Coronary/Structural Heart

Tenaya Therapeutics Presents Promising Interim Clinical Data from MYPEAK™-1 Phase 1b/2a Clinical Trial of TN-201 Gene Therapy for the Treatment of MYBPC3-Associated Hypertrophic Cardiomyopathy

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MyPEAK-1 Data Presented During Late-Breaking Session at AHA Scientific Sessions 2025 with Simultaneous Publication in Cardiovascular Research TN-201 Has Been Generally Well Tolerated at Both Doses Longer-term Follow Up of Cohort 1 Patients Showed Consistent, Deeper, and Durable Improvement in Measures of Hypertrophy Initial Cohort 2 Data Demonstrated Early Dose Responsive Increases in TN-201 Transduction and MyBP-C Protein Expression Tenaya Management to Host Webcast Call for Analysts and Investors on Monday, November 10 at 8:00 a.m. EST NEW ORLEANS and SOUTH SAN FRANCISCO, Calif., Nov. 08, 2025 (GLOBE NEWSWIRE) — Tenaya Therapeutics, Inc. (NASDAQ: TNYA) announced that new interim safety and efficacy data from the company’s MyPEAK™-1 Phase 1b/2a clinical trial of TN-201 were presented today during the Late-Breaking Science: Main Event session at the American Heart Association’s (AHA) Scientific Sessions 2025 by Milind Desai, M.D., MBA, director of the Hypertrophic Cardiomyopathy Center at Cleveland Clinic and vice chair of Cleveland Clinic’s Heart, Vascular & Thoracic Institute. These data, which included longer-term follow-up results for three patients dosed with TN-201 gene therapy at a dose of 3E13vg/kg (Cohort 1) and initial results for three patients who received TN-201 at a dose of 6E13 vg/kg (Cohort 2) were simultaneously published in Cardiovascular Research. TN-201 is being developed for the potential treatment of MYBPC3-associated hypertrophic cardiomyopathy (HCM), a condition caused by insufficient levels of myosin-binding protein C (MyBP-C). Single administration of TN-201 gene therapy was generally well-tolerated at both the 3E13 vg/kg and 6E13 vg/kg dose levels and immunogenicity was well managed through monitoring and individualized tapering of immunosuppressives. TN-201 achieved robust transduction and durable expression with early dose-dependent increase in both transduction and MyBP-C protein expression. Among Cohort 1 patients for whom there was greater than one year of follow up, decreases in circulating biomarkers and reductions in measures of left ventricular hypertrophy deepened over time. “These initial results are promising for a patient population that too often live with difficult, even dangerous, symptoms,” said Dr. Desai, an investigator for the MyPeak-1 Phase 1b/2a clinical trial. “In the past decade, we’ve made great progress in understanding and treating hypertrophic cardiomyopathy, and as our understanding of the genetic underpinnings of HCM increases, research into gene therapies such as TN-201 offer the opportunity to further advance and improve patient care.” “Results of TN-201 treatment are in line with our expectations for this stage of trial, with a manageable safety profile and dose-dependent MyBP-C protein level increases over time. In particular, the durable changes in multiple parameters of disease – biomarkers, hypertrophy and heart failure symptoms – all moving with directional consistency toward normalization after a single dose are an encouraging early signal of TN-201’s activity,” said Whit Tingley, M.D., Ph.D., Tenaya’s Chief Medical Officer. “We look forward to building on these data with continued long-term follow-up of Cohort 1 and the maturation of early results for Cohort 2, which will inform our plans for TN-201’s late-stage development.” Interim results from the MyPEAK-1 Phase 1b/2a Clinical TrialData reported today includes safety, biopsy and leading indicators of efficacy for the three patients enrolled in Cohort 1 with follow-up ranging from Week 52-78, and safety for the three patients in Cohort 2, Week 12 biopsy for Patient 6 and Week 26 assessments for Patient 4 as of the July 2025 data cut off. Patient 5 was lost to further follow-up after week 12. All patients other than Patient 5 have completed every visit and remain on study. All patients enrolled in MyPEAK-1 had serious burden of disease at baseline. All six had objectively severe nonobstructive HCM with levels of hypertrophy significantly above average for people with HCMAll six were at sufficiently high risk of sudden cardiac death to warrant an implantable cardiac defibrillator (ICD) deviceAll experienced mild-to-moderate symptoms of heart failure that interfered in activities of daily living (New York Heart Association, or NYHA, Class II-III)Four of the six have previously undergone surgical myectomy Safety data for all six patients in Cohorts 1 and 2 showed that TN-201 was generally well tolerated at both the 3E13 vg/kg and 6E13 vg/kg doses. No dose-limiting toxicities were observed and all patients have tapered off immunosuppressive medicines. Reversible, asymptomatic liver enzyme elevations (Grade 1-3) were the most common treatment-related adverse events (AEs) reportedThere were no signs