TRPC6

DUBLIN, May 5, 2023 /PRNewswire/ -- The "Chronic Kidney Disease - Competitive landscape, 2023" report has been added to ResearchAndMarkets.com's offering. This report provides comprehensive insights about 75+ companies and 95+ drugs in Chronic Kidney Disease Competitive landscape. It covers the therapeutics assessment by product type, stage, route of administration, and molecule type. It further highlights the inactive pipeline products in this space. In March 2023, POXEL SA, announced the publication of preclinical results in autosomal dominant polycystic kidney disease (ADPKD) for PXL770, a novel, first-in-class direct adenosine monophosphate-activated protein kinase (AMPK) activator. For the first time, POXEL SA showed beneficial effects of a direct and selective AMPK activator in preclinical ADPKD models from three species mouse, human, and dog. These results confirm the potential utility of AMPK activation for this disease and support the development of PXL770 in a Phase 2 clinical program for ADPKD. In February 2023, AstraZeneca announced the successful completion of the acquisition of CinCor Pharma, Inc. The acquisition bolsters AstraZeneca's cardiorenal pipeline by adding baxdrostat (CIN-107), an aldosterone synthase inhibitor (ASI) for blood pressure lowering in treatment-resistant hypertension, to its cardiorenal portfolio. In January 2023, The U.S. Food and Drug Administration (FDA) has accepted a supplemental New Drug Application (sNDA) for Jardiance (empagliflozin) tablets, which is being investigated as a potential treatment to reduce the risk of kidney disease progression and cardiovascular death in adults with chronic kidney disease (CKD), Boehringer Ingelheim and Eli Lilly and Company announced. In November 2022, The Medical Research Council Population Health Research Unit (MRC PHRU) at the University of Oxford, which designed, conducted and analyzed EMPA-KIDNEY in a scientific collaboration with Boehringer Ingelheim and Eli Lilly and Company, announced that EMPA-KIDNEY phase III clinical trial met its primary endpoint by demonstrating a significant kidney and cardiovascular benefit for adults living with chronic kidney disease (CKD). When treated with Jardiance (empagliflozin), the risk of kidney disease progression or cardiovascular death was significantly reduced by 28% vs. placebo (HR; 0.72; 95% CI 0.64 to 0.82; P< 0.0001). In October 2022, Revelation Biosciences Inc. announced positive results in a preclinical model of acute kidney injury (AKI), chronic kidney disease (CKD). Treatment with REVTx-300 significantly reduced renal cortical fibrosis in a dose dependent manner in the medium and high dose groups (21.7% reduction (p < 0.05) and 29.3% (p < 0.05), respectively) and was comparable to a known TGF inhibitor of fibrosis used as a positive control (38.1% reduction (P < 0.05)). In October 2022, French Biopharma Company, Poxel SA announced the U.S. Food and Drug Administration (FDA) has granted orphan drug designation (ODD) to PXL770 for the treatment of patients with autosomal-dominant polycystic kidney disease (ADPKD). PXL770 is a novel, first-in-class direct adenosine monophosphate-activated protein kinase (AMPK) activator - and is also a phase 2 ready ADPKD asset, subject to additional financing. In-depth Commercial Assessment: Chronic Kidney Disease Collaboration Analysis by Companies The Report provides in-depth commercial assessment of drugs that have been included, which comprises collaboration, agreement, licensing and acquisition - deals values trends. The sub-segmentation is described in the report which provide company-company collaboration (licensing/partnering), company academic collaboration and acquisition analysis in tabulated form. Current Treatment Scenario and Emerging Therapies: How many companies are developing Chronic Kidney Disease drugs? How many Chronic Kidney Disease drugs are developed by each company? How many emerging drugs are in mid-stage, and late-stage of development for the treatment of Chronic Kidney Disease? What are the key collaborations (Industry-Industry, Industry-Academia), Mergers and acquisitions, licensing activities related to the Chronic Kidney Disease therapeutics? What are the recent trends, drug types and novel technologies developed to overcome the limitation of existing therapies? What are the clinical studies going on for Chronic Kidney Disease and their status? What are the key designations that have been granted to the emerging and approved drugs? Key Players Boehringer Ingelheim Eli Lilly and Company Reata Pharmaceuticals Novo Nordisk KBP Biosciences AstraZeneca Allena Pharmaceuticals SCOHIA PHARMA DiaMedica Therapeutics CinCor Pharma Galapagos NV Sentien Biotechnologies, Inc. Regeneron Pharmaceuticals UnicoCell Biomed OccuRx Pharmicell Lisata Therapeutics Unicycive Therapeutics Senda Biosciences Sarfez Pharmaceuticals Rege Nephro Orgenesis GNI Group Algomedix Maze Therapeutics Chinook Therapeutics Angion Biomedica Corp Arch Biopartners Scohia Pharma Algernon Pharmaceuticals TICEBA GmbH Key Products Empagliflozin Bardoxolone methyl Ziltivekimab KBP-5074 AZD9977 ALLN-346 BI-685509 SCO-792 DM199 Baxdrostat GLPG2737 SBI-101 REGN5459 ELIXCYTE FT011 Cellgram-CKD CLBS201 UNI-494 Research Program SZ007 Renal progenitor cells MSCKD F351 Research programme: TRPC6 antagonist APOL1 Programme Research and discovery programs: severe chronic kidney disease ROCK2 Inhibitor LSALT peptide SCO-116 Repirinast Polycystic kidney disease (PKD) For more information about this report visit About ResearchAndMarkets.com ResearchAndMarkets.com is the world's leading source for international market research reports and market data. 