Latest news with #fibrosis
Associated Press
5 days ago
- Business
- Associated Press
Mediar Therapeutics Doses First Patient in Phase 2 WISPer Trial of MTX-463 for Idiopathic Pulmonary Fibrosis
First-in-class agent targets WISP1 in patients with IPF Primary endpoint in WISPer trial is change in Forced Vital Capacity (FVC) at 24 Weeks BOSTON, June 5, 2025 /PRNewswire/ -- Mediar Therapeutics, Inc., a clinical-stage biotechnology company advancing first-in-class therapies designed to halt fibrosis, today announced the first patient has been dosed in its Phase 2 WISPer clinical trial evaluating MTX-463, an investigational therapy for idiopathic pulmonary fibrosis (IPF). The study's primary endpoint is the change from baseline in forced vital capacity (FVC)—an important measure of lung function—at 24 weeks. The study aims to advance the development of a potential novel treatment for patients living with IPF, and targets the myofibroblast, the key pathogenic cell in fibrosis. Mediar recently entered into a global licensing agreement with Lilly to advance MTX-463 through the Phase 2 WISPer trial. IPF is a rare and progressive lung disease characterized by scarring and thickening of lung tissue, which leads to increasing shortness of breath and a persistent dry cough. Despite available treatments, there remains a high unmet medical need, with an average life expectancy of three to five years post-diagnosis. The WISPer trial is a randomized, double-blind, placebo-controlled 24-week Phase 2 study designed to evaluate the efficacy, safety, and tolerability of MTX-463 in patients living with IPF. 'Dosing the first patient in the WISPer trial represents an important step forward in the pursuit of new options to address the urgent needs of individuals living with IPF,' said Toby Maher, MD, PhD, Director of Interstitial Lung Disease, University of Southern California, and lead investigator in the Phase 2 clinical study. 'IPF is a devastating disease with limited treatment options. We are eager to evaluate the potential of MTX-463 to slow or halt disease progression and look forward to the insights this study will provide for patients and their physicians.' 'Today marks an important milestone in our ongoing commitment to pioneering novel therapies to impact people living with fibrotic diseases. We extend our gratitude to Dr. Ryan Klein and the dedicated team at NewportNativeMD whose expertise and collaboration have been instrumental in reaching this important step,' said Jeff Bornstein, MD, Chief Medical Officer, Mediar. 'The first patient dosed with this first-in-class anti-fibrotic marks the beginning of a new chapter in our research, and we look forward to working with our clinical sites as we continue to enroll the Phase 2 program.' Mediar is also independently advancing its two wholly owned programs to treat other fibrotic disorders. MTX-474, a first-in-class human IgG1 antibody designed to neutralize EphrinB2 signaling, recently completed its Phase 1 clinical study. Mediar anticipates initiating a Phase 2 trial for MTX-474 in systemic sclerosis in the second half of 2025. Mediar's third novel fibrosis program, targeting SMOC2 for renal fibrosis, is also advancing with a plan to nominate a clinical candidate in the first half of 2025. About MTX-463 MTX-463 is a first-in-class human IgG1 antibody developed against WNT1-inducible signaling pathway protein-1 (WISP1). WISP1 is a secreted matricellular protein shown to have a relevant role in fibrosis progression, is measurable in human blood, and correlates with disease severity. Data indicates that MTX-463 neutralizes WISP1-mediated fibrotic signaling and significantly reduced fibrosis in vitro and in various preclinical models. A Phase 1 study was recently completed and a Phase 2 study in patients with IPF is now open (NCT06967805). More information can be found at: About Mediar Therapeutics Mediar Therapeutics is pioneering a new approach to fibrosis treatment that aims to halt the disease at a different source – the myofibroblast, the key pathogenic cell in fibrosis that drives scarring, disease progression, and ultimately organ failure. Mediar was founded based on a deep understanding of the complex science underlying fibrosis progression. By combining novel targets with reliable, easily detectable blood biomarkers and familiar modalities, Mediar's goal is to bring forward novel anti-fibrotic therapies that potentially have a precision medicine approach. For more information, contact [email protected] or follow us on LinkedIn. Media Contact [email protected] View original content to download multimedia: SOURCE Mediar Therapeutics