of cardiotoxicities, including no declines in left ventricular ejection fraction, clinical myocarditis or ventricular arrhythmiasThere were two treatment-related AEs classified as serious due to inpatient treatment or monitoring: a Cohort 1 patient with Grade 2 transaminase elevation that responded to steroids and a Cohort 2 patient with Grade 1 elevation of complement factors that resolved without additional interventionAdjustments to monitoring and immunosuppression during Cohort 1 resulted in faster tapers and lower cumulative corticosteroid doses in Cohort 2, despite the higher TN-201 dose MyBP-C protein levels increased over time, with early evidence of a substantial increase commensurate with higher dose in Cohort 2. TN-201 DNA transduction and TN-201 mRNA expression following similar dose response. Tenaya reported that TN-201 transduction and TN-201 mRNA expression were robust. All three patients in Cohort 1 demonstrated sustained presence of TN-201 DNA in the heart and mRNA expression that increased over time, supporting the observed increases in MyBP-C level changes.In Cohort 1 patients, protein levels increased by an average of 4% from the first biopsy taken to Week 52. In Patient 3, the first patient for whom baseline biopsies were available, MyBP-C protein was shown to increase by 5% at Week 52.The first evaluable patient in Cohort 2 (Patient 6) demonstrated a clear dose response, and early MyBP-C expression increased by 14% after only 12 weeks post-dose. Of note, Patient 6 had a greater than 2-fold increase in transduction and expression at Week 12 relative to the averages for these measures observed across Cohort 1. Multiple parameters, including biomarkers, hypertrophy, heart failure symptoms, associated with increased risks of complications or reduced survival, have improved among a majority of patients with greater than 26 weeks of follow-up. Cardiac Troponin I levels declined significantly (48%-74%) to normal or near-normal levels in all Cohort 1 patients. Cardiac troponin I is a predictive risk factor of cardiac AEs such as ventricular arrhythmias, sudden cardiac death, and progression to end-stage heart failure.(1)NT-proBNP, a biomarker of cardiac muscle strain, improved or remained stable in two of three Cohort 1 patientsCardiac Troponin I remained within the normal range and NT-proBNP remained stable for Patient 4 from Cohort 2 at their 26-Week assessmentAll three patients in Cohort 1 now have evidence of significant improvement in one or more measures of hypertrophy at Week 52, including notable reductions in left ventricular posterior wall thickness (LVPWT) of between 21% and 39%. LVPWT for Patient 4 in Cohort 2 was stable at Week 26. Greater LVPWT is an independent risk factor for reduced long-term survival after septal myectomy.(2)Two out of three Cohort 1 patients saw reductions in overall left ventricular mass index (LVMI) of between 12% and 22% at Week 52. LVMI for Patient 4 in Cohort 2 was stable at Week 26NYHA classification, a measure of the impact of heart failure symptoms on activities of daily living, improved in all patients by at least one class by Week 26, and all Cohort 1 patients are now NYHA Class I (asymptomatic). While the interim results from MyPEAK-1 are promising, longer-term follow-up for all patients is required to further inform Tenaya’s understanding of TN-201’s potential as a treatment for MYBPC3-associated HCM. Tenaya plans to periodically report additional results from longer-term follow-up. These interim data were presented during the “Forgotten No More: The Current Belle of the Ball? Breakthrough Evolutions in Hypertrophic Cardiomyopathy” Late-Breaking Science: Main Event session during AHA 2025 and were published simultaneously in an article titled “First-in-human study of AAV9:MYBPC3 gene replacement therapy (TN-201) in hypertrophic cardiomyopathy: Initial safety, pharmacodynamic, and imaging results from MyPEAK-1” in Cardiovascular Research. Conference Call and WebcastTenaya management will host a conference call on Monday, November 10, 2025, at 8:00 a.m. ET/5:00 a.m. PT to discuss the TN-201 data presented and published today and the status of the MyPEAK-1 clinical trial.  The webcast conference call, including an accompanying slide presentation, can be accessed from the Investor section on the “Events and Presentations” page of the Tenaya website at www.tenayatherapeutics.com. About the MyPEAK-1 Phase 1b/2a Clinical TrialThe MyPEAK-1 Phase 1b/2 clinical trial (Clinicaltrials.gov ID: NCT05836259) is a multi-center, open-label, dose-escalating (3E13 vg/kg and 6E13 vg/kg) study of symptomatic adults (up to 24) who have been diagnosed with MYBPC3-associated HCM. MyPEAK-1 is designed to assess the safety, tolerability and clinical efficacy of a one-time intravenous infusion of TN-201 gene replacement therapy. MyPEAK-1 has tested doses of 3E13 vg/kg and 6E13 vg/kg in two cohorts of three patients each. On July 30, 2025, Tenaya reported that the trial’s independent Data Safety Monitoring Board (DSMB) concluded that TN-201 