Blood Institute

Framingham, MA, United States

Blood Institute

Framingham, MA, United States
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MARLBOROUGH, Mass.--(BUSINESS WIRE)--Sunovion Pharmaceuticals Inc. (Sunovion) announced that multiple data analyses from two Phase 3 studies demonstrating that Utibron™ Neohaler® (indacaterol/glycopyrrolate) inhalation powder improved lung function, health-related quality of life (HRQL), dyspnea and night-time symptoms compared to placebo in patients with moderate-to-severe chronic obstructive pulmonary disease (COPD), were presented at the 2017 American Thoracic Society International Conference (ATS 2017) held May 19-24, 2017, in Washington, D.C. Findings from the FLIGHT1 and FLIGHT2 pivotal efficacy and safety studies, as well as from the FLIGHT3 long-term safety study, were included in nine posters for UTIBRON NEOHALER presented at the meeting. UTIBRON NEOHALER is a twice-daily combination long-acting beta agonist (indacaterol) and long-acting muscarinic antagonist (glycopyrrolate) (LABA/LAMA) for the long-term maintenance treatment of airflow obstruction in people with COPD, including chronic bronchitis and/or emphysema. UTIBRON NEOHALER is not indicated to treat asthma or for the relief of sudden symptoms of COPD. “Improvement in health related quality of life, including reduction of difficult or labored breathing, is a key therapeutic goal for patients with COPD that is reflected in the updated 2017 Global Initiative for Chronic Obstructive Lung Disease (GOLD) report,” said lead investigator of FLIGHT1 and FLIGHT2 studies Donald A. Mahler, M.D., Emeritus Professor of Medicine, Geisel School of Medicine at Dartmouth, Lebanon, N.H. “These UTIBRON NEOHALER data show that the dual bronchodilator significantly improves and sustains bronchodilation and may improve health status and COPD symptoms in moderate-to-severe patients.” “UTIBRON NEOHALER has demonstrated the value of dual bronchodilation treatment for people living with COPD,” said Thomas H. Goodin, Ph.D., Senior Director, Clinical Development at Sunovion. “The data presented at ATS indicate that UTIBRON NEOHALER was associated with statistically significant and clinically important improvements in lung function as well as a reduction in the number of sleep disturbances and in the use of rescue medication, which may have a positive impact on patients’ quality of life.” About COPD Chronic obstructive pulmonary disease (COPD) is a common, preventable and treatable disease that is characterized by persistent respiratory symptoms and airflow limitation that is due to airway and/or lung abnormalities usually caused by significant exposure to toxic particles or gases. The main risk factor for COPD is tobacco smoking, but other environmental exposures may contribute.1 Approximately 15.7 million adults in the U.S. report that they have been diagnosed with COPD.2 It is estimated that several million more adults have undiagnosed COPD.3 COPD is responsible for over 120,000 deaths per year, making it the third leading cause of death in the U.S.2 COPD develops slowly and the symptoms often worsen over time, potentially limiting the ability to perform routine activities.2 Symptoms of COPD include coughing, wheezing, shortness of breath, excess production of mucus in the lungs, the inability to breathe deeply and the feeling of being unable to breathe.4 The symptoms of COPD can be most severe during the night and early morning.5 Morning symptoms can be associated with limitation of activities during the day, impaired health status and increased risk of exacerbation.6 Night-time symptoms disturb sleep, reduce sleep quality and, in the long term, may be associated with development or worsening of cardiovascular diseases, cognition, depression and increased mortality.7 About FLIGHT1 and FLIGHT2 Studies8 FLIGHT1 and FLIGHT2 were Phase 3, replicate, multicenter, double-blind, parallel group, placebo- and active-controlled studies that randomized (1:1:1:1) patients with moderate-to-severe COPD to receive indacaterol/glycopyrrolate 27.5/15.6 mcg, indacaterol 27.5 mcg, glycopyrrolate 15.6 mcg or placebo (all given twice daily) over a 12-week treatment period. All treatments were delivered via the Neohaler® device. The studies were funded by Novartis Pharmaceuticals Corporation. About Utibron™ Neohaler® (indacaterol/glycopyrrolate) Inhalation Powder9 UTIBRON NEOHALER (indacaterol/glycopyrrolate) inhalation powder is a combination bronchodilator indicated for the long-term maintenance treatment of airflow obstruction in patients with COPD, including chronic bronchitis and/or emphysema. It is not indicated to treat acute deteriorations of COPD or to treat asthma. UTIBRON NEOHALER combines two medicines in one twice-daily fixed-dose combination: indacaterol 27.5 mcg, a long-acting beta -adrenergic agonist (LABA), and the long-acting muscarinic antagonist (LAMA) glycopyrrolate 15.6 mcg. Sunovion entered into an exclusive license agreement with Novartis for the U.S. commercialization rights to UTIBRON NEOHALER, as well as Seebri™ Neohaler® (glycopyrrolate) inhalation solution and Arcapta® Neohaler® (indacaterol) inhalation solution, on December 21, 2016. Novartis received approval from the U.S. Food and Drug Administration (FDA) for UTIBRON NEOHALER in October 2015. UTIBRON™ NEOHALER® (indacaterol and glycopyrrolate) is a combination of a long-acting beta -agonist, or LABA, medicine (indacaterol) and an anticholinergic medicine (glycopyrrolate). UTIBRON NEOHALER is used long term, twice each day (morning and evening), to treat the symptoms of chronic obstructive pulmonary disease (COPD), including chronic bronchitis and/or emphysema. UTIBRON NEOHALER has been approved for COPD only and is NOT indicated for the treatment of asthma. People with asthma who take long-acting