Yahoo
31-05-2025
- Business
- Yahoo
Gyre Therapeutics, Inc. (GYRE) Raises $23M in Public Stock Offering to Fund Liver Fibrosis Trials
Gyre Therapeutics, Inc. (NASDAQ:GYRE), a biopharmaceutical company developing innovative fibrosis-focused therapies, has successfully closed a public offering, raising approximately $23 million in gross proceeds. The offering included 2,555,555 shares of common stock at $9.00 per share, with Jefferies serving as lead book-running manager and H.C. Wainwright & Co. as co-manager. A research scientist in an idiopathic pulmonary fibrosis laboratory, carrying out clinical trials. The capital infusion, which follows the full exercise of underwriters' options, will support Gyre Therapeutics, Inc. (NASDAQ:GYRE)'s ongoing Phase 2 clinical trial of F351, a promising treatment targeting liver fibrosis in patients with metabolic dysfunction-associated steatohepatitis (MASH) in the United States. The funds will also bolster research and development, manufacturing scale-up, and general corporate operations. The shares were offered under a shelf registration statement previously approved by the SEC. Gyre Therapeutics, Inc. (NASDAQ:GYRE)'s latest fundraising effort underscores its commitment to advancing therapies for chronic diseases marked by fibrosis, aiming to address significant unmet medical needs. While we acknowledge the potential of GYRE to grow, our conviction lies in the belief that some AI stocks hold greater promise for delivering higher returns and have limited downside risk. If you are looking for an AI stock that is more promising than GYRE and that has 100x upside potential, check out our report about this READ NEXT: and Disclosure: None. Sign in to access your portfolio
Yahoo
16-05-2025
- Health
- Yahoo
Nordic Bioscience launches novel Endotrophin assay
HERLEV, Denmark, May 16, 2025 /CNW/ -- Nordic Bioscience introduces nordicEndotrophin™, a fully automated high-precision assay that selectively quantifies the intact 77-amino-acid Endotrophin signaling hormone—qualified in the CAP/CLIA certified Nordic Bioscience laboratory. When integrated with the company's existing product line, the biomarker assay demonstrated prognostic utility in fibrosis and cancer studies1. NordicEndotrophin™ joins nordicPRO-C6™ and nordicPRO-C3™ (in-house versions of the FDA-supported PRO-C6 and CE approved PRO-C3 assays) to deliver a one-stop solution for assessing the fibro-inflammatory axis in chronic diseases, including cardiovascular, metabolic, renal and more. Following PRO-C3's recent deployment on Roche IVD platforms, the new Endotrophin assay strengthens risk stratification and pharmacodynamic monitoring. Endotrophin was first identified in 2012 as a collagen-derived hormone released from type VI collagen. Type VI collagen is a contributor to fibroblast activation and driver of fibrosis across organs—inflammatory processes that underlie roughly 40 percent of deaths in Western countries2. Obesity exacerbates this by activating fibroblasts in the liver, kidney and heart. Across a range of chronic diseases, patients with a two-fold increase of circulating Endotrophin levels increased risk of mortality by 100%1,2. Quantifying Endotrophin enables researchers to connect wound healing and fibrotic progression to patient outcomes, supporting precision-medicine approaches that pharmacodynamically modulate this dangerous hormone. Whereas PRO-C6, Nordic Bioscience's first hand-held ELISA assay measuring the formation of the total pool of type VI collagen (a3 chain encompassing 12 Von Willebrand binding domains), a collagen responsible for binding of platelets that cause fibroblast activation and would healing, nordicEndotrophin™ specifically measures the intact 77-amino-acid hormone. This specificity means additional risk stratification and prognostic value that complement PRO-C6's fibrosis-driven pharmacodynamic insights1. "Endotrophin is a significant prognostic biomarker to emerge," said CEO Dr. Morten Karsdal. "Evidenced in a study of HFpEF patients, Endotrophin and PRO-C6 outperformed NT-proBNP in HFpEF for mortality and hospitalization risk3. Together with PRO-C3, quantifying this fibro-inflammatory