Epoprostenol Sodium

GOTHENBURG, Sweden, March 31, 2026 /PRNewswire/ -- Cereno Scientific (NASDAQ First North: CRNO B) , an innovative biotech pioneering treatments to enhance and extend life for people with rare cardiovascular and pulmonary diseases, today announced initial learnings from the 12-month Expanded Access Program (EAP) with its lead drug candidate CS1 in pulmonary arterial hypertension (PAH). The data confirm a favorable safety and tolerability profile over long-term treatment, consistent with previous Phase IIa results, further strengthening the value proposition of CS1 as an oral, once-daily potentially disease-modifying therapy. The Expanded Access Program (EAP) enrolled ten patients who had completed the Phase IIa trial, enabling continued treatment with CS1 under physician supervision. Initial learnings from the completed 12-month treatment period show that CS1 was well tolerated, with no unexpected safety concerns observed. No deaths were reported, and no discontinuations were reported to be related to CS1. Six out of ten patients completed the full 12 months of continuous treatment with CS1. Of the remaining patients, two discontinued CS1 treatment following atrial fibrillation events, which was assessed as not related to CS1; one withdrew consent, and one was lost to follow-up. "These results provide important confirmation that the favorable safety and tolerability profile observed in the Phase IIa trial is maintained over longer-term use. In PAH, where existing therapies can be associated with safety and tolerability challenges, there remains a significant unmet need for safer, well-tolerated treatment options. These findings support the continued development of CS1 as a potential disease-modifying therapy," said Rahul Agrawal, CMO and Head of R&D of Cereno Scientific. The EAP was conducted under a formal FDA protocol and initiated following requests from patients and physicians. It enabled the generation of additional long-term data beyond the three-month Phase IIa trial, which had demonstrated that CS1 had favorable safety and tolerability and showed encouraging efficacy signals, including improvements in right heart function, functional class and patient quality of life, with signs consistent with reverse vascular remodeling. Together, the Phase IIa trial and the EAP provide up to 15 months of treatment experience in patients, further strengthening the overall clinical understanding of CS1 in PAH. "The accumulated clinical Phase II data representing up to 15 months of treatment with CS1 in patients with PAH, provides us with further confidence in our goal to develop and deliver CS1 as a new treatment for patients with PAH. The results from the EAP study support the value proposition of CS1 as an oral, once-daily PAH therapy with a favorable safety and tolerability profile and potential disease-modifying effects," said Sten R. Sörensen, CEO of Cereno Scientific. The EAP was initiated following positive results of the Phase IIa trial, which evaluated the safety, tolerability, pharmacokinetics, and exploratory efficacy of CS1 on top of standard therapy in patients with PAH. The Phase IIa trial was conducted at 10 US clinics over 3 months with a total of 25 patients of which 21 were evaluated for efficacy parameters. The trial successfully met its primary endpoint of safety and tolerability, with no drug-related serious adverse events. Encouraging efficacy signals were observed in the trial, including improvements in right heart function, functional class and patient quality of life, with early signs consistent with reverse vascular remodeling. Preparations for a larger, placebo-controlled global Phase IIb study of CS1 in PAH are ongoing, with first patient enrollment anticipated in June 2026. Further analyses from the EAP, including results from the exploratory imaging sub-study using Fluidda's technology, are planned to be communicated during Q2 2026. For further information, please contact: Tove Bergenholt, Head of IR & Communications Email: [email protected] Phone: +46 73- 236 62 46 About PAH PAH is a rare, progressive and life-threatening disease characterized by high blood pressure in the pulmonary arteries that leads to right heart failure and premature death. Current standard treatments mainly focus on managing symptoms, leaving a significant unmet need for disease-modifying therapies that can change the course of disease and improve long-term outcomes. About CS1 CS1 is an orally administered histone deacetylase inhibitor (HDACi) in development as a well-tolerated, disease-modifying therapy for pulmonary arterial hypertension (PAH) with favorable safety profile. Acting through epigenetic modulation, CS1 targets key disease-driving mechanisms such as vascular