beta -adrenergic agonist (LABA) medicines, such as indacaterol (one of the medicines in UTIBRON NEOHALER), have an increased risk of death from asthma problems. It is not known if LABA medicines, such as indacaterol, increase the risk of death in people with COPD. UTIBRON NEOHALER does not relieve sudden symptoms of COPD and should not be used more than twice daily. Always have a short-acting beta -agonist with you to treat sudden symptoms. Use UTIBRON NEOHALER exactly as your health care provider tells you to use it. Do not use UTIBRON NEOHALER more often than it is prescribed for you. Get emergency medical care if your breathing problems worsen quickly, you need to use your rescue medication more often than usual, or your rescue medication does not work as well to relieve your symptoms. Do not use UTIBRON NEOHALER if you are allergic to indacaterol, glycopyrrolate, or any of the ingredients in UTIBRON NEOHALER. Ask your health care provider if you are not sure. Tell your health care provider about all of your health conditions, including if you: Tell your health care provider about all the medicines you take, including prescription medicines, over-the-counter medicines, vitamins, and herbal supplements. UTIBRON NEOHALER and certain other medicines may interact with each other. This may cause serious side effects. Especially tell your health care provider if you take: UTIBRON NEOHALER can cause serious side effects, including: Common side effects of UTIBRON NEOHALER include sore throat and runny nose, high blood pressure, and back pain. These are not all of the possible side effects with UTIBRON NEOHALER. Tell your health care provider about any side effect that bothers you or that does not go away. Do not swallow UTIBRON capsules. UTIBRON capsules are for inhalation only with the NEOHALER device. Never place a capsule in the mouthpiece of the NEOHALER device. You are encouraged to report negative side effects of prescription drugs to the FDA. Visit www.fda.gov/medwatch or call 1-800-FDA-1088. This information is not comprehensive. How to get more information: For additional information, please see full Prescribing Information, including BOXED WARNING and Medication Guide, for UTIBRON NEOHALER, or visit www.UTIBRON.com. Expanding Sunovion’s Heritage in COPD Sunovion is committed to expanding its heritage of advancing new treatments for serious respiratory medical conditions, including the 15.7 million people in the U.S. who are living with chronic obstructive pulmonary disease (COPD).2 The company offers the broadest COPD portfolio in the U.S., providing treatment options for people at various stages of COPD, as well as the flexibility to choose handheld or nebulized delivery based on individual needs. Sunovion goes beyond treatment offerings to support awareness and understanding with the entire COPD community – health care providers, patients and caregivers – and to advancing disease state education through its partnerships with various organizations. About Sunovion Pharmaceuticals Inc. (Sunovion) Sunovion is a global biopharmaceutical company focused on the innovative application of science and medicine to help people with serious medical conditions. Sunovion’s vision is to lead the way to a healthier world. The company’s spirit of innovation is driven by the conviction that scientific excellence paired with meaningful advocacy and relevant education can improve lives. With patients at the center of everything it does, Sunovion has charted new paths to life-transforming treatments that reflect ongoing investments in research and development and an unwavering commitment to support people with psychiatric, neurological and respiratory conditions. Sunovion’s track record of discovery, development and commercialization of important therapies has included Utibron™ Neohaler® (indacaterol/glycopyrrolate) inhalation powder, Brovana® (arformoterol tartrate) inhalation solution, Latuda® (lurasidone HCI) and Aptiom® (eslicarbazepine acetate). Headquartered in Marlborough, Mass., Sunovion is an indirect, wholly-owned subsidiary of Sumitomo Dainippon Pharma Co., Ltd. Sunovion Pharmaceuticals Europe Ltd., based in London, England, Sunovion Pharmaceuticals Canada Inc., based in Mississauga, Ontario, and Sunovion CNS Development Canada ULC, based in Toronto, Ontario, are wholly-owned direct subsidiaries of Sunovion Pharmaceuticals Inc. Additional information can be found on the company’s web sites: www.sunovion.com, www.sunovion.eu and www.sunovion.ca. Connect with Sunovion on Twitter, LinkedIn, Facebook and YouTube. About Sumitomo Dainippon Pharma Co., Ltd. Sumitomo Dainippon Pharma is among the top-ten listed pharmaceutical companies in Japan operating globally in major pharmaceutical markets, including Japan, the United States, China and the European Union. Sumitomo Dainippon Pharma aims to create innovative pharmaceutical products in the Psychiatry & Neurology area and the Oncology area, which have been designated as the focus therapeutic areas. Sumitomo Dainippon Pharma is based on the merger in 2005 between Dainippon Pharmaceutical Co., Ltd., and Sumitomo Pharmaceuticals Co., Ltd. Today, Sumitomo Dainippon Pharma has about 6,500 employees worldwide. Additional information about Sumitomo Dainippon Pharma is available through its corporate website at www.ds-pharma.com. LATUDA and SUNOVION are registered trademarks of Sumitomo Dainippon Pharma Co., Ltd. BROVANA is a registered trademark of Sunovion Pharmaceuticals Inc. APTIOM is used under license from Bial. ARCAPTA and NEOHALER are registered trademarks of Novartis AG, used under license.  SEEBRI and UTIBRON are trademarks of Novartis AG, used under license. Sunovion Pharmaceuticals Inc. is a U.S. subsidiary of Sumitomo Dainippon Pharma Co., Ltd. For a copy of this release, visit Sunovion’s web site at www.sunovion.com 1 GOLD Guidelines 2017. http://www.goldcopd.org/guidelines-global-strategy-for-diagnosis-management.html. Accessed: March 16, 2017. 