had an acceptable safety profile to allow enrollment of expansion cohorts at either the 3E13 vg/kg (Cohort 1) or 6E13 vg/kg (Cohort 2) dose levels. On November 7, 2025, Tenaya announced the FDA placed MyPEAK-1 on a clinical hold. Tenaya is working with the FDA to address the agency’s concerns through an amendment to the trial protocol. To learn more about gene therapy for HCM and participation in the MyPEAK-1 study, please visit HCMStudies.com. About MYBPC3-Associated Hypertrophic Cardiomyopathy (HCM)Variants in the Myosin Binding Protein C3 (MYBPC3) gene are the most common genetic cause of hypertrophic cardiomyopathy (HCM), accounting for approximately 20% of the overall HCM population, or 120,000 patients, in the United States alone. MYBPC3-associated HCM is a severe and progressive condition affecting adults, teens, children and infants. Mutations of the MYBPC3 gene result in insufficient expression of a protein, called MyBP-C, needed to regulate heart contraction. The heart becomes hypercontractile and the left ventricle thickens, resulting in symptoms such as chest pain, shortness of breath, palpitations and fainting. Patients whose disease is caused by MYBPC3 mutations are more likely than those with non-genetic forms of HCM to experience earlier disease onset and have high rates of serious outcomes, including heart failure symptoms, arrhythmias, stroke and sudden cardiac arrest or death. There are currently no approved therapeutics that address the underlying genetic cause of HCM. About TN-201TN-201 is an adeno-associated virus serotype 9 (AAV9)-based gene therapy designed address the underlying cause of MYBPC3-associated hypertrophic cardiomyopathy (HCM) by delivering a working MYBPC3 gene to heart muscle cells via a single intravenous infusion and thereby increasing insufficient MyBP-C protein levels with the aim of halting or even reversing disease after a single dose. The U.S. Food and Drug Administration has granted TN-201 Fast Track, Orphan Drug and Rare Pediatric Drug Designations. TN-201 has also received orphan medicinal product designation from the European Commission. About Tenaya TherapeuticsTenaya Therapeutics is a clinical-stage biotechnology company committed to a bold mission: to discover, develop and deliver potentially curative therapies that address the underlying drivers of heart disease. Tenaya’s pipeline includes clinical-stage candidates TN-201, a gene therapy for MYBPC3-associated hypertrophic cardiomyopathy (HCM) and TN-401, a gene therapy for PKP2-associated arrhythmogenic right ventricular cardiomyopathy (ARVC). Tenaya has employed a suite of integrated internal capabilities, including modality agnostic target validation, capsid engineering and manufacturing, to generate a portfolio of novel medicines based on genetic insights, including TN-301, a clinical-stage small molecule HDAC6 inhibitor for the potential treatment of heart failure and related cardio/muscular disease, and multiple early-stage programs in preclinical development aimed at the treatment of both rare genetic disorders and more prevalent heart conditions. For more information, visit www.tenayatherapeutics.com.       (1)   Kubo, et al, Journal Am Coll Cardiol, 2013      (2)   Schaff, et al, JACC Heart Failure, 2022 Forward-Looking StatementsThis press release contains forward-looking statements as that term is defined in Section 27A of the Securities Act of 1933 and Section 21E of the Securities Exchange Act of 1934. Statements in this press release that are not purely historical are forward-looking statements. Words such as “promising,” “opportunity,” “expectations,” “encouraging,” “look forward,” “will,” “potential,” and similar expressions are intended to identify forward-looking statements. Such forward-looking statements include, among other things, the clinical, therapeutic and commercial potential of, and expectations regarding, TN-201 as a treatment for MYBPC3-associated HCM; the potential for additional MyPEAK-1 data to inform plans for TN-201’s late stage development; statements regarding the continued development of TN-201, clinical hold, anticipated timelines, TN-201 clinical outcomes and risk/benefit profile, which may materially change as more patient data become available and statements made by Tenaya’s Chief Medical Officer and the investigator for MyPEAK-1. The forward-looking statements contained herein are based upon Tenaya’s current expectations and involve assumptions that may never materialize or may prove to be incorrect. These forward-looking statements are neither promises nor guarantees and are subject to a variety of risks and uncertainties, including but not limited to: the expected timing and outcome of Tenaya’s regulatory interactions related to the clinical hold on MyPEAK-1; the timing and availability of MyPEAK-1 data; the potential progress of MyPEAK-1; the potential failure of TN-201 to demonstrate safety and/or efficacy in clinical testing; the potential for any MyPEAK-1 clinical trial results to differ from preclinical, interim, preliminary