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BOULDER, Colo., Nov. 10, 2025 /PRNewswire/ — Edgewise Therapeutics, Inc., (Nasdaq: EWTX), a leading muscle disease biopharmaceutical company developing novel therapeutics for muscular dystrophies and serious cardiac conditions, today announced the appointment of Michael Nofi, as Chief…
Three Late Breaking Science Presentations from MAPLE-HCM Provide Additional Data Including Responder Analyses, Patient Reported Outcomes, and Cardiac Biomarkers SOUTH SAN FRANCISCO, Calif., Nov. 10, 2025 (GLOBE NEWSWIRE) — Cytokinetics, Incorporated (Nasdaq: CYTK) today announced that additional data from MAPLE-HCM (Metoprolol vs Aficamten in Patients with LVOT Obstruction on Exercise Capacity in HCM) were presented in three Late Breaking Science sessions at the Hypertrophic Cardiomyopathy Medical Society Scientific Sessions and the American Heart Association Scientific Sessions 2025 in New Orleans, LA. Two of the presentations were simultaneously published in the Journal of the American College of Cardiology.1,2 “These additional analyses from MAPLE-HCM expand on the primary finding that aficamten is superior to metoprolol on exercise capacity, with new insights into the overall treatment effect of aficamten as well as its effect on symptoms and biomarkers in comparison to metoprolol,” said Fady I. Malik, M.D., Ph.D., Cytokinetics’ Executive Vice President of Research & Development. “What’s notable is patients treated with aficamten achieved a significantly greater number of clinical response categories compared with metoprolol, and that nearly 40% achieved significant improvements in patient reported symptoms.” Responder Analysis Shows Significantly More Patients on Aficamten Achieved Positive or Complete Response Compared to Metoprolol Andrew Wang, M.D., Cardiologist and Professor of Medicine, Duke University School of Medicine presented a pre-specified responder analysis from MAPLE-HCM evaluating five clinically relevant measures of disease burden: complete hemodynamic response, symptom improvement, cardiac biomarker response, enhanced exercise capacity and favorable cardiac remodeling. These results were also simultaneously published in the Journal of the American College of Cardiology.1 After 24 weeks of treatment, aficamten was associated with greater improvements than metoprolol in all outcome measures (all p
GOTHENBURG, Sweden, Nov. 10, 2025 /PRNewswire/ — Cereno Scientific (Nasdaq First North: CRNO B), an innovative biotech pioneering treatments to enhance and extend life for people with rare cardiovascular and pulmonary diseases, today announced the submission of the clinical trial…
Multicenter outcomes FISH&CHIPS study of nearly 8,000 patients confirms total plaque volume as a powerful independent predictor of long-term cardiovascular events
Heartflow Plaque Staging Personalizes Individual Cardiac Risk
*Heartflow Plaque Analysis is an FDA-cleared device. Heartflow Plaque Staging is an investigational only framework and its safety and effectiveness have not been reviewed by the FDA.