2 MMWR: Morbidity and Mortality Weekly Report. Employment and Activity Limitations Among Adults with Chronic Obstructive Pulmonary Disease — United States, 2013. March 27, 2015; 64(11). Available at http://www.cdc.gov/mmwr/ 3 National Heart, Lung, and Blood Institute. “What is COPD?” Available at: http://www.nhlbi.nih.gov/health/educational/copd/what-is-copd/index.htm. Accessed: March 2, 2016 4 National Heart, Lung and Blood Institute. (2013). What Are the Signs and Symptoms of COPD? Retrieved from https://www.nhlbi.nih.gov/health/health-topics/topics/copd/signs. 5 Partridge MR, Karlsson N, Small IR. Patient insight into the impact of chronic obstructive pulmonary disease in the morning: an internet survey. Curr Med Res Opin. 2009;25:2043–8. 6 Roche N, Small M, Broomfield S, Higgins V, Pollard R. Real world COPD: association of morning symptoms with clinical and patient reported outcomes. COPD. 2013;10:679–86. 7 Agusti A, Hedner J, Marin JM, Barbé F, Cazzola M, Rennard S. Night-time symptoms: a forgotten dimension of COPD. Eur Respir Rev. 2011;20:183–94. 8 Mahler DA, Kerwin E, Ayers T, et al. FLIGHT1 and FLIGHT2: Efficacy and Safety of QVA149 (Indacaterol/Glycoprrolate) versus its Monocomponents and Placebo and Patients with Chronic Obstructive Pulmonary Disease. Am J Respir Crit Care Med. 2015;192(9):1068-1079. 9 Utibron™ Neohaler® Full Prescribing Information. Novartis Pharmaceuticals Corporation. January 2017.


Dr. Chan was invited to speak on the development of new potassium lowering technologies that utilize novel potassium-binding sorbents to treat severe hyperkalemia, a potentially life-threatening elevation of potassium in the blood that can occur as a result of severe trauma, burn injury, and tissue ischemia.  These strategies were specifically designed to be used to stabilize our wounded warfighters in austere battlefield environments, where delays in evacuation necessitate prolonged field care for up to 72 hours before they can be brought to definitive care.  U.S. Special Operations Command (SOCOM) synchronizes the planning of Special Operations and provides Special Operations Forces to support persistent, networked, and distributed Global Combatant Command operations in order to protect and advance our Nation's interests.  This work was funded through two Small Business Innovation Research (SBIR) contracts by the U.S. Army Medical Research and Materiel Command (USAMRMC). 18th Annual B. Riley & Co. Investor Conference Presenter: Kathleen Bloch, CFO Where:  Loews Santa Monica Beach Hotel, 1700 Ocean Avenue, Santa Monica, CA When:    Wednesday, May 24, 2017 at 3:00PM PDT Presentation Room:   Arcadia D Ms. Bloch will be meeting with investors in one-on-one meetings during the two day conference (May 24-25th).  A copy of the presentation will be available on the company's investor relations website. CytoSorbents Corporation is a leader in critical care immunotherapy, specializing in blood purification. Its flagship product, CytoSorb® is approved in the European Union with distribution in 43 countries around the world, as a safe and effective extracorporeal cytokine adsorber, designed to reduce the "cytokine storm" or "cytokine release syndrome" that could otherwise cause massive inflammation, organ failure and death in common critical illnesses such as sepsis, burn injury, trauma, lung injury and pancreatitis, as well as in cancer immunotherapy. These are conditions where the risk of death is extremely high, yet no effective treatments exist. CytoSorb® is also being used during and after cardiac surgery to remove inflammatory mediators, such as cytokines and free hemoglobin, which can lead to post-operative complications, including multiple organ failure. CytoSorbents has completed its REFRESH (REduction in FREe Hemoglobin) 1 trial – a multi-center, randomized controlled study that has demonstrated the safety and efficacy of free hemoglobin reduction with intra-operative CytoSorb® use in a heart-lung machine during complex cardiac surgery.  In 2017, the company plans to initiate a pivotal REFRESH 2 trial intended to support U.S. FDA approval.  CytoSorb® has been used safely in more than 23,000 human treatments to date. CytoSorbents' purification technologies are based on biocompatible, highly porous polymer beads that can actively remove toxic substances from blood and other bodily fluids by pore capture and surface adsorption. Its technologies have received non-dilutive grant, contract, and other funding in excess of $18 million from DARPA, the U.S. Army, the U.S. Department of Health and Human Services, the National Institutes of Health (NIH), National Heart, Lung, and Blood Institute (NHLBI), U.S. Special Operations Command (SOCOM) and others. The Company has numerous products under development based upon this unique blood purification technology, protected by 32 issued U.S. patents and multiple applications pending, including CytoSorb-XL, HemoDefend™, VetResQ™, ContrastSorb, DrugSorb, and others.  