marketing application. The company recently completed a natural history study (FORWARD) and an open label study evaluating mavodelpar in patients with LC-FAOD that included multiple genotypes, including the LCHAD genotype. Mavodelpar is also being evaluated in a pivotal clinical trial (STRIDE study) in patients with primary mitochondrial myopathies (PMM) with mitochondrial DNA (mtDNA) defects. The company expects topline data from the STRIDE study in the fourth quarter of this year. About Reneo Pharmaceuticals Reneo is a clinical-stage pharmaceutical company focused on the development and commercialization of therapies for patients with rare genetic mitochondrial diseases, which are often associated with the inability of mitochondria to produce adenosine triphosphate (ATP). Our lead product candidate, mavodelpar (REN001), is a potent and selective agonist of the peroxisome proliferator-activated receptor delta (PPARδ). Mavodelpar has been shown to increase transcription of genes involved in mitochondrial function and increase fatty acid oxidation and may increase production of new mitochondria. For additional information, please see reneopharma.com. About Mavodelpar Mavodelpar (REN001) is a potent and selective peroxisome proliferator-activated receptor delta (PPARδ) agonist currently in clinical development for two rare genetic mitochondrial diseases that typically present with myopathy and have high unmet medical needs: primary mitochondrial myopathies (PMM) and long-chain fatty acid oxidation disorders (LC-FAOD). For additional information, please see clinicaltrials.gov. About PMM PMM are a group of rare, genetic metabolic disorders caused by mutations or deletions in the mitochondrial DNA (mtDNA) or nuclear DNA (nDNA). These genetic alterations hamper the ability of mitochondria to generate energy from nutrient sources, resulting in energy deficits that are most pronounced in tissues with high energy demand such as muscle, brain, and heart. The symptoms of PMM include muscle weakness, exercise intolerance, movement disorder, deafness, blindness, and droopy eyelids among others. The prognosis for these disorders ranges in severity from progressive weakness to death. About LC-FAOD LC-FAOD are a group of rare, genetic metabolic disorders caused by mutations or deletions in the nuclear DNA (nDNA). These genetic alterations prevent the body from breaking down long-chain fatty acids during metabolism. The most severe cases of LC-FAOD are diagnosed within the first few days or weeks of life. Young patients often present with a severe energy deficit that results in lethargy, liver dysfunction, hypoglycemia, encephalopathy, and high risk for sudden death. Older patients usually present with muscle weakness, exercise intolerance, muscle aches, or rhabdomyolysis which can damage the heart and kidneys and cause permanent disability or even death. Forward-Looking Statements Statements contained in this press release regarding matters that are not historical facts are “forward-looking statements” within the meaning of the Private Securities Litigation Reform Act of 1995. Such forward-looking statements include statements regarding, among other things, the potential development, registration, and commercialization of mavodelpar (REN001), results, conduct, progress, plans and timing of Reneo’s clinical studies, completion of enrollment of clinical trials, presentation of data from clinical trials, meetings with regulatory agencies and the regulatory approval path for REN001. Because such statements are subject to risks and uncertainties, actual results may differ materially from those expressed or implied by such forward-looking statements. Words such as “plans,” “will,” “believes,” “anticipates,” “expects,” “intends,” “goal,” “potential” and similar expressions are intended to identify forward-looking statements. These forward-looking statements are based upon Reneo’s current expectations and involve assumptions that may never materialize or may prove to be incorrect. Actual results could differ materially from those anticipated in such forward-looking statements as a result of various risks and uncertainties, which include, without limitation, risks and uncertainties associated with Reneo’s business in general, and the other risks described in Reneo’s filings with the Securities and Exchange Commission. All forward-looking statements contained in this press release speak only as of the date on which they were made. Reneo undertakes no obligation to update such statements to reflect events that occur or circumstances that exist after the date on which they were made, except as required by law. Contacts: Danielle Spangler Investor Relations Reneo Pharmaceuticals, Inc. dspangler@reneopharma.com David Melamed, Ph.D. Media Inquiries Russo Partners, LLC david.melamed@russopartnersllc.com