Hengrui Pharma and Braveheart Bio have announced positive results from a multi-centre, randomised, double-blind, placebo-controlled Phase 2 clinical study evaluating HRS-1893, also known as BHB-1893, for the treatment of non-obstructive hypertrophic cardiomyopathy (nHCM). The investigational next-generation cardiac myosin inhibitor demonstrated improvements across several clinical and structural measures, including biomarkers of cardiac stress, heart structure, diastolic function, patient symptoms and exercise capacity.

The study evaluated 84 adult patients with symptomatic nHCM and assessed the safety, tolerability and efficacy of multiple oral doses of the therapy. Patients enrolled in the trial had preserved Left Ventricular Ejection Fraction (LVEF), moderate-to-severe symptoms and elevated cardiac stress biomarkers. The trial’s primary endpoint focused on safety and tolerability, while secondary endpoints included improvements in biomarkers, cardiac imaging parameters, symptom scores and exercise performance.

According to the companies, patients receiving HRS/BHB-1893 reported notable improvements in quality of life and exercise tolerance. The high-dose treatment group recorded a placebo-adjusted improvement of 5.5 points in the Kansas City Cardiomyopathy Questionnaire Clinical Summary Score (KCCQ-CSS), with more than half of patients achieving clinically meaningful symptom improvement. Patients also demonstrated improved peak oxygen consumption, indicating enhanced exercise capacity.

The therapy additionally showed encouraging results in reversing structural abnormalities associated with nHCM. Echocardiographic assessments revealed improvements in myocardial relaxation velocity, reductions in left atrial volume index and decreases in left ventricular mass and wall thickness, indicating structural reverse remodeling of the heart. Researchers noted that these findings suggest the therapy may directly target the underlying disease process rather than only relieving symptoms.

HRS/BHB-1893 also produced rapid and sustained reductions in key cardiac biomarkers. Patients treated with the therapy experienced reductions of approximately 68–69 percent in NT-proBNP, a marker of cardiac wall stress, and 55–60 percent in cardiac troponin I, a marker of myocardial injury, compared with placebo. Both outcomes achieved high statistical significance.

The investigational therapy was generally well tolerated during the study. Most treatment-emergent adverse events were mild or moderate, with no severe treatment-related adverse events or discontinuations reported. A small number of patients experienced temporary reductions in LVEF, which resolved following dose adjustments. Serious adverse events reported during the trial were assessed as unrelated to the treatment.

Anjali Owens, Associate Professor of Medicine at the Hospital of the University of Pennsylvania and member of Braveheart Bio’s Clinical Advisory Board, said the absence of left ventricular outflow tract obstruction in nHCM allows researchers to better assess whether therapies are directly modifying disease biology. She noted that the observed structural reverse remodeling could represent an important signal of disease-modifying potential.

Sheng Qi, Executive Director and Head of Cardiovascular at Hengrui Pharma, said the findings demonstrate the possibility of directly targeting the underlying mechanisms of non-obstructive hypertrophic cardiomyopathy, an area with limited treatment options. Travis Murdoch, Chief Executive Officer and President of Braveheart Bio, added that the company plans to further evaluate the therapy in a global registrational study.

The study findings were presented during a late-breaking featured clinical research session at Heart Failure 2026, the annual congress of the Heart Failure Association of the European Society of Cardiology.