For more information, please visit the Company's websites at www.cytosorbents.com and www.cytosorb.com or follow us on Facebook and Twitter This press release includes forward-looking statements intended to qualify for the safe harbor from liability established by the Private Securities Litigation Reform Act of 1995. These forward-looking statements include, but are not limited to, statements about our plans, objectives, representations and contentions and are not historical facts and typically are identified by use of terms such as "may," "should," "could," "expect," "plan," "anticipate," "believe," "estimate," "predict," "potential," "continue" and similar words, although some forward-looking statements are expressed differently. You should be aware that the forward-looking statements in this press release represent management's current judgment and expectations, but our actual results, events and performance could differ materially from those in the forward-looking statements. Factors which could cause or contribute to such differences include, but are not limited to, the risks discussed in our Annual Report on Form 10-K, filed with the SEC on March 3, 2017, as updated by the risks reported in our Quarterly Reports on Form 10-Q, and in the press releases and other communications to shareholders issued by us from time to time which attempt to advise interested parties of the risks and factors which may affect our business. We caution you not to place undue reliance upon any such forward-looking statements. We undertake no obligation to publicly update or revise any forward-looking statements, whether as a result of new information, future events, or otherwise, other than as required under the Federal securities laws. Please Click to Follow Us on Facebook and Twitter To view the original version on PR Newswire, visit:http://www.prnewswire.com/news-releases/cytosorbents-selected-to-present-at-special-operations-somsa-2017-conference-and-18th-annual-b-riley--co-investor-conference-300463018.html


News Article | May 24, 2017
Site: www.eurekalert.org

PHILADELPHIA -- Blood platelets shore up open wounds and help cuts heal, but they can also cause heart attacks and strokes when a congealed ball of platelets known as a thrombus breaks free from a site of injury and gets lodged in blood vessels that feed oxygen to the brain or heart. Blood thinners, such as aspirin, reduce the risk of thrombus formation but also interfere with the initial clot formation that is essential for preventing blood loss from the wounds. Now researchers have discovered that a molecule plays a role in thrombus development, but not the initial clot formation, suggesting a new avenue for developing more specific and protective blood thinners. The results were published May 24 in the journal PLOS ONE. "The Holy Grail of our field is to reduce unwanted thrombus formation without completely blocking other important platelet functions," says senior author Ulhas Naik, Ph.D., Director of the Center for Vascular Biology at Thomas Jefferson University's Cardeza Foundation for Hematologic Research. After platelets become activated at the site of an injury, they become linked to one another forming a platelet plug. The platelets then continue to change shape, trap red blood cells and the clot begins to tighten and pull together, which can help bring two sides of a wound in closer. But this process of clot retraction is also responsible for creating the free-floating ball of a thrombus capable of blocking vital blood flow. Clot retraction is governed by a signaling process called outside-in signaling. In earlier work Dr. Naik and colleagues showed that the protein called CIB1 was involved in thrombus formation. Mice that lacked the CIB1 gene were less likely to form a thrombus. That work also suggested that mice lacking the CIB1 were still able to form a platelet plug, suggesting that this gene was involved only in the process of thrombus formation. To investigate this possibility further, and to demonstrate that the process was relevant to human physiology, the current study used human platelets, and probed the molecules that interacted with CIB1 at different time points after platelet activation. The researchers showed that CIB1 does not begin to bind and interact with platelet molecular machinery until after platelets send out sticky protrusions that allow them to cross-link to one another and begin to form a plug. The paper, to which Dr. Naik's entire nuclear family contributed, also elucidated a number of molecules that CIB1 interacts with during outside-in signaling and thrombus formation. A clearer picture of this process could in turn be useful for researchers studying other diseases that involve platelets, such as cancer, specifically the role platelets play in metastasis or helping seed cancer in distant parts of the body. "This work demonstrates that CIB1 could be a good anti-thrombotic drug target," says Dr. Naik. "If we block CIB1, it hampers thrombus formation without interfering with platelet plug formation. If developed further, blocking CIB1 could reduce the risk of heart attack and stroke without increasing the risk for excessive bleeding that is the trade-off of current medication." The next steps for Dr. Naik and collaborating researchers include screening for small-molecule compounds that would inhibit CIB1 and which could be developed into new therapies. Article Reference: M.U. Naik, et al., "Binding of CIB1 to the αIIb tail of αIIbβ3 is required for FAK recruitment and activation in platelets" PLOS ONE. 2017. https:/ This work was supported by the grants from the NHLBI (National Heart, Lung, Blood Institute) HL 57630 and HL113188. The authors report no conflicts of interest. Jefferson, through its academic and clinical entities of Thomas Jefferson University and Jefferson Health, including Abington Health and Aria Health, is reimagining health care for the greater Philadelphia region and southern New Jersey. Jefferson has 23,000 people dedicated to providing the highest-quality, compassionate clinical care for patients, educating the health professionals of tomorrow, and discovering new treatments and therapies to define the future of care. With a university and hospital that date back to 1824, today Jefferson is comprised of six colleges, nine hospitals, 35 outpatient and urgent care locations, and a multitude of physician practices throughout the region, serving more than 100,000 inpatients, 373,000 emergency patients and 2.2 million outpatients annually.