Overall Considerations
3. Tzimas, et al. JACC. 2023. https://doi.org/10.1016/j.jcmg.2023.05.011
NEW ORLEANS, Nov. 09, 2025 (GLOBE NEWSWIRE) — Heartflow, Inc. (Heartflow) (Nasdaq: HTFL), the leader in AI technology for coronary artery disease (CAD), today announced late-breaking data from the FISH&CHIPS Study presented at the American Heart Association (AHA) Scientific Sessions 2025. The new data add to the robust and growing body of evidence supporting AI-powered Heartflow Plaque Analysis with Heartflow Plaque Staging* — the most clinically validated framework for actionable CAD care. The retrospective analysis, which evaluated nearly 8,000 symptomatic patients from a cohort of the FISH&CHIPS Study, represents the largest validation to date of the Heartflow Plaque Staging framework based on total plaque volume (TPV) measurement.1 Key findings include: Patients in the highest TPV stage experienced more than a 5x greater risk of major cardiovascular events compared with patients in the lowest stage (hazard ratio 5.10, p-value < 0.0001).Higher plaque volume stages were independently associated with significantly increased rates of cardiovascular death and myocardial infarction over a median 3.3 years of follow-up.Associations remained significant after adjustment for coronary stenosis, FFRCT values and cardiovascular risk factors. “This study provides strong validation of TPV-based staging measured with Heartflow Plaque Analysis as a predictor of future heart attacks or cardiovascular death,” said Timothy Fairbairn, Ph.D., principal investigator for the FISH&CHIPS study, Liverpool Heart and Chest Hospital, and Associate Professor at the University of Liverpool, UK. “The ability to accurately measure plaque will enable cardiologists to better predict which patients are most at risk above the traditional risk factors, and thus personalize treatment, in order to prevent heart attacks or death in the future.” The findings build on results from the DECIDE Registry presented at the Society of Cardiovascular Computed Tomography (SCCT) 2025 Annual Scientific Meeting in July. DECIDE data showed that Heartflow Plaque Analysis with Plaque Staging led to changes in medical management for more than half of patients, resulting in an average reduction in LDL cholesterol of 18.7 mg/dL at 90 days. These results indicate management changes guided by Heartflow Plaque Staging result in an expected 15% decrease in risk of a cardiac event.2,3,4 “We are demonstrating how AI-powered Heartflow Plaque Analysis with Heartflow Plaque Staging can fundamentally change the way we manage CAD,” said Campbell Rogers, M.D., F.A.C.C., Chief Medical Officer at Heartflow. “These latest findings show that by embedding plaque insights directly into the diagnostic pathway, we can help physicians make more confident decisions to guide personalized and precise treatment for their patients.” *Heartflow Plaque Analysis is an FDA-cleared device. Heartflow Plaque Staging is an investigational-only framework, and its safety and effectiveness have not been reviewed by the FDA. About Heartflow’s Technology and ResearchHeartflow’s technology is redefining precision cardiovascular care through clinically-proven AI and the world’s largest coronary imaging dataset. Heartflow has been adopted by more than 1,400 institutions globally and continues to strengthen its commercial presence to make this cutting-edge solution more widely available to an increasingly diverse patient population. Backed by ACC/AHA guidelines and supported by more than 600 peer-reviewed publications, Heartflow has redefined how clinicians manage care for nearly 500,000 patients worldwide. Key benefits include: Proprietary data pipeline: Built from more than 110 million annotated CTA images, Heartflow’s data foundation powers advanced AI models that deliver highly accurate, reproducible insights across diverse patient populations.Extensive clinical and real-world validation: Heartflow’s AI-driven solutions have been validated through clinical evidence in over 100 studies assessing over 365,000 patients. Proven in real-world practice with reproducibility and accuracy, Heartflow’s coronary CTA image acceptance rates exceed 96%.Seamless clinical integration via upgraded workflow: Heartflow delivers final quality-reviewed analyses instantly upon order, enabling clinicians to move from diagnosis to decision without delay.Quality system, global security and patient-data integrity compliance: Heartflow meets or exceeds leading international standards, including HITRUST, SOC 2 Type 2, GDPR, HIPAA, CCPA, ISO 13485, and ISO 27001. About Heartflow, Inc.Heartflow is transforming coronary artery disease from the world’s leading cause of death into a condition that can be detected early, diagnosed accurately, and managed for life. The