remodeling, fibrosis and inflammation. CS1 has shown disease-modifying potential in early clinical evaluation and is being evaluated as an add-on (on top of standard-of-care) therapy with the potential to improve outcomes for patients with high unmet medical needs. It has been granted Orphan Drug Designation (ODD) in both the U.S. and the EU and received Fast Track designation from the U.S. FDA in August 2025, underscoring its potential to address a serious condition with high unmet medical need. CS1 has first-in-class potential and is currently in preparation for a global Phase IIb trial. About Cereno Scientific AB Cereno Scientific is pioneering treatments to enhance and extend life. The company's innovative pipeline offers disease-modifying drug candidates to empower people suffering from rare cardiovascular and pulmonary diseases to live life to the fullest. Lead candidate CS1 is an HDAC inhibitor that works through epigenetic modulation and represents a novel therapeutic approach by targeting the root mechanisms of the pulmonary arterial hypertension (PAH). CS1 is a well-tolerated oral therapy with a favorable safety profile that has shown encouraging efficacy signals in a Phase IIa trial in patients with PAH, including improvements in right heart function, functional class and patient quality of life, with early signs consistent with reverse vascular remodeling. An Expanded Access Program enables patients that have completed the Phase IIa trial to gain access to CS1. CS014 is a new chemical entity and HDAC inhibitor with a multimodal mechanism of action as an epigenetic modulator having the potential to address the underlying pathophysiology of a range of cardiovascular and pulmonary diseases with high unmet needs. CS014 showed favorable safety and tolerability profile in Phase I, development focus for Phase II is pulmonary hypertension associated with interstitial lung disease (PH-ILD). Cereno Scientific is also pursuing a preclinical program with CS585, an oral, highly potent and selective prostacyclin (IP) receptor agonist that has demonstrated the potential to significantly improve disease mechanisms relevant to cardiovascular diseases. While CS585 has not yet been assigned a specific indication for clinical development, preclinical data indicates that it could potentially be used in rare thrombotic diseases. The Company is headquartered in GoCo Health Innovation City, in Gothenburg, Sweden, and has a US subsidiary; Cereno Scientific Inc. based in Kendall Square, Boston, Massachusetts, US. Cereno Scientific is listed on the Nasdaq First North (CRNO B). The Company's Certified Adviser is DNB Carnegie Investment Bank AB, [email protected]. More information can be found on . This information was brought to you by Cision . The following files are available for download: 21% more press release views with Request a Demo

RAHWAY, N.J.--(BUSINESS WIRE) March 29, 2026 -- Merck (NYSE: MRK), known as MSD outside of the United States and Canada, today announced detailed results from the Phase 2 CADENCE study, which was designed to evaluate the efficacy, safety and tolerability of two doses (0.3 mg/kg and 0.7 mg/kg) of WINREVAIR™ (sotatercept-csrk) for the treatment of adults with the syndrome of combined post- and precapillary pulmonary hypertension and heart failure with preserved ejection fraction (CpcPH-HFpEF). In this distinct patient population, WINREVAIR showed a statistically significant and clinically meaningful reduction from baseline in pulmonary vascular resistance (PVR) versus placebo (n=55) at week 24, with a 1.02 Wood units reduction for the 0.3 mg/kg dose (n=54, [95% CI, -1.81, -0.23], p=0.004) and a 0.75 Wood units reduction for the 0.7 mg/kg dose (n=55, [95% CI -1.52, 0.03], p=0.024). As noted below, important secondary endpoints explored include six-minute walk distance (6MWD), echocardiographic measures, N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels and time to clinical worsening (TTCW). These late-breaking data were presented today in a late-breaking clinical trial presentation at the American College of Cardiology’s Annual Scientific Session and Expo (ACC.26), simultaneously published in Circulation and featured as part of an ACC.26 press conference. Merck’s WINREVAIR met primary endpoint of change in pulmonary vascular resistance (PVR), significantly improving the ability of blood to flow through the lungs to the heart Totality of evidence across hemodynamic, functional, echocardiographic and clinical endpoints supports advancing development of WINREVAIR for this distinct patient population into a registrational Phase 3 study “CpcPH-HFpEF is a distinct, identifiable and well-characterized condition that develops in people with advanced heart failure and typically