PHILADELPHIA--A new strategy - an injectable antibody - for lowering blood lipids and thereby potentially preventing coronary artery disease and other conditions caused by the build-up of fats, cholesterol, and other substances on the artery walls, is supported by findings from two new studies from researchers in the Perelman School of Medicine at the University of Pennsylvania. The new approach targets a protein called ANGPTL3, a regulator of enzymes that clear triglycerides and other fat molecules from the blood. Research in recent years has hinted that inherited mutations in the ANGPTL3 gene that disable its function can decrease triglyceride, LDL cholesterol and HDL cholesterol levels. As reported in a paper published today online in the New England Journal of Medicine, researchers from Penn Medicine, Regeneron Pharmaceuticals, and a group of international collaborators studied ANGPTL3 in both humans and mice. They found that blocking ANGPTL3 activity with an investigative injectable antibody, known as evinacumab, reduced triglycerides by up to 76 percent and lowered LDL cholesterol 23 percent in human study participants, and largely reversed signs of atherosclerosis in a mouse models. Researchers also included a human genetics study of approximately 188,000 people, which found that carriers of mutations that disable ANGPTL3 had nearly 40 percent fewer incidents of coronary artery disease as compared to those with fully functioning ANGPTL3. "In the clinic, I treat many patients with very high triglycerides, but our current medications aren't lowering triglycerides enough in many cases. I'm delighted at the prospect of a new treatment that's a lot more potent, all the more because it lowers LDL at the same time," said study co-author Richard L. Dunbar, MD, assistant professor of Cardiovascular Medicine and member of Penn's Division of Translational Medicine and Human Genetics. "It's very reassuring to see that people with this genetic defect actually seem to be protected from heart disease. I think that really bodes well for a therapeutic that's targeting the ANGPTL3 pathway." In a separate study, published in the March issue of the Journal of the American College of Cardiology (JACC) researchers from Penn Medicine, Harvard Medical School, Washington University in St. Louis, and nine other institutions, who also studied humans and mice, reported on a similar set of findings. Among these was the discovery from another large population sample that carriers of ANGPTL3-inactivating mutations had a 34 percent lower rate of coronary artery disease compared to non-carriers. "We used different lines of evidence to show that ANGPTL3 deficiency is associated with a reduced risk of coronary artery disease," said study co-author Kiran Musunuru, MD, PhD, MPH, an associate professor of Cardiovascular Medicine at Penn. "But ultimately we were able to identify that fact that carriers of this genetic mutation did in fact experience a benefit - with little other health risk." The trial of research on ANGPTL3 as a potential target for atherosclerosis prevention began over a decade ago when scientists reported on two cases of familial hypolipidemia, a rare inherited condition involving abnormally low blood levels of cholesterol and triglycerides. Most cases of familial hypolipidemia are linked to other gene mutations that cause liver and digestive problems, but in members of this American family with the condition, Musunuru found mutations in the gene for ANGPTL3, and no associated health problems. In the NEJM study from Dunbar and colleagues, the antibody had similar effects in an initial clinical trial in 83 people, lowering the blood levels of triglycerides measured after fasting by about 75 percent at the highest dose, and lowering LDL cholesterol by about 30 percent. Statins and other drugs are already widely used to lower LDL cholesterol, but there are fewer options for lowering triglycerides. "For treating high triglyceride levels there's really nothing out there that's quite this potent, so that's where I expect this new approach to have its greatest therapeutic benefit," Dunbar said. Hypertriglyceridemia, a condition in which fasting triglyceride levels are greater than 150 mg/dL, is estimated to affect at least tens of millions of American adults. It is associated with coronary artery disease and other forms of atherosclerosis, and can lead to potentially fatal inflammation of the pancreas. In principle, the strategy of targeting ANGPTL3 could have an even broader use in treating atherosclerosis in the general population. The researchers found that in a mouse model of atherosclerosis, treatment with evinacumab reduced the area of atherosclerotic lesions by 39 percent. The population study findings, including those from the JACC study, suggest that even the partial inactivation of ANGPTL3--carriers typically have one mutant copy of the gene and one working copy--may be powerfully protective against coronary artery disease, which has long been one of the leading causes of death in developed countries. In the JACC study, for example, carriers of inactivating ANGPTL3 mutations had only a 17 percent reduction in triglycerides on average. But that modest reduction was associated with a 34 percent reduction in coronary artery disease risk. Moreover, Musunuru and his colleagues found that the people in their sample with the lowest blood levels of ANGPTL3 had a 35 percent lower rate of heart attacks compared to those with the highest ANGPTL3 levels. Dunbar noted that the population study findings probably have lain to rest a lingering concern about targeting ANGPTL3, namely its effect in lowering not just LDL and triglycerides but also the so-called "good cholesterol," known as HDL cholesterol. "If lowering HDL were a major concern, then I don't think we would have seen the evidence of overall benefit that we did in this study," he said. The two studies together suggest that single copies of inactivating ANGPTL3 mutations are found in roughly one of every 250 people of European descent, whereas people with mutations in both copies of the gene--as in the family studied by Musunuru and colleagues--are much rarer. According to Dunbar, the next logical step would be to take evinacumab into larger clinical trials to study its safety, effectiveness, and optimal dosing. "The effect of even a single dose lasts for several months, and it's plausible that with multiple doses we would see an even deeper and more sustained effect," he said. Additional Penn authors on the NEJM study include Scott Damrauer, MD, Aeron Small, and Daniel J. Rader MD, and the Journal of the American College of Cardiology study include Xiao Wang, PhD, Daniel J. Rader, MD, and Danish Saleheen, MBBS, PhD. Funding sources for the studies detailed in this press release included grants from the National Heart, Lung, and Blood Institute (NHLBI) (R01HL131961), (K08HL114642), (R01HL118744), (R01HL127564) and (R21HL120781) and Regeneron Pharmaceuticals. Editor's Note: Dunbar has received grant support from and consulted for Regeneron Pharmaceuticals, Inc. Penn Medicine is one of the world's leading academic medical centers, dedicated to the related missions of medical education, biomedical research, and excellence in patient care. Penn Medicine consists of the Raymond and Ruth Perelman School of Medicine at the University of Pennsylvania (founded in 1765 as the nation's first medical school) and the University of Pennsylvania Health System, which together form a $6.7 billion enterprise. The Perelman School of Medicine has been ranked among the top five medical schools in the United States for the past 20 years, according to U.S. News & World Report's survey of research-oriented medical schools. The School is consistently among the nation's top recipients of funding from the National Institutes of Health, with $392 million awarded in the 2016 fiscal year. The University of Pennsylvania Health System's patient care facilities include: The Hospital of the University of Pennsylvania and Penn Presbyterian Medical Center -- which are recognized as one of the nation's top "Honor Roll" hospitals by U.S. News & World Report -- Chester County Hospital; Lancaster General Health; Penn Wissahickon Hospice; and Pennsylvania Hospital -- the nation's first hospital, founded in 1751. Additional affiliated inpatient care facilities and services throughout the Philadelphia region include Good Shepherd Penn Partners, a partnership between Good Shepherd Rehabilitation Network and Penn Medicine. Penn Medicine is committed to improving lives and health through a variety of community-based programs and activities. In fiscal year 2016, Penn Medicine provided $393 million to benefit our community.