or expected results; the potential for the FDA and/or other regulatory agencies to conclude at any time that TN-201 may not have an appropriate risk/benefit profile; Tenaya’s ability to enroll and maintain patients in clinical trials, including MyPEAK-1; risks associated with the process of discovering, developing and commercializing drugs that are safe and effective for use as human therapeutics and operating as an early stage company; Tenaya’s continuing compliance with applicable legal and regulatory requirements; Tenaya’s ability to raise any additional funding it will need to continue to pursue its product development plans; Tenaya’s reliance on third parties; Tenaya’s manufacturing, commercialization and marketing capabilities and strategy; the loss of key scientific or management personnel; competition in the industry in which Tenaya operates; Tenaya’s ability to obtain and maintain intellectual property protection for its product candidates; general economic and market conditions; and other risks. Information regarding the foregoing and additional risks may be found in the section titled “Risk Factors” in Tenaya’s Quarterly Report on Form 10-Q for the fiscal quarter ended June 30, 2025, and other documents that Tenaya files from time to time with the Securities and Exchange Commission. These forward-looking statements are made as of the date of this press release, and Tenaya assumes no obligation to update or revise any forward-looking statements, whether as a result of new information, future events or otherwise, except as required by law. Tenaya ContactsMichelle CorralVP, Corporate Communications and Investor RelationsIR@tenayathera.com InvestorsAnne-Marie FieldsPrecision AQannemarie.fields@precisionaq.com MediaWendy RyanTen Bridge Communicationswendy@tenbridgecommunications.com

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CRISPR Therapeutics Announces Positive Phase 1 Clinical Data for CTX310® Demonstrating Deep and Durable ANGPTL3 Editing, Triglyceride and Lipid Lowering

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-Data presented in a late-breaking presentation at the American Heart Association (AHA) Scientific Sessions 2025- -Phase 1 clinical data for CTX310® demonstrate robust, dose-dependent reductions in circulating ANGPTL3 with a mean reduction from baseline of -73% (maximum -89%), a mean reduction in triglycerides (TG) of -55% (maximum -84%), and a mean reduction of low-density lipoprotein (LDL) of -49% (maximum -87%) at the highest dose- -Among participants with elevated baseline TG ( >150 mg/dL), a mean reduction of 60% in TG were observed at therapeutic doses- -CTX310 was well tolerated with no treatment-related serious adverse events and no ≥Grade 3 changes in liver transaminases- -Findings simultaneously published in The New England Journal of Medicine entitled “First-in-Human Phase 1 Trial of CRISPR-Cas9 Gene Editing Targeting ANGPTL3”- ZUG, Switzerland and BOSTON, Nov. 08, 2025 (GLOBE NEWSWIRE) — CRISPR Therapeutics (Nasdaq: CRSP), a biopharmaceutical company focused on creating transformative gene-based medicines for serious diseases, today announced positive Phase 1 data from its ongoing clinical trial evaluating CTX310®, an investigational, in vivo CRISPR/Cas9 gene-editing therapy targeting ANGPTL3. A single-course treatment with CTX310 produced dose-dependent, durable reductions in circulating ANGPTL3 with a mean reduction from baseline of -73% (maximum -89%), a mean reduction in triglycerides (TG) of -55% (maximum -84%) and a mean reduction of low-density lipoprotein (LDL) of -49% (maximum -87%) at the highest dose. These data demonstrate the potential of CTX310 to deliver meaningful and sustained lipid lowering following a single-course intravenous (IV) infusion. These data were presented today during a late-breaking session at the American Heart Association (AHA) Scientific Sessions and published simultaneously in The New England Journal of Medicine (NEJM) in a peer-reviewed article entitled “Phase 1 Trial of CRISPR-Cas9 Gene Editing Targeting ANGPTL3.” “The publication and presentation of these Phase 1 results mark an important milestone for CRISPR Therapeutics and for the field of in vivo gene editing,” said Naimish Patel, M.D., Chief Medical Officer of CRISPR Therapeutics. “For the first time, we’ve shown that a single-course in vivo CRISPR treatment can safely and durably lower ANGPTL3, leading to clinically meaningful reductions in triglycerides and LDL. These data provide strong support for continued advancement of CTX310 and our broader cardiovascular gene-editing portfolio.” “Seeing a single-course treatment safely lower both LDL cholesterol and triglycerides is truly unprecedented,” said Stephen J. Nicholls, lead study investigator and director of the Victorian Heart Institute at Monash University. “If these findings are confirmed in larger studies, a one-time therapy could redefine how we manage lifelong lipid disorders and help prevent cardiovascular disease.” “Adherence to cholesterol-lowering therapy remains a major