Heartflow One platform uses AI to turn coronary CTA images into personalized 3D models of the heart, providing clinically meaningful, actionable insights into plaque location, volume, and composition and its effect on blood flow — all without invasive procedures. Discover how we’re shaping the future of cardiovascular care at heartflow.com. Media ContactElliot Levyelevy@heartflow.com Investor ContactNick Laudiconlaudico@heartflow.com Photos accompanying this announcement are available at https://www.globenewswire.com/NewsRoom/AttachmentNg/4702aa38-c48c-4291-91aa-937325c8206f https://www.globenewswire.com/NewsRoom/AttachmentNg/a2a0e458-a265-4790-90b4-33f7403b0b2e 1 Fairbairn et al. AHA 2025.2 Rinehart SJ, et al. DECIDE Primary Outcomes. J Cardiovasc Comput Tomogr. 2025; 19(4):S78-79. doi.org/10.1016/j.jcct.2025.05.1853 Collins et al. Lancet 2016. DOI: 10.1016/S0140-6736(16)31357-54 Fairbairn et al. HEART. 2025. doi:10.1136/heartjnl-2025-BSCI.5
BOSTON, Nov. 09, 2025 (GLOBE NEWSWIRE) — Medera Inc. (“Medera”), a clinical-stage biopharmaceutical company focused on targeting cardiovascular diseases by developing next-generation therapeutics, today announced that positive interim data from its ongoing MUSIC-HFpEF Phase 1/2a clinical trial was presented at the American Heart Association (AHA) Scientific Sessions 2025 taking place November 7-10, 2025, in New Orleans, Louisiana. The late-breaking presentation, titled “First-in-Human Gene Therapy Trial for Patients with Heart Failure with Preserved Ejection Fraction (HFpEF): MUSIC-HFpEF – Modulation of SERCA2a of Intra-myocytic Calcium Trafficking in Heart Failure With Preserved Ejection Fraction,” was delivered by Marat Fudim, MD, MHS, Advanced Heart Failure Specialist and Associate Professor at Duke University Medical Center, during the Featured Science session on Biological and Pragmatic Interventions in Heart Failure: From Present to Future on Sunday, November 9, 2025, at 8:00 AM CST. The MUSIC-HFpEF trial is investigating SRD-002, a one-time gene therapy treatment for heart failure with preserved ejection fraction (HFpEF) delivered through a proprietary minimally invasive intracoronary infusion methodology. SRD-002 utilizes an adeno-associated type 1 virus vector carrying the cardiac isoform of the sarcoplasmic reticulum calcium ATPase pump (SERCA2a) to directly target the molecular pathways underlying the core pathology of HFpEF by enhancing myocardial relaxation and reducing stiffness. The presentation highlighted data from the ongoing trial, which, as of the interim data cutoff date of October 15, 2025, has treated five patients in Cohort A with a low dose of 3E13 viral genomes (vg) who completed the twelve-month follow-up and five patients in Cohort B with a high dose of 4.5E13 vg. SRD-002 demonstrated a favorable safety profile and early clinical benefits. With follow-up ranging from 6 to 12 months, no gene therapy-related serious adverse events have been reported. Patients in the low-dose cohort have shown improvements in New York Heart Association (NYHA) heart failure classification and Kansas City Cardiomyopathy Questionnaire at both 6 and 12 months, with clinically meaningful stabilizations and improvements in pulmonary capillary wedge pressure (PCWP) at rest and peak exercise. The data support progression to the Phase 2 portion of the ongoing trial to test durable disease-modification in HFpEF by SRD-002. Patients in Cohort A and B received higher optimized doses of 3.0E13 vg and 4.5E13 vg, respectively—substantially higher than in prior studies, yet still significantly lower than systemic intravenous (IV) infusion. The dosing strategy was rationally designed and optimized using Medera’s proprietary human-based mini-Heart™ technology platform, including its HFpEF disease model co-developed with AstraZeneca, which has contributed to a US Food and Drug Administration (FDA) Investigational New Drug (IND) clearance and Fast Track Designation. “The data presented today at the AHA Scientific Sessions demonstrate continued safety and clinical benefits with SRD-002,” said Marat Fudim, MD, MHS. “These results reinforce the potential of gene therapy to address the fundamental pathophysiological mechanisms in HFpEF and provide hope for patients with this challenging condition.” “We are pleased to announce the completion of enrollment for this innovative clinical trial and are encouraged by the outcomes observed in the low dose cohort,” said Ronald Li, PhD, CEO and Founder of Medera. “We remain dedicated to advancing this investigational gene therapy, which targets a condition characterized by significant unmet medical needs.” The AHA Scientific Sessions is the premier global event in cardiovascular health and science offering unmatched access to groundbreaking research, dynamic learning, and career-defining