impacts people who are older and have other comorbid conditions. While it is an uncommon condition and underdiagnosed, it is associated with a high morbidity and mortality rate and there are no approved treatment options specifically for CpcPH-HFpEF,” said Dr. Mardi Gomberg-Maitland, MSc, Walter G. Ross professor of clinical research, director of Pulmonary Hypertension Program, George Washington University School of Medicine and Health Sciences. “The Phase 2 CADENCE study results suggest that WINREVAIR has direct pulmonary vascular and cardiac effects in this distinct population, which may translate to clinically meaningful improvements. These proof-of-concept data provide strong rationale for further evaluation in a Phase 3 study.” In this Phase 2 study designed to assess proof-of-concept and different doses, patients in the WINREVAIR 0.7 mg/kg arm showed an increase of 5.8 meters in 6MWD that did not reach statistical significance (95% CI, -17.3, 28.9). While subsequent secondary endpoints were not formally tested due to the prespecified hierarchical testing strategy, there was a 20.3-meter increase from baseline in 6MWD in patients treated with WINREVAIR 0.3 mg/kg (95% CI, 1.5, 39.1). Additional findings from the week 24 analysis of these secondary endpoints compared to placebo include: the reduction in mean pulmonary arterial pressure (mPAP) from baseline was -9.19 for WINREVAIR 0.3 mg/kg (95% CI, -13.00, -5.38) and was -9.22 for WINREVAIR 0.7 mg/kg (95% CI, -12.97, -5.46); the reduction in pulmonary arterial wedge pressure (PAWP) from baseline was -3.04 for WINREVAIR 0.3 mg/kg (95% CI, -5.77, -0.32) and -2.53 for WINREVAIR 0.7 mg/kg (95% CI, -5.33, 0.28); the reduction in NT-proBNP levels from baseline was -344 pg/mL for WINREVAIR 0.3 mg/kg (95% CI, -656, -31); and -402 pg/mL for WINREVAIR 0.7 mg/kg (95% CI, -846, 42); the time to first occurrence of a clinical worsening event was prolonged with WINREVAIR 0.3 mg/kg (HR: 0.18 [95% CI, 0.05, 0.62]) and WINREVAIR 0.7 mg/kg (HR: 0.59 [95% CI, 0.25, 1.36]). The safety profile observed in CpcPH-HFpEF was generally consistent with the known safety profile for WINREVAIR in pulmonary arterial hypertension (PAH). “The totality of evidence and consistency in trends across multiple endpoints from the CADENCE study support advancement of WINREVAIR into a registrational Phase 3 program in CpcPH-HFpEF. While both doses suggest efficacy, CADENCE results support that the 0.3 mg/kg dose may optimize the benefit-risk profile of WINREVAIR in the distinct population of CpcPH-HFpEF,” said Dr. Mahesh Patel, vice president, global clinical development, Merck Research Laboratories. “We are working with regulatory agencies to design a Phase 3 registrational study with endpoints that focus on clinical outcomes most relevant to the needs of this population, with the ultimate goal of providing the first treatment option for CpcPH-HFpEF.” About the CADENCE study and additional results CADENCE is a double-blind, randomized, placebo-controlled Phase 2 proof-of-concept study (NCT04945460) evaluating the efficacy, safety and tolerability of WINREVAIR versus placebo in adults with CpcPH-HFpEF. Adult patients in the trial had a diagnosis of CpcPH-HFpEF with New York Heart Association (NYHA) FC II or III. The study enrolled 164 participants, and the demographics and clinical characteristics at baseline were generally balanced. The median age was 75 years old (69-79) and 69.5% of the patients were female (n=114). 65.9% of patients had a NYHA FC III diagnosis and 34.1% had a NYHA FC II diagnosis. At baseline, 34.8% had atrial fibrillation and 46.3% had diabetes. A total of 164 participants were randomized in a 1:1:1 ratio to one of the three treatment groups: placebo once every three weeks (Q3W) (n=55), 0.3 mg/kg WINREVAIR Q3W (n=54) and 0.7 mg/kg WINREVAIR Q3W (n=55) during the placebo-controlled treatment period. For those randomized to the 0.7 mg/kg dose of WINREVAIR, participants received a starting dose level of WINREVAIR 0.3 mg/kg for the initial three dosing visits, then escalated to the 0.7 mg/kg dose Q3W. The CADENCE trial was designed as a proof-of-concept study with biomarkers, invasive hemodynamics, non-invasive imaging and exercise capacity. The primary endpoint is change from baseline in PVR. The study also evaluated exercise capacity, as well as echocardiographic, biomarker and clinical endpoints. Time to clinical worsening was defined by a composite endpoint of death, ≥1 hospitalization due to cardiopulmonary indication; ≥1 administration of intravenous diuretics or subcutaneous furosemide or ≥15 percent decrease from baseline in 6MWD confirmed by two tests. At baseline, the median PVR was 5.2 Wood units (4.0, 6.9), mPAP was 43 mmHg (38.0, 50.0), PAWP was 21.0 