hormone will refine patient stratification and treatment monitoring across obesity, fibrotic diseases, and autoimmune endotypes." Offered in Nordic Bioscience's CAP/CLIA-certified laboratory in Herlev, Denmark, the nordicEndotrophin™ high-precision sandwich assay is available on fully automated, high-accuracy, high-throughput platforms. To accelerate drug fibro-inflammatory profiling, clients considering nordicEndotrophin™ are invited to co-measure nordicPRO-C3™ and nordicPRO-C6™. Together, these assays facilitate precise risk stratification, dose selection, patient enrichment, proof-of-mechanism and treatment monitoring in anti-fibrotic and oncology trials2. About Nordic Bioscience Nordic Bioscience is a Danish biomarker company headquartered in Herlev, Denmark. We are engaged in biomarker development using our unique neoepitope technology. We combine our expertise in biomarker development with preclinical and clinical research. This enables us to develop biomarkers that provide fast and objective decision-making for compound selection and development in clinical trials as well as provide value for patients in a diagnostic setting. For more information about Nordic Bioscience, visit us at References: [1] [2] [3] For product related inquires please use Logo: View original content to download multimedia: SOURCE Nordic Bioscience View original content to download multimedia: Sign in to access your portfolio
Medscape
09-05-2025
- Health
- Medscape
Efruxifermin Shows Fibrosis Reduction in MASH Cirrhosis
AMSTERDAM — A once daily, 50 mg dose of efruxifermin reduced fibrosis at 96 weeks in patients with compensated cirrhosis due to metabolic dysfunction-associated steatohepatitis (MASH) compared with placebo, but it did not significantly reduce fibrosis at 36 weeks (primary endpoint), according to results from the phase 2b SYMMETRY trial. Efruxifermin is a long-acting, bivalent fibroblast growth factor 21 analogue. At 96 weeks of treatment, a statistically significant 29% of patients had at least one stage of fibrosis improvement without MASH worsening (secondary outcome) compared with 11% on placebo. Results also suggested improvements in MASH-related histologic findings, non-invasive markers of liver injury and fibrosis, as well as markers of glucose and lipid metabolism at 96 weeks. Now the 50 mg dose of efruxifermin is being investigated in phase 3 development. Mazen Noureddin, MD, MHSc Academic-clinician Mazen Noureddin, MD, MHSc, of the Sherrie and Alan Conover Center for Liver Disease and Transplantation at Houston Methodist Hospital, Texas, presented the findings here at the at the European Association for the Study of the Liver (EASL) Congress 2025. The work was published simultaneously in The New England Journal of Medicine . Noureddin said that, for the first time, they showed 'significant, unprecedented improvement in fibrosis' on the regimen. He added that the 'histologic improvement in fibrosis corroborated with non-invasive tests, presenting an overall picture of liver injury and function that suggests liver health is maintained or slightly improved by efruxifermin compared to placebo.' Despite being a major cause of liver failure and transplantation, there are currently no approved therapies that reverse fibrosis in MASH-related cirrhosis. Efruxifermin has shown antifibrotic effects in earlier studies of patients with less advanced disease (F2-F3 fibrosis). Now, this phase 2b, randomized, placebo-controlled, double-blind trial, shows efficacy and safety with efruxifermin in patients with MASH who had biopsy-confirmed compensated cirrhosis at stage 4 fibrosis. The Trial SYMMETRY was conducted across 45 sites in the US, Mexico, and Puerto Rico. It enrolled 181 adults with biopsy-confirmed compensated cirrhosis due to MASH (Child-Pugh A), 80% of whom had diabetes and obesity. Patients were at high risk for hepatic decompensation. Participants were 18-75 years of age, had liver histologic features consistent with MASH, and had compensated cirrhosis (stage 4 fibrosis with a Child-Pugh score of 5 or 6). They also had type 2 diabetes or two components of metabolic syndrome comprising obesity, dyslipidemia, elevated blood pressure, and elevated fasting glucose level. Approximately 80% of the patients had biopsy-confirmed MASH. Patients received weekly subcutaneous efruxifermin (28 mg or 50 mg) or placebo in a 1:1:1 ratio. Liver