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Researchers report that an experimental drug first developed to treat kidney disease prolongs survival and improves muscle function in mice genetically engineered to develop a severe form of Duchenne muscular dystrophy (DMD). Researchers at Johns Hopkins Medicine report that an experimental drug first developed to treat kidney disease prolongs survival and improves muscle function in mice genetically engineered to develop a severe form of Duchenne muscular dystrophy (DMD). According to the Muscular Dystrophy Association (MDA), DMD affects 1 in every 5,000 live male births and results in severe muscle wasting and weakness because of the lack of a protein called dystrophin, which is needed to strengthen muscle cells and protect them from mechanical injury. The dystrophin gene is in the X chromosome, so DMD mainly affects boys. Girls only get the disease if both X chromosomes are affected. Muscle symptoms begin between the ages of 2 and 4, and by their early teens, most individuals with DMD are unable to walk. Dystrophin is also important to heart muscle, so heart failure often occurs in later teenage years into the early 20s. According to the MDA, people with DMD generally live until their late 20s or early 30s. There is no cure, but physical therapy and corticosteroids reduce inflammation and help delay muscle decline, helping symptoms and improving quality of life. Newer gene-targeting treatments are being tested, but they remain limited to a small number of patients targeted. The new study, published Sept. 13 in the Journal of Clinical Investigation -- Insight, reports that a drug blocking the ion channel called TRPC6 in mice with severe DMD doubled their survival and improved their skeletal and cardiac muscle function. It also reduced bone deformities associated with weak muscles. Ion channels are groups of proteins mostly found at the outer cell membrane that act like pores to allow elements like calcium or sodium to pass into or out of the cell in a controlled way. TRPC6 is one of these proteins that mostly allows calcium to pass into the cell. It is activated by stress hormones and mechanical forces, and has been found to contribute to abnormal calcium entry into muscle cells lacking dystrophin. This can result in cell damage and ultimately cell death, according to David Kass, M.D., Abraham and Virginia Weiss Professor of Cardiology at the Johns Hopkins University School of Medicine and senior author of the study. "In 2014, my laboratory first showed that calcium entering heart muscle cells from Duchenne mice rose more when they were stretched as compared to normal cells. This induced abnormal rhythms. We found that blocking TRPC6 prevented this excess calcium from entering the heart and reduced arrhythmia," Kass says. "We thought maybe a long-term TRPC6 blocker would help with this syndrome. Unfortunately, the drug we had back then worked fine in cells but was metabolized too fast in animals, so it was not usable." For the new study, the researchers used a mouse model of DMD that mimics the severe disease found in humans. The mice had a median lifespan of two months (equal to late teens for a human). Starting three days after birth, researchers treated male and female DMD mice with a TRPC6 inhibitor drug (BI 749327, developed by Boehringer-Ingelheim Pharmaceuticals) or with a placebo. Mice receiving the placebo had a median survival rate of four weeks and 100% mortality by nine weeks. Mice getting the inhibitor had nearly double this lifespan. Heart function improved by nearly 50%, and mice moved around 50% more and faster when compared with DMD mice that did not get the drug. These findings were supported by another experiment in which TRPC6 was genetically removed so the DMD mice never expressed the protein. They also had prolonged lifespan (nearly three times controls) and improved muscle function. "We believe this may be one of the first studies to prolong survival in this very severe model of Duchenne with a compound that can be administered orally. While the molecule does not restore dystrophin, it blocks abnormal behavior of another protein that is caused by the lack of dystrophin," says Kass. "This is not a cure for Duchenne, but if human trials replicate these findings, it could mean patients may survive into their late 40's and 50's with the possibility for an improved quality of life." According to the Muscular Dystrophy Association, an estimated 20,000 children globally are diagnosed with Duchenne each year. Authors of the study include Brian Lin, Joseph Shin, William Jeffreys, Nadan Wang, Clarisse Lukban, Megan Moorer, Esteban Velarde, Olivia Hanselman, Seoyoung Kwon, Suraj Kannan, and Ryan Riddle from The Johns Hopkins University, Christopher Ward from the University of Maryland, and Steven Pullen and Antonio Filareto (RBB) from Boehringer-Ingelheim Pharmaceuticals in Ridgefield, Connecticut. Funding was supported by sponsored research from Research Beyond Borders Boehringer-Ingelheim and NIH R35 HL 135827, AHA PD fellowship 20POST35180102 and 1K99HL 155840. Steven Pullen and Antonio Filareto are employees of Boehringer-Ingelheim. All other authors do not have any conflicts of interest to report.