challenge in treating patients with heart disease,” said Steven E. Nissen, M.D., senior author of the study and Chief Academic Officer at the Cleveland Clinic Heart, Vascular and Thoracic Institute. “Many patients discontinue therapy within the first year. The prospect of a one-time treatment with durable effects would be a major advance in cardiovascular prevention.” CTX310 CTX310 is an investigational, lipid nanoparticle (LNP) delivered CRISPR/Cas9 therapy designed to precisely edit the ANGPTL3 gene in hepatocytes following a single-course IV administration. ANGPTL3 encodes a key protein that regulates TG and LDL levels, both well-established risk factors for atherosclerotic cardiovascular disease (ASCVD). Individuals with naturally occurring loss-of-function mutations in ANGPLT3 have lower TG, lower LDL and a reduced lifetime risk of cardiovascular disease compared to those without such mutations. By reducing ANGPTL3 expression, CTX310 has the potential to durably lower TG and LDL cholesterol in patients with severe or refractory dyslipidemia. More than 40 million people in the United States have elevated TG, elevated LDL, or both, underscoring the significant unmet medical need. CTX310 is initially being developed for patients at highest cardiovascular risk who have limited effective treatment options despite current lipid-lowering therapies. Phase 1 Clinical Trial Design The Phase 1, open label, dose-escalation trial evaluated single-course IV doses of CTX310 ranging from 0.1 to 0.8 mg/kg (lean body weight) targeting ANGPTL3 in four patient groups: homozygous familial hypercholesterolemia (HoFH), severe hypertriglyceridemia (sHTG), heterozygous familial hypercholesterolemia (HeFH), or mixed dyslipidemias (elevated TG and LDL). Eligible participants had uncontrolled TG levels >150 mg/dL and/or LDL cholesterol >100 mg/dL (or >70 mg/dL for those with established ASCVD) despite background standard of care per local guidelines. The majority of participants were receiving statins and/or ezetimibe, while 40% were taking PCSK9 inhibitors. The trial was designed to evaluate safety and tolerability as primary endpoints, with changes in circulating ANGPTL3 protein, TG, and LDL as secondary endpoints. Safety and Tolerability Single-course ascending doses of CTX310 were administered to 15 participants across sequential cohorts, and all participants completed at least 28 days of follow-up as of the data cutoff. CTX310 was generally well tolerated, and no dose-limiting toxicities or serious adverse events related to treatment. Adverse events were generally mild to moderate. One participant experienced an allergic reaction that resolved the following day with supportive care. Infusion-related reactions occurred in three participants (two at 0.6 mg/kg and one at 0.8 mg/kg dose), all Grade 2. All events resolved, and all participants completed their infusions. One participant with elevated transaminases level at baseline had a Grade 2 elevation of transaminases that peaked by Day 4 and resolved completely by Day 14 without any rise in bilirubin. Overall, CTX310 demonstrated a well-tolerated safety and tolerability profile that supports continued advancement of the program. Efficacy Highlights These new results build upon previously disclosed top-line data from 12 participants across the first four sequential cohorts, corresponding to lean body weight-based doses of DL1 [0.1 mg/kg], DL2 [0.3 mg/kg], DL3 [0.6 mg/kg] and DL4 [0.8 mg/kg]. All participants had at least 30 days of follow-up. Dose-dependent reductions in circulating ANGPTL3 protein: Mean (range) among participants treated with 0.1, 0.3, 0.6, 0.7, and 0.8 mg/kg doses were 10% (-22 to 71), 9% (-25 to 64), -33% (-51 to -19), -80% (-87 to -73), and -73% (-89 to -67), respectively, at Day 30 following CTX310 infusion.Among participants treated at 0.8 mg/kg, TG reductions of up to 84% were observed, with a mean reduction of 55% at Day 60 following CTX310 infusion. In participants with elevated TG ( >150 mg/dL) at baseline, mean reductions of 60% were observed at the therapeutic dose levels at Day 60 following CTX310 infusion.   Among participants treated at 0.8 mg/kg, LDL reductions of up to 87% were observed, with a mean reduction of 49% at Day 60 following CTX310 infusion.Two participants on background PCSK9 inhibitors achieved >80% reduction in LDL from baseline. Next Steps Results from the Phase 1 clinical trial highlight the potential of CTX310 to safely and durably lower both TG and LDL following a single-course IV administration. These findings underscore its promise as a potentially transformative treatment approach for patients with severe or refractory dyslipidemia. CRISPR Therapeutics is advancing CTX310 into Phase 1b clinical trials, prioritizing development in sHTG and mixed dyslipidemia. About In Vivo Programs CRISPR Therapeutics has established a proprietary lipid nanoparticle (LNP) delivery platform to enable gene editing in the liver using both CRISPR/Cas9 and its novel, proprietary SyNTase™ editing technologies. The