connections. For additional information about the MUSIC-HFpEF trial, visit ClinicalTrials.gov using the study identifier NCT06061549. About Heart Failure with Preserved Ejection Fraction (HFpEF) Heart failure (HF) is a global pandemic with an estimated 64.3 million cases worldwide and a rising prevalence trend. Accounting for 50% or more of the overall HF population, HFpEF is an age-related condition that has become increasingly prevalent in recent years. This surge is partly due to better awareness and identification of the condition and partly due to lifestyle changes affecting cardiac myocytes. Individuals affected by HFpEF experience similar morbidity and mortality to patients with HF with reduced ejection fraction (HFrEF). Despite the growing epidemic of this emerging syndrome, HFpEF-focused interventional trials have had little success, except for the use of sacubitril-valsartan (Entresto™) and the sodium glucose transporter-2 (SGLT-2) inhibitor empagliflozin (Jardiance™) for reducing cardiovascular mortality and heart failure hospitalization. However, these agents are not disease-modifying, highlighting the critical need for therapeutic interventions targeting the physiological mechanisms involved in HFpEF. About Medera Inc. Medera is a clinical-stage biopharmaceutical company focused on targeting difficult-to-treat and currently incurable diseases by developing a range of next-generation therapeutics. Medera operates via its two preclinical and clinical business units, Novoheart and Sardocor, respectively. Novoheart capitalizes on the world’s first and award-winning “mini-Heart” Technology for revolutionary disease modelling and drug discovery, uniquely enabling the modelling of human-specific diseases and discovery of therapeutic candidates free from species-specific differences in accordance to the FDA Modernization Act 2.0. Novoheart’s versatile technology platform provides a range of state-of-the-art automation hardware and software as well as screening services, for human-specific disease modelling, therapeutic target discovery and validation, drug toxicity and efficacy screening, and dosage optimization carried out in the context of healthy and/or diseased human heart chambers and tissues. Global pharmaceutical and academic leaders are using Novoheart’s technology platform for their drug discovery and development purposes. The Novoheart platform has facilitated and accelerated the development of Sardocor’s lead therapeutic candidates that are currently in clinical trials. Sardocor is dedicated to the clinical development of novel next-generation therapies for Medera. Leveraging Novoheart’s human-based drug discovery and validation platforms, Sardocor aims to expedite drug development and regulatory timelines for its gene and cell therapy pipeline. Sardocor has received Investigational New Drug (IND) clearances from the FDA for three ongoing AAV-based cardiac gene therapy clinical trials targeting Heart Failure with Reduced Ejection Fraction (HFrEF), Heart Failure with Preserved Ejection Fraction (HFpEF) with the Fast Track Designation, and Duchenne Muscular Dystrophy-associated Cardiomyopathy (DMD-CM) with the Orphan Drug Designation. Additionally, Sardocor’s pipeline includes four preclinical gene therapy and three preclinical small molecule candidates targeting various cardiac, pulmonary, and vascular diseases. For more information, please visit www.medera.bio. Contacts Ally StubinPublic RelationsICR HealthcareAlly.stubin@icrhealthcare.com 646.667.1861 Stephanie CarringtonInvestor RelationsICR HealthcareStephanie.carrington@icrhealthcare.com 646.277.1282
Oral presentation highlights sotagliflozin’s unique benefits to HFpEF patients in significantly improving cardiac and physical performance, and quality of life Oral presentation highlights sotagliflozin’s unique benefits to HFpEF patients in significantly improving cardiac and physical performance, and quality of life
Data support NEK7 as a potential novel and differentiated therapeutic approach to modulate the NLRP3 inflammasome in multiple cardiovascular and cardiometabolic diseases, including pericarditis and atherosclerosis Initial data from a Phase 1 study of MRT-8102 in healthy volunteers and elevated CVD-risk subjects on track for first half of 2026 Poster presentation on November 8 at 10:30 a.m. CST BOSTON, Nov. 08, 2025 (GLOBE NEWSWIRE) — Monte Rosa Therapeutics, Inc. (Nasdaq: GLUE), a clinical-stage biotechnology company developing novel molecular glue degrader (MGD)-based medicines, today announced the company will present preclinical data on the potential of MRT-8102, a first-in-class, NEK7-directed MGD for inflammatory diseases driven by the NLRP3 inflammasome, at the American Heart Association’s Scientific Sessions 2025, held November 7-10 in New