mmHg (18.0, 25.0), the median 6MWD was 273.8 meters (199.5, 343.8), and the median NT-proBNP level was 1119 pg/mL (554-2383). Serious adverse events (SAEs) were reported in 20% of participants receiving WINREVAIR 0.3 mg/kg, 33% of participants receiving WINREVAIR 0.7 mg/kg and 22% receiving placebo. Adverse events leading to treatment discontinuation were comparable between WINREVAIR 0.3 mg/kg and placebo, with no discontinuations in either group. There were three discontinuations due to an AE and one discontinuation due to a drug-related AE in the WINREVAIR 0.7 mg/kg group. Bleeding events occurred in 26% of patients in the WINREVAIR 0.3 mg/kg group, 27% in the WINREVAIR 0.7 mg/kg group and 24% of patients in the placebo group. Adverse events leading to death occurred in one patient in the WINREVAIR 0.7 mg/kg group and two patients in the placebo group. Adverse events with an incidence of ≥10% in any group included diarrhea, fatigue, peripheral edema, influenza, nasopharyngitis, urinary tract infection, dizziness, headache and dyspnea. About the syndrome of combined post- and precapillary pulmonary hypertension and heart failure with preserved ejection fraction (CpcPH-HFpEF) Combined post- and precapillary pulmonary hypertension and heart failure with preserved ejection fraction (CpcPH-HFpEF) is a distinct, identifiable and well-characterized condition that develops in people with long-term or advanced heart failure. Different from Group 1 pulmonary arterial hypertension (PAH), CpcPH-HFpEF is caused by two interrelated components: pulmonary vascular disease and cardiac disease. CpcPH-HFpEF is thought to be uncommon and underdiagnosed, typically impacting people who are older and have other comorbid conditions. It is associated with a worse prognosis and higher mortality rate compared to HFpEF alone. There are no treatments specifically approved for CpcPH-HFpEF. About WINREVAIR™ (sotatercept-csrk) for injection, for subcutaneous use, 45 mg, 60 mg WINREVAIR is FDA-approved for the treatment of adults with pulmonary arterial hypertension (PAH, WHO Group 1 pulmonary hypertension) to improve exercise capacity and World Health Organization (WHO) functional class (FC), and reduce the risk of clinical worsening events, including hospitalization for PAH, lung transplantation and death. WINREVAIR is the first activin signaling inhibitor therapy approved to treat PAH. WINREVAIR improves the balance between pro-proliferative and anti-proliferative signaling to modulate vascular proliferation. In preclinical models, WINREVAIR induced cellular changes that were associated with thinner vessel walls, partial reversal of right ventricular remodeling and improved hemodynamics. WINREVAIR is the subject of a licensing agreement with Bristol Myers Squibb. Selected Safety Information for WINREVAIR WINREVAIR may increase hemoglobin (Hgb). Severe erythrocytosis may increase the risk of thromboembolic events or hyperviscosity syndrome. Monitor Hgb before each dose for the first 5 doses, or longer if values are unstable, and periodically thereafter, to determine if dose adjustments are required. WINREVAIR may decrease platelet count. Severe thrombocytopenia may increase the risk of bleeding. Thrombocytopenia occurred more frequently in patients also receiving prostacyclin infusion. Do not initiate treatment if platelet count is <50,000/mm 3 . Monitor platelets before each dose for the first 5 doses, or longer if values are unstable, and periodically thereafter to determine whether dose adjustments are required. In clinical studies, serious bleeding (e.g., gastrointestinal, intracranial hemorrhage) was reported in 4% vs 1% (STELLAR) and 7% vs 5% (ZENITH) of patients taking WINREVAIR vs placebo, respectively. Patients with serious bleeding were more likely to be on prostacyclin background therapy and/or antithrombotic agents, or have low platelet counts. Advise patients about signs and symptoms of blood loss. Evaluate and treat bleeding accordingly. Do not administer WINREVAIR if the patient is experiencing serious bleeding. WINREVAIR may cause fetal harm when administered to a pregnant woman. Advise pregnant women of the potential risk to a fetus. Advise females of reproductive potential to use an effective method of contraception during treatment with WINREVAIR and for at least 4 months after the final dose. Pregnancy testing is recommended for females of reproductive potential before starting WINREVAIR treatment. Based on findings in animals, WINREVAIR may impair female and male fertility. Advise patients on the potential effects on fertility. The most common adverse reactions (≥10% for WINREVAIR and at least 5% more than placebo) occurring in the STELLAR Phase 3 clinical trial were headache (24.5% vs 17.5%), epistaxis (22.1% vs 1.9%), rash (20.2% vs 8.1%), telangiectasia (16.6% vs 4.4%), diarrhea (15.3% vs 10.0%), dizziness (14.7% vs 6.3%) and erythema (13.5% vs 3.1%). The most common adverse reactions in the ZENITH trial were infections (67.4% vs 44.2%), epistaxis (45.3% vs 9.3%), diarrhea (25.6 % vs 17.4%), telangiectasia (25.6 % vs 3.5%), increased hemoglobin (15.1% vs 1.2%), rash (10.5% vs 4.7%), erythema (10.5% vs 3.5%) and gingival bleeding (10.5% vs 2.3%). Because of the potential for serious adverse reactions in the breastfed child, advise patients that breastfeeding is not recommended during treatment with WINREVAIR, and for 4 months after the final dose. Merck’s focus on cardiometabolic and respiratory diseases Merck has a long history of developing treatments for cardiometabolic and respiratory diseases. Building on a legacy that began nearly 70 years ago with the introduction of our first cardiovascular therapy, we are committed to advancing research for patients impacted by cardiometabolic and respiratory diseases. Our focus spans a range of diseases, including atherosclerotic cardiovascular disease, heart failure, pulmonary hypertension and chronic obstructive pulmonary disease (COPD). Advancements in the treatment of cardiometabolic and respiratory diseases can make a critical difference for patients and health systems around the world. At Merck, we strive for scientific excellence and innovation in all stages of research, from discovery through approval and life cycle management. We partner with experts in the community to advance research that can help improve the lives of patients. For more information, visit https://www.merck.com/research/cardiometabolic-and-respiratory-diseases/. About Merck At Merck, known as MSD outside of the United States and Canada, we are unified around our purpose: We use the power of leading-edge science to save and improve lives around the world. For more than 130 years, we have brought hope to humanity through the development of important medicines and vaccines. We aspire to be the premier research-intensive biopharmaceutical company in the world – and today, we are at the forefront of research to deliver innovative health solutions that advance the prevention and treatment of diseases in people and animals. We foster a diverse and inclusive global workforce and operate responsibly every day to enable a safe, sustainable and healthy future for all people and communities. For more information, visit www.merck.com and connect with us on X (formerly Twitter), Facebook, Instagram, YouTube and LinkedIn. Forward-Looking statement of Merck & Co., Inc., Rahway, N.J., USA This news release of Merck & Co., Inc., Rahway, N.J., USA (the “company”) includes “forward-looking statements” within the meaning of the safe harbor provisions of the U.S. Private Securities Litigation Reform Act of 1995. These statements are based upon the current beliefs and expectations of the company’s management and are subject to significant risks and uncertainties. There can be no guarantees with respect to pipeline candidates that the candidates will receive the necessary regulatory approvals or that they will prove to be commercially successful. If underlying assumptions prove inaccurate or risks or uncertainties materialize, actual results may differ materially from those set forth in the forward-looking statements. Risks and uncertainties include but are not limited to, general industry conditions and competition; general economic factors, including interest rate and currency exchange rate fluctuations; the impact of pharmaceutical industry regulation and health care legislation in the United States and internationally; global trends toward health care cost containment; technological advances, new products and patents attained by competitors; challenges inherent in new product development, including obtaining regulatory approval; the company’s ability to accurately predict future market conditions; manufacturing difficulties or delays; financial instability of international economies and sovereign risk; dependence on the effectiveness of the company’s patents and other protections for innovative products; and the exposure to litigation, including patent litigation, and/or regulatory actions. The company undertakes no obligation to publicly update any forward-looking statement, whether as a result of new information, future events or otherwise. Additional factors that could cause results to differ materially from those described in the forward-looking statements can be found in the company’s Annual Report on Form 10-K for the year ended December 31, 2025 and the company’s other filings with the Securities and Exchange Commission (SEC) available at the SEC’s Internet site ( www.sec.gov ).