DALLAS, May 24, 2017 -- People with a common cluster of risk factors for heart disease and diabetes were approximately twice as likely to die of heart disease or stroke as people without the same set of risk factors if they failed to get more than six hours of sleep, according to a new observational study published in the association's open access publication Journal of the American Heart Association. For those who got more sleep, the risk of death was more modest. The study, funded in part by the American Heart Association, is the first to measure sleep duration in the laboratory rather than rely on patient reports and the first to examine the impact of sleep duration on the risk of death in those with a common cluster of heart disease risk factors. The researchers randomly selected 1,344 adults (average age 49 years, 42 percent male) who agreed to spend one night in a sleep laboratory as part of the Penn State Adult Cohort. Based on their test results, 39.2 percent of the participants were found to have at least three of the risk factors, that when clustered together are known as the metabolic syndrome. For this study, the cluster included body mass index (BMI) higher than 30 and elevated total cholesterol, blood pressure, fasting blood sugar and triglyceride levels. During an average follow-up of 16.6 years, 22 percent of the participants died. Compared to people without the same cluster of risk factors, those with metabolic syndrome who clocked more than six hours of sleep time in the lab were about 1.49 times more likely to die of stroke during the 16.6-year follow-up period, while those who slept less than six hours in the lab were about 2.1 times more likely to die of heart disease or stroke. The short sleepers with metabolic syndrome were also 1.99 times more likely to die from any cause compared to those without metabolic syndrome. The relationship was particularly striking because the researchers adjusted for sleep apnea - sleep interrupted by pauses in breathing that is a known heart disease risk. "If you have several heart disease risk factors, taking care of your sleep and consulting with a clinician if you have insufficient sleep is important if you want to lower your risk of death from heart disease or stroke," said study lead author Julio Fernandez-Mendoza, Ph.D., an assistant professor at Penn State College of Medicine and sleep psychologist at the Sleep Research & Treatment Center of the Penn State Health Milton S. Hershey Medical Center in Hershey, Pennsylvania. He noted that sleep lab studies are often used to rule out sleep apnea, but physicians should also note insufficient sleep in the lab because it may signal a higher risk of death in patients with risk factors for heart disease. A recent scientific statement from the American Heart Association on sleep duration and quality noted that an increasing number of Americans suffer from sleep difficulties or choose to curtail sleep in favor of other social, leisure, or work-related activities and this may be associated with adverse cardiovascular risks and outcomes. As the Fernandez-Mendoza research was an observational study, the results cannot establish a cause-and-effect, only an association between short sleep and mortality in people with the metabolic syndrome. Additional limitations include that the study used only one day of sleep lab results and enrolled too few minority patients to determine whether there are racial differences in the relationship between short sleep times and mortality. "Future clinical trials are needed to determine whether lengthening sleep, in combination with lowering blood pressure and glucose, improves the prognosis of people with the metabolic syndrome" said Fernandez-Mendoza. Co-authors are Fan He, M.S.; Caitlin LaGrotte, Psy.D.; Alexandros N. Vgontzas, M.D.; Duanping Liao, M.D., Ph.D.; and Edward O. Bixler, Ph.D. Author disclosures are on the manuscript. The American Heart Association and the National Heart, Lung, and Blood Institute funded the study. Statements and conclusions of study authors published in American Heart Association scientific journals are solely those of the study authors and do not necessarily reflect the association's policy or position. The association makes no representation or guarantee as to their accuracy or reliability. The association receives funding primarily from individuals; foundations and corporations (including pharmaceutical, device manufacturers and other companies) also make donations and fund specific association programs and events. The association has strict policies to prevent these relationships from influencing the science content. Revenues from pharmaceutical and device corporations and health insurance providers are available at http://www. . The American Heart Association is devoted to saving people from heart disease and stroke - the two leading causes of death in the world. We team with millions of volunteers to fund innovative research, fight for stronger public health policies, and provide lifesaving tools and information to prevent and treat these diseases. The Dallas-based association is the nation's oldest and largest voluntary organization dedicated to fighting heart disease and stroke. To learn more or to get involved, call 1-800-AHA-USA1, visit heart.org or call any of our offices around the country. Follow us on Facebook and Twitter.