Company’s in vivo portfolio includes its lead investigational programs, CTX310 (directed towards angiopoietin-related protein 3 (ANGPTL3)) and CTX320™ (directed towards LPA, the gene encoding apolipoprotein(a) (apo(a)), a major component of lipoprotein(a) [Lp(a)]). Both are validated therapeutic targets for cardiovascular disease. CTX310 and CTX320 are in ongoing clinical trials in patients with heterozygous familial hypercholesterolemia, homozygous familial hypercholesterolemia, mixed dyslipidemias, or severe hypertriglyceridemia, and in patients with elevated lipoprotein(a), respectively. In addition, the Company’s research and preclinical development candidates include: CTX460™, targeting SERPINA1 for the treatment of alpha-1 antitrypsin deficiency (AATD); CTX340™, targeting AGT for the treatment of refractory hypertension; and CTX450™, targeting ALAS1 for the treatment of acute hepatic porphyria (AHP).  About CRISPR TherapeuticsFounded over a decade ago, CRISPR Therapeutics is a leading gene editing company focused on developing transformative medicines for serious diseases. The Company has evolved from a pioneering research-stage organization into an industry leader, marking a historic milestone with the approval of CASGEVY® (exagamglogene autotemcel [exa-cel]), the world’s first CRISPR-based therapy, approved for eligible patients with sickle cell disease and transfusion-dependent beta thalassemia. CRISPR Therapeutics is advancing a broad and diversified pipeline across hemoglobinopathies, oncology, regenerative medicine, cardiovascular and autoimmune, and rare diseases. The Company continues to expand its leadership in gene editing through the development of SyNTase™ editing, a novel and proprietary gene-editing platform designed to enable precise, efficient, and scalable gene correction. To accelerate and expand its impact, CRISPR Therapeutics has established strategic collaborations with leading biopharmaceutical partners, including Vertex Pharmaceuticals. CRISPR Therapeutics AG is headquartered in Zug, Switzerland, with its wholly-owned U.S. subsidiary, CRISPR Therapeutics, Inc., and R&D operations based in Boston, Massachusetts and San Francisco, California. To learn more, visit www.crisprtx.com.  CRISPR THERAPEUTICS® standard character mark and design logo, SyNTase™, CTX310®, CTX320™, CTX340™, CTX450™ and CTX460™ are trademarks and registered trademarks of CRISPR Therapeutics AG. CASGEVY® and the CASGEVY logo are registered trademarks of Vertex Pharmaceuticals Incorporated. All other trademarks and registered trademarks are the property of their respective owners.   CRISPR Therapeutics Forward-Looking StatementStatements contained in this press release regarding matters that are not historical facts are “forward-looking statements” within the meaning of the Private Securities Litigation Reform Act of 1995. Because such statements are subject to risks and uncertainties, actual results may differ materially from those expressed or implied by such forward-looking statements. Such statements include, but are not limited to, statements made by Drs. Nicholls, Nissen and Patel in this press release as well as statements regarding any or all of the following: (i) CRISPR Therapeutics preclinical studies, clinical trials and pipeline products and programs, including, without limitation, manufacturing capabilities, status of such studies and trials, potential expansion into new indications and expectations regarding data, safety and efficacy generally; (ii) data included in the above-described oral presentation and any associated abstracts or posters, data included in the above-described article in The New England Journal of Medicine as well as the ability to use data from ongoing and planned clinical trials for the design and initiation of further clinical trials; and (iii) the therapeutic value, development, and commercial potential of gene editing technologies and therapies, including CRISPR/Cas9 and SyNTase, as well as other technologies. Risks that contribute to the uncertain nature of the forward-looking statements include, without limitation, the risks and uncertainties discussed under the heading “Risk Factors” in CRISPR Therapeutics most recent annual report on Form 10-K and in any other subsequent filings made by CRISPR Therapeutics with the U.S. Securities and Exchange Commission. Existing and prospective investors are cautioned not to place undue reliance on these forward-looking statements, which speak only as of the date they are made. We disclaim any obligation or undertaking to update or revise any forward-looking statements contained in this press release, other than to the extent required by law. Investor Contact: +1-617-307-7503 ir@crisprtx.com Media Contact: +1-617-315-4493 media@crisprtx.com

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Cardiosense Presents New Analysis of the SEISMIC-HF I Study Validating its AI Algorithm for Noninvasive PCWP Assessment at the American Heart Association’s 2025 Scientific Sessions

