Tenax Therapeutics Provides Update on Phase 2 Pulmonary Hypertension Clinical Trial - Business Wire
Tenax Therapeutics Provides Update on Phase 2 Pulmonary Hypertension Clinical Trial - Business Wire |
| Tenax Therapeutics Provides Update on Phase 2 Pulmonary Hypertension Clinical Trial - Business Wire Posted: 31 Oct 2019 05:00 AM PDT MORRISVILLE, N.C.--(BUSINESS WIRE)--Tenax Therapeutics, Inc. (Nasdaq: TENX), a specialty pharmaceutical company focused on identifying, developing and commercializing products that address cardiovascular and pulmonary diseases with high unmet medical need, today provided an update on its on-going clinical trial of levosimendan. Enrollment Update Tenax is conducting a multi-center, double-blind placebo controlled Phase 2 trial designed to evaluate levosimendan in patients with pulmonary hypertension and heart failure with preserved ejection fraction (PH-HFpEF). The study is also known as the HELP Trial (Hemodynamic Evaluation of Levosimendan in Patients with PH-HFpEF). The Company has activated all of its anticipate 15 sites which it believes will be sufficient to fully enroll the trial. 15 patients, up from eight at the end of August, are currently enrolled, out of the targeted 36 patients. Given the current pace of patient enrollment, we continue to expect full enrollment and top-line data in the first quarter of 2020. Initial Response The trial has a predefined response criterion that patients must meet following a 24-hour open-label infusion of levosimendan before they can be randomized to the 6-week double-blind phase of the trial. The criterion for randomization is that PCWP measured during supine exercise is ≥ 4mmHg less after the open-label infusion than at baseline. 15 of the 18 patients, approximately 83%, achieved this predefined responder criterion with a mean reduction of 8 mmHg in PCWP. Adverse Events There have been no drug-related serious adverse events, and no patients have withdrawn from the study. All of the patients who have completed the 6-week double-blind phase of the trial have elected to enroll in the open-label extension study. Tenax CEO Tony DiTonno stated, "We are excited to provide this interim update regarding the HELP Study enrollment and preliminary responder information. While these open-label hemodynamic responses are preliminary, it is encouraging to see such favorable responses. We are very fortunate to have so many prominent investigators and leading academic centers participating in the HELP Study." Dr. Stuart Rich, Director of the Pulmonary Vascular Disease Program at the Bluhm Cardiovascular Institute at Northwestern University and the principal investigator and architect for the HELP Study stated, "The high initial response rate, and the magnitude of the initial response with exercise has exceeded my expectations. I remain very hopeful that we may have an effective treatment for PH-HFpEF for the first time." About Tenax Therapeutics Tenax Therapeutics, Inc., is a specialty pharmaceutical company focused on identifying, developing and commercializing products that address cardiovascular and pulmonary diseases with high unmet medical need. The Company has a world-class scientific team including recognized global experts in pulmonary hypertension. The Company owns North American rights to develop and commercialize levosimendan and is currently enrolling their Phase 2 clinical trial for the use of levosimendan in the treatment of Pulmonary Hypertension associated with Heart Failure and preserved Ejection Fraction (PH-HFpEF). For more information, visit www.tenaxthera.com. About Levosimendan Levosimendan is a calcium sensitizer that works through a unique triple mechanism of action. It initially was developed for intravenous use in hospitalized patients with acutely decompensated heart failure. It was discovered and developed by Orion Pharma, Orion Corporation of Espoo Finland, and is currently approved in over 60 countries for this indication and not available in the United States. Tenax Therapeutics acquired North American rights to develop and commercialize levosimendan from Phyxius Pharma, Inc. Caution Regarding Forward-Looking Statements This news release contains certain forward-looking statements by the Company that involve risks and uncertainties and reflect the Company's judgment as of the date of this release. The forward-looking statements are subject to a number of risks and uncertainties, including, but not limited to matters beyond the Company's control that could lead to delays in the clinical study, new product introductions and customer acceptance of these new products; matters beyond the Company's control that could impact the Company's continued compliance with Nasdaq listing requirements; the impact of management changes on the Company's business and unanticipated charges, costs and expenditures not currently contemplated that may occur as a result of management changes; and other risks and uncertainties as described in the Company's filings with the Securities and Exchange Commission, including in its annual report on Form 10-K filed on April 1, 2019, its quarterly report on Form 10-Q filed on August 14, 2019 as well as its other filings with the SEC. The Company disclaims any intent or obligation to update these forward-looking statements beyond the date of this release. Statements in this press release regarding management's future expectations, beliefs, goals, plans or prospects constitute forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995.  |