biopsies were obtained at weeks 36 and 96 and were included in the intention-to-treat and safety analyses. Overall, liver biopsy data were available for 154 patients at week 36 and for 134 patients at week 96. The primary endpoint comprised a reduction of at least one stage of fibrosis without worsening of MASH at week 36, while the same measure comprised the secondary outcome at week 96. At 36 weeks, in the intent-to-treat analysis, a reduction in fibrosis without worsening of MASH was seen in 8/61 patients (13%) in the placebo group, 10/57 patients (18%) in the 28 mg efruxifermin group (95% CI, -11 to 17; P = .62), and 12/63 patients (19%) in the 50 mg efruxifermin group (95% CI, -10 to 18; P = .52). Referring to the 36-week completer analysis, Noureddin reported, 'We see here, 24% in the 50 mg group compared with 14% in those on placebo [and 22% on the 28-mg dose]. When they continue treatment up to 96 weeks, we saw up to 39% improvement [50-mg dose] in fibrosis by one stage without worsening of MASH compared to 15% placebo [and 29% with 28 mg]. This is a difference of 24% [between placebo and 50 mg] that was statistically significant [ P < .01],' he reported. In the intent-to-treat analysis, at week 96, a reduction in fibrosis without worsening of MASH occurred in 7/61 patients (11%) in the placebo group, in 12/57 patients (21%) in the 28 mg efruxifermin group (95% CI, -4 to 24), and in 18/63 patients (29%) in the 50 mg efruxifermin group (95% CI, 2-30). 'It was up to 29% in the 50 mg compared with 11%, and that's an 18% statistically significant difference [ P < .05].' The proportion of week 36 responders who sustained response to week 96 were 50% (n = 4), 67% (n = 6), and 75% (n = 9), in the placebo, 28 mg, and 50 mg groups, respectively. Expanded response (non-response at week 36 but response at week 96) was 8% (n = 3), 19% (n = 6), and 26% (n = 9) respectively. 'This emphasizes the role of ongoing treatment in cirrhotic patients,' said Noureddin. He also added that they saw 'consistent responses across multiple baseline subgroups for the primary histological endpoint and at week 96 with the 50 mg.' Nearly all participants (99% on efruxifermin and 97% on placebo) reported adverse events. Any serious adverse events were reported in 26%, 24%, and 18% in the 28 mg, 50 mg, and placebo groups, respectively. Gastrointestinal side effects were most common: diarrhea (42%, 54%, and 30% on 28 mg, 50 mg, and placebo, respectively), nausea (30%, 46%, 30%, respectively), and increased appetite (16%, 40%, 7%, respectively) and mostly of mild-to-moderate nature. Administration-site reactions (erythema) were also more common with efruxifermin (13%, 16%, and 6%, respectively). After week 36 and prior to week 96, discontinuations due to adverse events were 0%, 2%, and 3% in the placebo, 28 mg, and 50 mg, respectively. 'After week 36, there were very few discontinuations due to side effects,' reported Noureddin. Poor bone health is a common complication of cirrhosis, and across all treatment groups, 43% of participants had osteopenia at baseline, but only 4% were treated with bisphosphonates. Placebo-adjusted, significant relative reductions in bone mineral density (-5%) for spine and hip were observed for both treatment groups at week 96 or about 2%-3% per year. The number of participants experiencing fractures was equal across all treatment groups, added Noureddin. Commenting on the study, delegate and chairman of the Global NASH Council, Zobair M Younossi, MD, professor and chairman of the department of medicine at Inova Fairfax Medical Campus, Fairfax County, Virgina, told Medscape Medical News , 'The key to this whole area is that there are treatments that have been developed for non-cirrhotic MASH, F2 and F3, but there is currently nothing that is positive for people with cirrhosis and MASH. This study shows there is improvement in all categories even in those with diabetes and even when they are controlled for some alcohol consumption.' He added, 'I think that the best aspect of this is that it gives us a potential treatment for those patients who are at highest risk for bad outcomes in MASLD, which are those with cirrhosis.' The study was supported by Akero Therapeutics. Noureddin declared grants, consultant roles, and stock options from many pharmaceutical companies, including Akero. Younossi reported no relevant financial relationships.