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CHICAGO–(BUSINESS WIRE)–Cardiosense, a digital health company pioneering AI-enabled solutions for cardiac disease management, today announced a secondary analysis from the SEISMIC-HF I study on the performance of an AI algorithm for noninvasive congestion assessment at the point of care. The new analysis will be presented by Marat Fudim, MD, Associate […]

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Elixir Medical Highlights Results From “Real World” MY-IVL Study Demonstrating Performance of LithiX™ Hertz Contact (HC) Intravascular Lithotripsy System (IVL) in Treating Calcified Coronary Lesions

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LithiX™ HC-IVL is a novel lithotripsy system designed to facilitate treatment of heart disease exacerbated by the presence of calcium within coronary artery plaques MY-IVL study enrolled 102 real world complex patients (130 lesions) with core lab adjudicated intravascular imaging analysis MILPITAS, Calif., Nov. 06, 2025 (GLOBE NEWSWIRE) —  Elixir Medical, a developer of disruptive technologies to treat cardiovascular disease, announced results from the MY-IVL Study at the Transcatheter Cardiovascular Therapeutics (TCT) Conference 2025 in San Francisco. The data showed excellent clinical outcomes for LithiX™ Hertz Contact (HC) Intravascular Lithotripsy System (IVL) in the treatment of severely calcified coronary lesions among complex and high-risk percutaneous coronary intervention (PCI) patients. The MY-IVL Study evaluated 102 consecutive all-comer patients with notable severe calcified coronary artery disease treated with LithiX HC-IVL between April and September 2025 at Cardiac Vascular Sentral Kuala Lumpur Hospital (CVSKL), Malaysia’s first and leading private heart and vascular center. Angiographic and intravascular imaging from all patients was analyzed and adjudicated by an independent core lab MedStar Cardiovascular Research Network Core Laboratory at Washington Hospital Center, Washington, DC. The study included a broad range of clinically complex patients with multiple comorbidities clinically presenting with stable angina or acute coronary syndrome, including patients in cardiogenic shock, reflecting the device’s use and performance in everyday practice. Patient and lesion characteristics include: 102 patients with 130 lesions treatedAverage lesion length was 19.72 ± 14.09 mm and more than 30% of lesions were longer than 20 mm with an average length of 35.7 mm88% of lesions had severe calcificationCalcification in 41% of lesions was eccentric (arc of ≤ 270°), including 20% of lesions with an arc ≤ 180°94.6% of lesions were Class B2/C by American Heart Association (AHA) classification, which is associated with almost a two-fold risk of target lesion failure events within 30 days as compared to noncomplex lesions 1 Key clinical and procedural findings include: 96.1% of freedom from MACE at 30 days (Primary Safety Endpoint)Angiographic diameter stenosis of < 30% without intra-procedural MACE was achieved in 96.3% of patients following DES treatment There were no LithiX HC-IVL device-related angiographic procedural complications Key core lab adjudicated intravascular imaging results: Post procedure mean minimum stent area (MSA) was 6.89 mm², exceeding the powered performance goal (PG) of 4.9 mm² (p 100% was achieved in all lesion morphologies, including concentric and eccentric calcification “LithiX represents an important advancement in PCI. In our experience, its notable advantages include versatility and high treatment effect in modifying the most complex calcified lesions using a simpler procedure flow, particularly in this study with only a single device used per procedure, including multiple and long lesions,” said Dr. Tamil Selvan Muthusamy, Consultant Cardiologist at CVSKL and Co-Principal Investigator of the MY-IVL Study. The LithiX HC-IVL System is an advanced intravascular lithotripsy technology designed to optimize device expansion in calcified coronary artery blockages during a PCI procedure. Unlike energy-based systems dependent on an external energy generator, LithiX device is a highly deliverable mechanical lithotripsy device using a balloon with integrated low-profile metallic hemispheres to create focal pressure amplification based on Hertz Contact Stress theory. “Our study demonstrates excellent calcium modification potential of this novel Hertz Contact Lithotripsy technology, with MSA above 100% in all treated lesions, even those with less than 180% degree arc of calcium, which, based on our experience, are often difficult to treat with existing calcium modification devices,” added Dr. Rosli Mohd Ali, Consultant Cardiologist at CVSKL and Co-Principal Investigator of the MY-IVL Study. The Hertz Contact Lithotripsy hemispheres work selectively on calcium within the lesion, breaking and fragmenting the hardened plaque under low balloon inflation pressure. The hemispheres (27 to 45 depending on device size) are designed to create highly localized points of amplified force to create