| Posted: 09 Oct 2019 12:00 AM PDT Loss of a hormone called secretin (SCT) induces hypertension, scarring, and structural alterations in the heart and lungs, a study in mice reports. The study "Loss of secretin results in systemic and pulmonary hypertension with cardiopulmonary pathologies in mice" was published in the journal Nature Scientific Reports, and led by a team from Hong Kong. SCT is released by cells in the intestine and the brain, and its receptors are found at high levels in both the heart and lungs. Prior studies showed that SCT reduces blood pressure in the heart, increases cardiac blood flow, and regulates water and salt balance, among other mechanisms. Blood serum levels of SCT are also known to be markedly lower in people with congestive heart failure. However, "no studies have clearly shown the significance of SCT in these systems and explained how SCT plays a role in regulating blood pressure," the researchers wrote. The team investigated the severity of SCT's loss to the heart and lungs using mice in which the gene coding for secretin had been deleted. Compared to normal mice serving as controls, mice with no SCT showed increased blood pressure. This was accompanied by changes in the heart's chambers, namely right ventricular hypertrophy (enlargement) and fibrosis, or scarring. The heart's left ventricle was smaller than in control mice. Loss of secretin also led to pulmonary arterial hypertension (PAH), as shown by increased right ventricular systolic pressure in mice without SCT compared to control mice. This increase was detected as early as 3 months of age, and maintained until the age of 12 months. Right ventricular enlargement, another hallmark of PAH, was also seen in 3-month-old mice with SCT deficiency. Animals with no SCT also showed changes in lung tissue compared to the controls; namely, a significant increase in pulmonary artery thickness, severe structural alterations in blood vessels (vascular remodeling), and inflammation. Other changes associated with a complete lack of SCT included lower serum levels of nitric oxide (NO) and vascular endothelial growth factor (VEGF). In line with the previously shown role of VEGF in stimulating NO production to widen blood vessels, this suggests that a lack of SCT could lead to persistent vasoconstriction and elevated blood pressure, the researchers said. In contrast, levels of aldosterone were higher than normal in plasma and the heart of mice without SCT, as seen in people with congestive heart failure. The scientists then tested whether administration of SCT up to three months could effectively treat hypertension. Three-month-old mice lacking SCT were given this hormone (at 2.5 nmol/kg/day) via a pump into the abdomen. After three months, blood levels of SCT in these animals were similar to those of control mice. Mice given SCT also showed significantly reduced thickening of heart and lung arteries, as well as less cardiac scarring and inflammation. Overall, the findings suggest that "SCT can be an essential hormone for the cardiovascular and pulmonary systems in humans, since SCT deficiency can result in pulmonary and systemic hypertension in mice," the researchers wrote. Measuring SCT levels "can provide interesting information, such as whether SCT deficiency has a role in pulmonary and systemic hypertension in humans," they added.  Patricia holds her Ph.D. in Cell Biology from University Nova de Lisboa, and has served as an author on several research projects and fellowships, as well as major grant applications for European Agencies. She also served as a PhD student research assistant in the Laboratory of Doctor David A. Fidock, Department of Microbiology & Immunology, Columbia University, New York. × Patricia holds her Ph.D. in Cell Biology from University Nova de Lisboa, and has served as an author on several research projects and fellowships, as well as major grant applications for European Agencies. She also served as a PhD student research assistant in the Laboratory of Doctor David A. Fidock, Department of Microbiology & Immunology, Columbia University, New York. Latest Posts  |
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