Yahoo
09-05-2025
- Business
- Yahoo
Akero Therapeutics Presents Week 96 Results from Phase 2b SYMMETRY Clinical Trial of Efruxifermin in Patients with Compensated Cirrhosis Caused by MASH Showing Fibrosis Improvement without Worsening of MASH at the EASL Congress 2025
SOUTH SAN FRANCISCO, Calif., May 09, 2025 (GLOBE NEWSWIRE) -- Akero Therapeutics, Inc. (Nasdaq: AKRO), a clinical-stage company developing transformational treatments for patients with serious metabolic diseases marked by high unmet medical need, presented results from the Phase 2b SYMMETRY trial demonstrating the potential of efruxifermin (EFX) to improve fibrosis in compensated cirrhosis (F4) caused by metabolic dysfunction-associated steatohepatitis (MASH), in a late-breaking oral presentation at the European Association for the Study of the Liver (EASL) Congress 2025 taking place May 7-10, in Amsterdam, the Netherlands. 'Compensated cirrhosis due to MASH remains a high unmet medical need, leaving patients with a poor prognosis and currently no effective treatment options beyond liver transplant,' said Kitty Yale, chief development officer of Akero. 'These data presented at the EASL Congress 2025 differentiate EFX from other approved or investigational MASH treatments as the first to demonstrate fibrosis reversal in patients with MASH caused by cirrhosis. We look forward to continuing evaluation of EFX across all stages of MASH in our Phase 3 SYNCHRONY program.' 'Patients with cirrhosis caused by MASH could face a 50 percent chance of dying within five years without a liver transplant,' said Mazen Noureddin, M.D., Professor of Medicine and Transplant Hepatologist at Houston Methodist Hospital, and principal investigator for the SYMMETRY study. 'EFX's powerful anti-fibrotic activity, as observed in the Phase 2b SYMMETRY trial and currently being evaluated in Phase 3, has the potential to be the most substantial medical breakthrough in my career as a treating physician.' Week 96 data presented from SYMMETRY, a Phase 2b trial evaluating the efficacy and safety of Akero's lead product candidate, EFX, in patients with biopsy-confirmed compensated cirrhosis (F4) due to MASH, showed fibrosis reduction without MASH worsening by both completer and intent-to-treat (ITT) analyses after 96 weeks. In the pre-specified analysis of patients with baseline and week 96 biopsies (N=134), 39% of patients treated with EFX 50mg had fibrosis improvement compared to 15% of placebo-treated patients (p=0.009). In the ITT population (N=181), with missing week 96 biopsies treated as non-responders, 29% of patients in the EFX 50mg group experienced this improvement, compared to 11% for placebo (p=0.031). The primary endpoint of the SYMMETRY study was ≥1 stage fibrosis improvement with no worsening of MASH at Week 36. A numerical improvement was observed in the EFX groups vs. placebo at Week 36 but the differences were not statistically significant. Summary of Week 96 Fibrosis Improvement without MASH Worsening Secondary Endpoint Primary Analysis (N=134)1 ITT Analysis (N=181)2 Histology Endpoint3 (Proportion of Patients) Placebo(N=47) EFX 28mg(N=41) EFX 50mg(N=46) Placebo(N=61) EFX 28mg(N=57) EFX 50mg(N=63) ≥1 stage fibrosis improvement without worsening MASH (%) 15 29 39 ** 11 21 29 * 1 All patients with baseline and week 96 biopsies2 The 47 randomized and dosed patients who had missing biopsies at week 96 are treated as non-responders in the ITT analysis (without imputation).3 Biopsies scored independently by two pathologists; third available to adjudicate (which was not required)* p<0.05, ** p<0.01, versus placebo (Cochran-Mantel-Haenszel test). Comparison of the proportion of patients with a fibrosis reduction at Week 36 and Week 96 in the pre-specified analysis of patients with baseline and week 96 biopsies, showed more than a doubling of placebo-adjusted treatment effect for the EFX 50mg group, from 10% to 24%. This increase in effect size shows the importance of longer treatment with EFX for patients with compensated cirrhosis (F4) as compared to responses observed in trials of EFX in patients with earlier stage fibrosis (F2 or F3). The larger treatment effect observed after 96 weeks is corroborated by changes in noninvasive measures of liver fibrosis and injury. For example, two key non-invasive measures of the extent of fibrosis development in the whole liver, ELF test score and liver stiffness by Fibroscan, showed continuing improvement over 96 weeks for the 50mg EFX group. Newly presented analyses showed EFX's potential to improve fibrosis among patients with compensated cirrhosis across key subgroups. Patients responded to EFX 50mg after 96 weeks regardless of type 2 diabetes status or treatment with GLP-1 medications or statins at baseline. The safety and tolerability profile of EFX was consistent with previous trials. The most frequent adverse events with EFX were gastrointestinal (diarrhea, nausea, increased appetite) and most were mild to moderate and transient. All serious adverse events were deemed to be unrelated to study drug. Details for the presentation are as follows: Title: Efruxifermin improves fibrosis in participants with compensated cirrhosis due to MASH: results of a 96-week, randomized, double-blind, placebo-controlled, phase 2b trial (SYMMETRY)Speaker: Mazen