Orleans, LA. “These promising findings reinforce our belief in the highly differentiated profile of MRT-8102, the only clinical-stage degrader targeting NEK7, as a potential treatment for cardiovascular and cardiometabolic diseases such as pericarditis, atherosclerosis, and others,” said Sharon Townson, Ph.D., Chief Scientific Officer of Monte Rosa Therapeutics. “By modulating the NLRP3/IL-1/IL-6 pathway upstream of other approaches, MRT-8102 potently inhibited pyroptotic cell death and inhibited the release of multiple inflammatory cytokines. Furthermore, MRT-8102 has the potential to block cholesterol crystal-induced cardiovascular inflammation characterized by pyroptosis and cytokine release that leads to atherosclerotic plaque pathogenesis. We are encouraged by the growing interest in targeting the NLRP3/NEK7 inflammasome to treat cardiovascular disease, and we believe we have a unique approach to achieve this. We continue to enroll our Phase 1 study of MRT-8102 and look forward to presenting initial data in healthy volunteers and elevated CVD-risk subjects in the first half of 2026.” The poster, entitled, “Selective Degradation of NIMA-related kinase 7 (NEK7) via a Molecular Glue Degrader Inhibits IL-1 Downstream of NLRP3 Inflammasome Activation: A Novel Therapeutic Approach for Cardiovascular Inflammation” (Poster Number #Sa4063), will be displayed on Saturday, November 8, 2025 from 10:30 to 11:30 a.m. CST in a poster session entitled, “Novel Cellular Stress Sensors in Cardiovascular Pathology: Metabolic, Mechanical, and Immune Interactions.” The poster will be presented by Daric Wible, Ph.D., Senior Scientist II, Biology, Monte Rosa Therapeutics. Summary of key findings: MRT-8102 is a selective, potent, and durable NEK7 degrader. Activation of the NLRP3 inflammasome critically depends on NEK7.Administration of MRT-8102 led to inhibition of NLRP3 inflammasome in vitro and in vivo and subsequently inhibited production of multiple inflammatory cytokines.In in vitro assays, MRT-8102 inhibited pyroptotic membrane permeabilization in stimulated human monocyte-derived macrophages (hMDM), unlike anti-IL-1 and anti-IL-6 therapies. Additionally, only MRT-8102 inhibited release of multiple cytokines from stimulated hMDM.In vitro, NEK7 degradation inhibited cholesterol crystal-induced NLRP3 inflammasome activation, a key driver of atherosclerotic plaque pathogenesis, more potently than selnoflast, an NLRP3 inhibitor currently in development.In a mouse peritonitis model, MRT-8102 led to potent inhibition of the cytokines IL-1β, IL-1α, IL-6, and TNF in peritoneal lavage.MRT-8102 demonstrated near-complete suppression of IL-1β and Caspase-1 activity in ex vivo-stimulated whole blood from orally dosed cynomolgus monkeys.Degrading NEK7 to modulate the inflammasome represents a novel and differentiated approach with potential therapeutic application in multiple cardiovascular and cardiometabolic diseases, including pericarditis and atherosclerosis. About MRT-8102MRT-8102 is a potent, highly selective, and orally bioavailable investigational molecular glue degrader (MGD) that targets NEK7 for the treatment of inflammatory diseases linked to NLRP3, IL-1β, and IL-6 dysregulation. NEK7 has been shown to be required for NLRP3 inflammasome assembly, activation and IL-1β release both in vitro and in vivo. Aberrant NLRP3 inflammasome activation and the subsequent release of active IL-1β and interleukin-18 (IL-18) has been implicated in multiple inflammatory disorders, including cardiovascular disease, gout, osteoarthritis, neurologic disorders including Parkinson’s disease and Alzheimer’s disease, and metabolic disorders. In a non-human primate model, MRT-8102 was shown to potently, selectively, and durably degrade NEK7, and resulted in near-complete reductions of IL-1β and caspase-1 following ex vivo stimulation of whole blood. MRT-8102 has demonstrated a considerable safety margin ( >200-fold exposure margin over projected human efficacious dose) in GLP toxicology studies. MRT-8102 is currently being investigated in a Phase 1 study (clinicaltrials.gov identifier NCT07119125) in healthy participants and participants at elevated cardiovascular disease risk. About Monte RosaMonte Rosa Therapeutics is a clinical-stage biotechnology company developing highly selective molecular glue degrader (MGD) medicines for patients living with serious diseases. MGDs are small molecule protein degraders that have the potential to treat many diseases that other modalities, including other degraders, cannot. Monte Rosa’s QuEEN™ (Quantitative and Engineered Elimination of Neosubstrates) discovery engine combines AI-guided chemistry, diverse chemical libraries, structural biology, and proteomics to rationally design MGDs with unprecedented selectivity. Monte Rosa has developed the