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

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.”