Noureddin, M.D., Professor of Medicine, Houston Methodist Hospital and Director, Houston Research InstituteDate/Time: Friday, May 9, 2025, from 12:15 pm – 12:30 pm CET Abstract Identifier: GS-012Oral Session: General Session 2 About Cirrhosis Due to MASH Cirrhosis due to MASH (metabolic dysfunction-associated steatohepatitis) is a life-threatening disease with high risk of liver failure, cancer, and death. By 2030, an estimated 3 million Americans are projected to have MASH cirrhosis, which is the fastest growing cause of liver transplants and liver cancer in the United States and Europe. About the SYMMETRY Study SYMMETRY was a Phase 2b, multicenter, randomized, double-blind, placebo-controlled, dose-ranging trial in adult patients with biopsy-confirmed compensated cirrhosis (F4, Child-Pugh A) due to MASH. The study randomized 182 patients, and 181 received once-weekly subcutaneous EFX 28mg or 50mg, or placebo for 96 weeks. The primary efficacy endpoint was the proportion of patients with ≥1 stage fibrosis improvement without worsening of MASH at Week 36. Secondary efficacy measures at Week 96 included ≥1 stage fibrosis improvement without worsening of MASH, MASH resolution, change from baseline in liver enzymes, noninvasive markers of liver fibrosis, serum markers of glucose and lipid metabolism, as well as safety and tolerability measures. About EFXEfruxifermin (EFX), Akero's lead product candidate for MASH, is currently being evaluated in three ongoing Phase 3 studies. In multiple Phase 2 studies, EFX has been observed to reverse fibrosis (including compensated cirrhosis), resolve MASH, reduce non-invasive markers of fibrosis and liver injury, and improve insulin sensitivity and lipoprotein profile. This holistic profile offers the potential to address the complex, multi-system disease state of all stages of MASH, including improvements in risk factors linked to cardiovascular disease – the leading cause of death among MASH patients. Engineered to mimic the biological activity profile of native FGF21, EFX is designed to offer convenient once-weekly dosing and has been generally well-tolerated in clinical trials to date. About Akero Therapeutics Akero Therapeutics is a clinical-stage company developing transformational treatments for patients with serious metabolic diseases marked by high unmet medical need, including metabolic dysfunction-associated steatohepatitis (MASH). Akero's lead product candidate, efruxifermin (EFX), is currently being evaluated in three ongoing Phase 3 clinical studies: SYNCHRONY Histology in patients with pre-cirrhotic (F2-F3 fibrosis) MASH, SYNCHRONY Outcomes in patients with compensated cirrhosis (F4) due to MASH, and SYNCHRONY Real-World in patients with MASH or MASLD (metabolic dysfunction-associated steatotic liver disease). The Phase 3 SYNCHRONY program builds on the results of two Phase 2b clinical trials, the HARMONY study in patients with pre-cirrhotic MASH and the SYMMETRY study in patients with compensated cirrhosis due to MASH. Akero is headquartered in South San Francisco. Visit us at and follow us on LinkedIn and X for more information. 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. Because such statements are subject to risks and uncertainties, actual results may differ materially from those expressed or implied by such forward-looking statements, including, but not limited to, statements regarding Akero's business plans and objectives; the potential therapeutic effects and anti-fibrotic activity of EFX, as well as the dosing, safety and tolerability of EFX, the future potential and long-term benefits of EFX following the preliminary topline week 96 results of Akero's Phase 2b SYMMETRY study and the ongoing SYNCHRONY Phase 3 program. Any forward-looking statements in this press release are based on management's current expectations of future events and are subject to a number of risks and uncertainties that could cause actual results to differ materially and adversely from those set forth in or implied by such forward-looking statements. Risks that contribute to the uncertain nature of the forward-looking statements include: the success, cost, and timing of Akero's product candidate development activities and planned clinical trials; Akero's ability to execute on its strategy; positive results from any of its clinical studies may not necessarily be predictive of the results of future or ongoing clinical studies; regulatory developments in the United States and foreign countries; Akero's ability to fund operations; as well as those risks and uncertainties set forth more fully under the caption "Risk Factors'' in Akero's most recent Annual Report on Form 10-K and Quarterly Report on Form 10-Q, as filed with the Securities and Exchange Commission (SEC) as well as discussions of potential risks, uncertainties and other important factors in Akero's other filings and reports with the SEC. All forward-looking statements contained in this press release speak only as of the date on which they were made. Akero undertakes no obligation to update such statements to reflect events that occur or circumstances that exist after the date on which they were made. Investor Contact:Christina TartagliaPrecision AQ212.362.1200IR@ Media Contact:Peg RusconiDeerfield in to access your portfolio