industry’s leading pipeline of first-in-class and only-in-class MGDs, spanning autoimmune and inflammatory diseases, oncology, and beyond, with three programs in the clinic. Monte Rosa has ongoing collaborations with leading pharmaceutical companies in the areas of immunology, oncology and neurology. For more information, visit www.monterosatx.com. Forward-Looking Statements This communication includes express and implied “forward-looking statements,” including forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. Forward-looking statements include all statements that are not historical facts and in some cases, can be identified by terms such as “may,” “might,” “will,” “could,” “would,” “should,” “expect,” “intend,” “plan,” “objective,” “anticipate,” “believe,” “estimate,” “predict,” “potential,” “continue,” “ongoing,” or the negative of these terms, or other comparable terminology intended to identify statements about the future. Forward-looking statements contained herein include, but are not limited to, statements around the potential of the Company’s NEK7-directed MGD, referred to as MRT-8102, to address inflammatory diseases driven by the NLRP3 inflammasome, including cardiovascular disease and cardiometabolic disease, including pericarditis and atherosclerosis, the Company’s belief that MRT-8102 could offer a differentiated approach to treating multiple inflammatory diseases based on the potency, selectivity, and durable pharmacodynamics seen in its preclinical studies, the Company’s belief in the potential for MRT-8102 to treat cardiovascular disease by blocking cholesterol crystal-induced cardiovascular inflammation characterized by pyroptosis and cytokine release that leads to atherosclerotic plaque pathogenesis, our expectations for the continuing advancement of our Phase 1 study and the timing thereof, including updates related to status, safety data, pharmacokinetics, NEK7 protein degradation, and key downstream pharmacodynamic markers and the timing of any clinical data read-outs, including the potential readout of initial data in healthy volunteers and elevated CVD-risk subjects expected in the first half of 2026, as well as our expectations of success for our programs, including for MRT-8102, among others. By their nature, these statements are subject to numerous risks and uncertainties, including those risks and uncertainties set forth in our most recent Annual Report on Form 10-K for the year ended December 31, 2024, filed with the U.S. Securities and Exchange Commission on March 20, 2025, and any subsequent filings, that could cause actual results, performance or achievement to differ materially and adversely from those anticipated or implied in the statements. You should not rely upon forward-looking statements as predictions of future events. Although our management believes that the expectations reflected in our statements are reasonable, we cannot guarantee that the future results, performance, or events and circumstances described in the forward-looking statements will be achieved or occur. Recipients are cautioned not to place undue reliance on these forward-looking statements, which speak only as of the date such statements are made and should not be construed as statements of fact. We undertake no obligation to publicly update any forward-looking statements, whether as a result of new information, any future presentations, or otherwise, except as required by applicable law. Certain information contained in these materials and any statements made orally during any presentation of these materials that relate to the materials or are based on studies, publications, surveys and other data obtained from third-party sources and our own internal estimates and research. While we believe these third-party studies, publications, surveys and other data to be reliable as of the date of these materials, we have not independently verified, and make no representations as to the adequacy, fairness, accuracy or completeness of, any information obtained from third-party sources. In addition, no independent source has evaluated the reasonableness or accuracy of our internal estimates or research and no reliance should be made on any information or statements made in these materials relating to or based on such internal estimates and research. Investors Andrew Funderburkir@monterosatx.com Media Cory Tromblee, Scient PRmedia@monterosatx.com
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
-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
The investigational device evaluated in the trial, previously known as the GORE® VIAFORT Vascular Stent, will now be referred to as the GORE® VIABAHN® FORTEGRA Venous Stent. CAUTION: Investigational device. Limited by United States law to investigational use. LAS VEGAS and FLAGSTAFF, Ariz….
