Medera Presents Late-Breaking Clinical Trial Data at ESC Congress 2026 Demonstrating Durable Improvement in HFpEF Cardiac Filling Pressures Following SRD-002 Gene Therapy

80% (8/10) met the prespecified threshold for normalization of cardiac filling pressures at 12 months, and mean peak exercise pulmonary capillary wedge pressure (PCWP) was reduced by approximately 30% at 12 months following a single intracoronary dose of SRD-002

Favorable safety profile maintained across all 10 treated patients, with no treatment-related serious adverse events

BOSTON, Aug. 31, 2026 (GLOBE NEWSWIRE) -- Medera Inc. ("Medera"), a clinical-stage biopharmaceutical company pioneering next-generation therapeutics for cardiovascular disease, today announced 12-month data from its ongoing MUSIC-HFpEF Phase 1/2a clinical trial were presented as a Late-Breaking Clinical Trial (LBCT) at the European Society of Cardiology (ESC) Congress 2026 taking place August 28-31 in Munich, Germany. The selection marks the fourth LBCT recognition awarded to the MUSIC-HFpEF program at major international cardiology conferences, spanning successive stages of the trial’s development.

The presentation, titled “Outcomes of Intracoronary AAV1/SERCA2a Gene Therapy in Patients With Heart Failure With Preserved Ejection Fraction: 12-Month Results From the MUSIC-HFpEF Phase 1b Trial” was delivered by Marat Fudim, MD, MHS, Medical Director for the Heart Failure Research Unit and Heart Failure Remote Monitoring at Duke University Medical Center, during the session “Transforming the Heart: Novel Therapies for Myocardial Disease and Heart Failure” on Monday, August 31, 2026, from 11:15 a.m. to 12:15 p.m. CEST.

The open-label, dose-escalation MUSIC-HFpEF trial is evaluating a single intracoronary infusion of SRD-002, a next-generation adeno-associated virus serotype 1 (AAV1).SERCA2a — sarcoplasmic reticulum Ca²⁺-ATPase 2a, the cardiac calcium pump that is down-regulated in heart failure and whose restoration improves calcium reuptake and diastolic relaxation—gene therapy, in adults with symptomatic HFpEF. Ten patients received either low-dose SRD-002 (3x10¹³ vg; n=5) or high-dose SRD-002 (4.5x10¹³ vg; n=5).

Across patients from both cohorts, 80% (8/10) met the prespecified threshold for normalization of cardiac filling pressures at 12 months, and reduction in mean peak exercise pulmonary capillary wedge pressure (PCWP) was approximately 30% at 12 months, representing one of the largest sustained reductions in exercise filling pressure reported to date in an interventional HFpEF trial. The improvements were durable and showed a dose-response, with reductions generally greater from 6 to 12 months and from low to high dose.

Supporting symptomatic, quality-of-life, and functional findings were consistent with the hemodynamic results: 83% (5/6) of patients with baseline New York Heart Association (NYHA) class III symptoms improved to class II, mean improvement in Kansas City Cardiomyopathy Questionnaire (KCCQ) score was +17.8 points, and functional capacity stabilized or improved in all patients.

"These 12-month results are among the first to show sustained normalization of invasive exercise hemodynamics following a gene therapy in HFpEF," said Marat Fudim, MD, MHS, Medical Director for the Heart Failure Research Unit and Heart Failure Remote Monitoring at Duke University Medical Center. “The magnitude and durability of the filling pressure reductions we observed, paired with meaningful improvements in symptoms and quality of life, support impaired calcium handling as a disease-defining mechanism in HFpEF and reinforce the case for advancing this approach into randomized evaluation.”

SRD-002 continued to demonstrate a favorable safety profile across all 10 treated patients, with no treatment-related serious adverse events, dose-limiting toxicities, treatment discontinuations, or Grade 3 or higher liver enzyme elevations reported. Intracoronary delivery enabled approximately 100- to 300-fold lower vector exposure compared with systemic intravenous AAV approaches while achieving targeted myocardial delivery without routine immunosuppression.

"These data reinforce what we’ve seen across our HFpEF program: a favorable safety profile paired with durable and clinically meaningful improvement in the physiological abnormalities that define the disease. Particularly encouraging is that the improvement in cardiac filling pressures continued to evolve following a single administration of SRD-002," said Ronald Li, PhD, Co-Founder and CEO of Medera. “We believe these findings support the potential for SRD-002 to become a one-time, disease-modifying therapy for HFpEF, and we look forward to advancing the program into randomized development.”

These Phase 1/2a results support advancement to a randomized Phase 2b trial to further evaluate the efficacy and safety of SRD-002 as a potential one-time therapy for patients with HFpEF.

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 affects more than 64 million people worldwide, with HFpEF accounting for approximately half of all heart failure cases. Patients with HFpEF experience morbidity and mortality comparable to those with heart failure with reduced ejection fraction (HFrEF). Despite its growing prevalence, currently approved therapies primarily improve symptoms and reduce cardiovascular risk rather than directly targeting the underlying myocardial abnormalities responsible for the disease. Consequently, HFpEF remains one of the largest unmet needs in cardiovascular medicine and an area of active therapeutic development.

About Medera Inc.

Medera is a clinical-stage biopharmaceutical company focused on targeting difficult-to-treat and currently incurable diseases by developing next-generation therapeutics. Medera operates via two business units: Sardocor, its clinical development arm advancing a pipeline of cardiac gene therapy trials (HFpEF, HFrEF, DMD-CM), and Novoheart, its preclinical subsidiary pioneering the world’s first and award-winning “mini-Heart” technology for human-based disease modelling, drug discovery, and toxicity testing. Novoheart’s human cardiac disease models have supported the preclinical development of Medera programs that have subsequently received FDA IND clearance, Fast Track designation for HFpEF and Orphan Drug Designation for DMD-CM, and the Company is advancing a broader pipeline of gene therapy, cell therapy, and small molecule candidates. For more information, visit www.medera.bio.

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