TNYA News & Events

Reports Q1 revenue $225,000, consensus $7.5M. "We are entering a catalyst-rich period for Tenaya, with multiple clinical milestones expected across our lead gene therapy programs throughout 2026. Building on the encouraging initial readouts we reported in 2025, we believe the additional data expected this year from both TN-201 and TN-401 may support alignment on registrational pathways for these novel gene therapies," said Faraz Ali, Chief Executive Officer of Tenaya.

Tenaya Therapeutics' treatment of Duchenne muscular dystrophy was granted FDA orphan designation status, according to a post to the agency's website.

"As we enter 2026, we are energized by the momentum and clinical advances achieved over the past year," said Faraz Ali, CEO of Tenaya. "The encouraging data presented in 2025 from both of our lead gene therapy programs underscore the transformative potential of our science. In the first half of 2026, we expect to share additional updates, including longer-term follow-up data from the MyPEAK-1 clinical trial of TN-201 for MYBPC3-associated HCM, as well as one-year Cohort 1 data and early Cohort 2 data from the RIDGE-1 clinical trial of TN-401 for PKP2-associated ARVC. Over the course of the year, we also plan to pursue regulatory agency alignment on pivotal trial plans for both programs, a critical step toward accelerating the delivery of safe and effective gene therapies to patients with serious cardiac conditions."

Tenaya Therapeutics presented preclinical data evaluating TN-301, the company's highly selective HDAC6 inhibitor, at the Muscular Dystrophy Association's Clinical & Scientific Conference 2026. In in vitro and in vivo models of Duchenne muscular dystrophy, TN-301 improved muscle performance and corrected key drivers of DMD cardiomyopathy. Key findings presented at MDA 2026 include: TN-301 treatment at doses as low as 3 mg/kg improved grip strength to wild-type levels within five weeks, whereas mdx mice treated with givinostat failed to reach wild-type performance. TN-301-mediated functional improvements were accompanied by reductions in circulating creatine kinase activity and favorable changes in gene expression, indicating reduced muscle cell injury. In cardiomyocytes derived from human DMD induced pluripotent stem cells, TN-301 corrected calcium handling abnormalities and mitochondrial dysfunction, while givinostat exacerbated these established drivers of DMD cardiomyopathy.