MARLBOROUGH, Mass.--(BUSINESS WIRE)--Sunovion Pharmaceuticals Inc. (Sunovion) presented data from the Phase 3 GOLDEN trials, showing that treatment with SUN-101/eFlow® significantly improved lung function, health related quality of life and respiratory symptoms among people with moderate-to-very severe chronic obstructive pulmonary disease (COPD), at the American Thoracic Society 2017 International Conference (ATS 2017) held May 19-24, 2017, in Washington D.C. Sunovion also presented data from the long-term safety trial showing a high rate of patient reported satisfaction and confidence with the use of the investigational eFlow® closed system nebulizer. “There are no approved nebulized, long-acting muscarinic antagonists (LAMAs) currently available for use in COPD,” said Thomas H. Goodin, Ph.D., Senior Director, Clinical Development at Sunovion. “These data suggest that for moderate-to-very severe patients, SUN-101/eFlow® could potentially be an effective and well-tolerated maintenance therapy.” If approved, SUN-101/eFlow® will be the first nebulized LAMA approved for the treatment of COPD in the U.S. The investigational eFlow® closed system nebulizer, developed by PARI Pharma GmbH, is portable, virtually silent, designed to deliver the medication in two to three minutes and, unlike handheld inhalers, allows patients to breathe normally while using the device. “COPD symptoms can severely impact patients’ daily activities and health related quality of life, and it is important for any treatment to be not only well-tolerated and effective, but also easy to administer,” said Gary Ferguson, M.D., Pulmonary Research Institute of Southeast Michigan and Principal Investigator for the GOLDEN-5 clinical trial. “With its efficacy and tolerability profile as well as the portability and short administration time, SUN-101/eFlow® could be a valuable treatment option for patients with COPD.” Results from three Phase 3 studies (GOLDEN-3, GOLDEN-4, GOLDEN-5) demonstrate the efficacy and safety of SUN-101/eFlow® in a population of patients with real-world characteristics representing its potential as an important maintenance therapy in patients with moderate-to-very severe COPD. Key data presented included: The expected action date by the U.S. Food and Drug Administration (FDA) under the Prescription Drug User Fee Act (PDUFA) for SUN-101/eFlow® is May 29, 2017. SUN-101 (glycopyrrolate) is a long-acting muscarinic antagonist (LAMA) bronchodilator delivered via the proprietary investigational eFlow® closed system nebulizer. SUN-101/eFlow® is currently in development as a nebulized treatment for patients with moderate-to-very-severe chronic obstructive pulmonary disease (COPD). The investigational combined product, consisting of SUN-101 and the investigational eFlow® closed system nebulizer, which has been optimized for SUN-101 delivery, has not been approved by the U.S. Food and Drug Administration (FDA) for the treatment of COPD. A long-acting muscarinic antagonist (LAMA) is a type of long-acting bronchodilator, along with long-acting beta agonists (LABAs). According to the GOLD report, these are currently the first-line standard of care maintenance therapy for symptomatic patients with COPD, and helps the muscles around the airways in lungs stay relaxed to prevent symptoms such as wheezing, coughing, chest tightness, and shortness of breath.1 LAMAs and LABAs are widely used and important therapeutic approaches for people with COPD. GOLDEN-3 and GOLDEN-4 were pivotal Phase 3, 12-week, randomized, double-blind, placebo-controlled, parallel-group, multicenter, efficacy and safety trials comparing SUN-101/eFlow® with placebo in adults with moderate-to-very severe COPD. The GOLDEN-3 trial enrolled 653 people who were at least 40 years old at 45 sites in the United States. The GOLDEN-4 trial enrolled 641 people who were at least 40 years old at 49 sites in the United States. SUN-101/eFlow® 25 mcg, SUN-101/eFlow® 50 mcg or placebo was administered twice daily in these studies. The primary endpoint was the change from baseline in trough FEV at Week 12. Secondary endpoints included standardized change from baseline at Week 12 in FEV area under the curve (AUC), change from baseline in trough forced vital capacity (FVC) at Week 12, change from baseline in health status measured by St. George’s Respiratory Questionnaire and change in rescue medication use. Safety was assessed by the number of treatment-emergent adverse events (TEAE), serious adverse events (SAE) or major adverse cardiac events (MACE) and the number and percentage of study participants who discontinued the study due to TEAE. Both GOLDEN-3 and GOLDEN-4 studies included not only patients who were taking effective background long acting bronchodilator therapy but also patients with very severe disease and co-existing cardiovascular illness. Approximately 10 percent of the population were elderly (>75 years), 65 percent were classified as being high-risk cardiovascular patients and approximately 30 percent were taking long acting bronchodilator therapy [NCT02347761 and NCT02347774]. GOLDEN-5 was a Phase 3, 48-week, randomized, open-label, active-controlled, parallel-group, multicenter safety trial designed to evaluate the long term safety and tolerability of SUN-101/eFlow® in adults with moderate-to-very severe COPD. The study enrolled 1,087 patients at 111 investigational sites in the United States and Europe. The study evaluated 50 mcg of SUN-101/eFlow® delivered twice-daily and active comparator 18 mcg of Spiriva® (tiotropium bromide) delivered once-daily by the HandiHaler® device. The primary safety endpoints were: the number and percentage of study participants with treatment-emergent adverse events (TEAE), the number and percentage of study participants with treatment-emergent serious adverse events (SAE), the number and percentage of study participants who discontinued the study due to TEAEs and the number and incidence of subjects with MACE. The secondary endpoint was the mean change from baseline over 48 weeks in trough FEV for all subjects. The study included not only patients who were taking effective background long acting bronchodilator therapy but also patients with very severe disease and co-existing significant cardiovascular illness. Approximately 10 percent of the population were elderly (>75 years), 65 percent were classified as being high-risk cardiovascular