deep and wide fractures at the multiple points of contact with calcium while being atraumatic to the adjacent non-calcified vessel due to the tissue’s elasticity. About Elixir Medical Elixir Medical Corporation, a privately held company based in Milpitas, California, develops disruptive platforms to treat coronary and peripheral artery disease. Our transformative technologies have multiple applications across the cardiovascular space capable of delivering improved clinical outcomes for millions of patients. Elixir Medical was named to Fast Company’s prestigious list of the World’s Most Innovative Companies of 2025 and Fierce Medtech’s 2025 Fierce 15 list. Visit us at www.elixirmedical.com and on LinkedIn and X. The LithiX HC-IVL System is CE Mark approved and is not available in the United States. Media Contact Richard Laermer, RLM PR, elixir@rlmpr.com  (212) 741-5106 X 216 1 Konigstein M et al. J Am Heart Assoc. 2022;11:e025275. DOI: 10.1161/JAHA.121.025275

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Tenax Therapeutics to Host Virtual KOL Call to Discuss TNX-103 (Oral Levosimendan) for the Treatment of PH-HFpEF

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CHAPEL HILL, N.C., Nov. 06, 2025 (GLOBE NEWSWIRE) — Tenax Therapeutics, Inc. (Nasdaq: TENX) (“Tenax Therapeutics” or the “Company”), a Phase 3, development-stage pharmaceutical company using clinical insights to develop novel cardiopulmonary therapies, today announced that the Company will host a conference call and webcast on Thursday, November 13, 2025, at 4:30 p.m. ET. Members of the management team will be joined by the below recognized key opinion leaders in cardiovascular medicine to discuss the treatment landscape for pulmonary hypertension in heart failure with preserved ejection fraction (PH-HFpEF) and the ongoing late-stage development program for TNX-103 (oral levosimendan). Barry A. Borlaug, M.D., Professor of Medicine, Department of Cardiovascular Medicine, and Professor of Cardiology, Mayo ClinicSanjiv J. Shah, M.D., Director of Research, Bluhm Cardiovascular Institute and Director, HFpEF Program, Northwestern University Feinberg School of Medicine Tenax is advancing TNX-103 in patients with PH-HFpEF in two registrational Phase 3 studies, LEVEL and LEVEL-2. Enrollment is ongoing in the North American LEVEL study and LEVEL-2, a global study of TNX-103, remains on track to initiate in 2025. To participate in the conference call, please dial one of the following numbers and ask to join the Tenax Therapeutics call: +1-877-317-6789 for callers in the United States+1-412-317-6789 for international callers The live and archived webcast of the call will be accessible from the Company’s investor relations webpage. About Levosimendan (TNX-101, TNX-102, TNX-103) Levosimendan is a novel, first-in-class K-ATP channel activator/calcium sensitizer currently being evaluated to treat pulmonary hypertension (PH) associated with heart failure with preserved ejection fraction (PH-HFpEF). Levosimendan was first developed for intravenous use in hospitalized patients with acutely decompensated heart failure, and it has received market authorization in 60 countries in this indication, although it is not available in the United States or Canada. Tenax’s Phase 2 HELP study, including its open-label extension stage, demonstrated the potential of IV (TNX-101) and oral (TNX-103) levosimendan to bring durable improvements in exercise capacity and quality of life, as well as other clinical assessments, in patients with PH-HFpEF. TNX-103 (oral levosimendan) is currently being evaluated in LEVEL, a Phase 3, double-blind, randomized, placebo-controlled clinical trial in patients with PH-HFpEF. About Tenax Therapeutics Tenax Therapeutics, Inc. is a Phase 3, development-stage pharmaceutical company using clinical insights to develop novel cardiopulmonary therapies. The Company owns global rights to develop and commercialize levosimendan, which it is developing for the treatment of PH-HFpEF, the most prevalent form of pulmonary hypertension globally, for which no product has been approved to date. For more information, visit tenaxthera.com. Tenax Therapeutics’ common stock is listed on The Nasdaq Stock Market LLC under the symbol “TENX”. Contact: Investor and Media: Argot Partnerstenax@argotpartners.com

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SIS Medical AG Welcomes the Results of the VICTORY Trial Demonstrating Non-inferiority of OPN NC to Intravascular Lithotrispy (IVL) for Lesion Preparation and Stent Expansion in Severely Calcified Lesions

Coronary/Structural Heart by 0 comments

FRAUENFELD, Switzerland & SAN FRANCISCO–(BUSINESS WIRE)–SIS Medical AG, a Swiss manufacturer of the Super-High-Pressure PTCA balloon catheter (OPN NC), is pleased to announce that the results of the investigator-initiated VICTORY trial were presented during the late-breaking clinical session at TCT 2025 by the Cardiovascular Research Foundation (CRF). The randomized, multi-center […]

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