patients and more than 40 percent were taking long acting bronchodilator therapy [NCT02276222]. Chronic obstructive pulmonary disease (COPD) is a common, preventable and treatable disease that is characterized by persistent respiratory symptoms and airflow limitation that is due to airway and/or lung abnormalities usually caused by significant exposure to toxic particles or gases. The main risk factor for COPD is tobacco smoking, but other environmental exposures may contribute.1 Approximately 15.7 million adults in the U.S. report that they have been diagnosed with COPD.2 It is estimated that several million more adults have undiagnosed COPD.3 COPD is responsible for over 120,000 deaths per year, making it the third leading cause of death in the U.S.2 COPD develops slowly and the symptoms often worsen over time, potentially limiting the ability to perform routine activities.2 Symptoms of COPD include coughing, wheezing, shortness of breath, excess production of mucus in the lungs, the inability to breathe deeply and the feeling of being unable to breathe.4 The symptoms of COPD can be most severe during the night and early morning.5 Morning symptoms can be associated with limitation of activities during the day, impaired health status and increased risk of exacerbation.6 Night-time symptoms disturb sleep, reduce sleep quality and, in the long term, may be associated with development or worsening of cardiovascular diseases, cognition, depression and increased mortality.7 Sunovion is committed to expanding its heritage of advancing new treatments for serious respiratory medical conditions, including the 15.7 million people in the U.S. who are living with chronic obstructive pulmonary disease (COPD).2 The company offers the broadest COPD portfolio in the U.S., providing treatment options for people at various stages of COPD, as well as the flexibility to choose handheld or nebulized delivery based on individual needs. Sunovion goes beyond treatment offerings to support awareness and understanding with the entire COPD community – health care providers, patients and caregivers – and to advancing disease state education through its partnerships with various organizations. Sunovion is a global biopharmaceutical company focused on the innovative application of science and medicine to help people with serious medical conditions. Sunovion’s vision is to lead the way to a healthier world. The company’s spirit of innovation is driven by the conviction that scientific excellence paired with meaningful advocacy and relevant education can improve lives. With patients at the center of everything it does, Sunovion has charted new paths to life-transforming treatments that reflect ongoing investments in research and development and an unwavering commitment to support people with psychiatric, neurological and respiratory conditions. Sunovion’s track record of discovery, development and commercialization of important therapies has included Utibron™ Neohaler® (indacaterol/glycopyrrolate) inhalation powder, Brovana® (arformoterol tartrate) inhalation solution, Latuda® (lurasidone HCI) and Aptiom® (eslicarbazepine acetate). Headquartered in Marlborough, Mass., Sunovion is an indirect, wholly-owned subsidiary of Sumitomo Dainippon Pharma Co., Ltd. Sunovion Pharmaceuticals Europe Ltd., based in London, England, Sunovion Pharmaceuticals Canada Inc., based in Mississauga, Ontario, and Sunovion CNS Development Canada ULC, based in Toronto, Ontario, are wholly-owned direct subsidiaries of Sunovion Pharmaceuticals Inc. Additional information can be found on the company’s web sites: www.sunovion.com, www.sunovion.eu and www.sunovion.ca. Connect with Sunovion on Twitter, LinkedIn, Facebook and YouTube. About Sumitomo Dainippon Pharma Co., Ltd. Sumitomo Dainippon Pharma is among the top-ten listed pharmaceutical companies in Japan operating globally in major pharmaceutical markets, including Japan, the United States, China and the European Union. Sumitomo Dainippon Pharma aims to create innovative pharmaceutical products in the Psychiatry & Neurology area and the Oncology area, which have been designated as the focus therapeutic areas. Sumitomo Dainippon Pharma is based on the merger in 2005 between Dainippon Pharmaceutical Co., Ltd., and Sumitomo Pharmaceuticals Co., Ltd. Today, Sumitomo Dainippon Pharma has about 6,500 employees worldwide. Additional information about Sumitomo Dainippon Pharma is available through its corporate website at www.ds-pharma.com. LATUDA and SUNOVION are registered trademarks of Sumitomo Dainippon Pharma Co., Ltd. BROVANA is a registered trademark of Sunovion Pharmaceuticals Inc. APTIOM is used under license from Bial. ARCAPTA and NEOHALER are registered trademarks of Novartis AG, used under license. SEEBRI and UTIBRON are trademarks of Novartis AG, used under license. eFlow® is a registered trademark of PARI Pharma GmbH. Spiriva® and HandiHaler® are registered trademarks of Boehringer Ingelheim Pharma GMBH & Co KG. Sunovion Pharmaceuticals Inc. is a U.S. subsidiary of Sumitomo Dainippon Pharma Co., Ltd. For a copy of this release, visit Sunovion’s web site at www.sunovion.com 1 GOLD Guidelines 2017. http://www.goldcopd.org/guidelines-global-strategy-for-diagnosis-management.html. Accessed: March 16, 2017. 2 MMWR: Morbidity and Mortality Weekly Report. Employment and Activity Limitations Among Adults with Chronic Obstructive Pulmonary Disease — United States, 2013. March 27, 2015; 64(11). Available at http://www.cdc.gov/mmwr/ 3 National Heart, Lung, and Blood Institute. “What is COPD?” Available at: http://www.nhlbi.nih.gov/health/educational/copd/what-is-copd/index.htm. Accessed: March 2, 2016 4 National Heart, Lung and Blood Institute. (2013). What Are the Signs and Symptoms of COPD? Retrieved from https://www.nhlbi.nih.gov/health/health-topics/topics/copd/signs. 5 Partridge MR, Karlsson N, Small IR. Patient insight into the impact of chronic obstructive pulmonary disease in the morning: an internet survey. Curr Med Res Opin. 2009;25:2043–8. 6 Roche N, Small M, Broomfield S, Higgins V, Pollard R. Real world COPD: association of morning symptoms with clinical and patient reported outcomes. COPD. 2013;10:679–86. 7 Agusti A, Hedner J, Marin JM, Barbé F, Cazzola M, Rennard S. Night-time symptoms: a forgotten dimension of COPD. Eur Respir Rev. 2011;20:183–94.

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