Results with next-generation cardiac myosin inhibitor provide evidence of potential disease-modifying treatment in non-obstructive HCM

 

HRS/BHB-1893 treatment resulted in rapid and sustained reductions in key biomarkers, structural remodeling and meaningful improvements in symptoms

 

Safety and tolerability profile was favorable

 

Data highlighted in a late-breaking featured clinical research presentation at Heart Failure 2026, the annual congress of the Heart Failure Association of the European Society of Cardiology

 

SHANGHAI, China, and SAN FRANCISCO, May 11, 2026 — Hengrui Pharma (Hengrui) and Braveheart Bio today announced results from a multi-center, randomized, double-blind, placebo-controlled Phase 2 study evaluating HRS-1893 (also known as BHB-1893), an investigational next-generation cardiac myosin inhibitor (CMI), in patients with non-obstructive hypertrophic cardiomyopathy (nHCM). HRS/BHB-1893 treatment resulted in improvements across biomarkers of cardiac wall stress and tissue injury, echocardiographic (echo) measures of diastolic function and cardiac structure, patient-reported symptoms and exercise capacity, with a generally favorable tolerability profile.

 

“In obstructive HCM, it has been difficult to separate the direct biological effect of a therapeutic candidate from the mechanical consequence of relieving the gradient,” said Anjali Owens, MD, Associate Professor of Medicine at the Hospital of the University of Pennsylvania and member of Braveheart’s Clinical Advisory Board. “In non-obstructive HCM, where there is no LVOT gradient, that confounding variable does not exist. The structural reverse remodeling toward normal observed here is a compelling [early] signal that BHB/HRS-1893 may be modifying the underlying disease in nHCM, in addition to helping manage the condition.”

 

 

“Non-obstructive HCM has long represented one of the most difficult challenges in cardiovascular medicine, a disease with clear pathophysiology and significant patient burden, but limited treatment options,” said Sheng Qi, M.D., Executive Director and Head of Cardiovascular, Hengrui Pharma. “The breadth of improvement we have observed here across biomarkers, cardiac structure and patient-reported outcomes, in a population with no gradient to relieve, points to a mechanism that may act directly on the disease. We look forward to advancing this program and continuing our partnership with Braveheart to bring a meaningful treatment option to patients.”

 

 "These results give us real conviction that HRS/BHB-1893 could change the course of nHCM," said Travis Murdoch, M.D., Chief Executive Officer and President, Braveheart Bio. "The rapid and meaningful responses across diastolic function, cardiac structure, biomarkers, and clinical endpoints, in this placebo-controlled study, suggest that we may be engaging  the underlying pathophysiology in a unique and direct way.. We seek to prove that at scale in an upcoming global registrational study."

 

The multi-center, randomized, double-blind, placebo-controlled Phase 2 study (NCT06816251) enrolled 84 adults with symptomatic nHCM and left ventricular ejection fraction (LVEF) ≥60%, New York Heart Association (NYHA) Class II–III, maximal wall thickness of ≥15 mm (≥13 mm with family history of HCM), LVOT-G <30 mmHg,NT-proBNP > 300 pg/mL, and KCCQ-CSS ≥30 and ≤85. Patients were randomized 1:1:1 to placebo, low-dose HRS/BHB-1893 (20–40 mg twice daily) or high-dose HRS/BHB-1893 (20–40–60 mg twice daily) for 12 weeks. Dose titration was guided by LVEF assessed by transthoracic echocardiogram. A washout phase and 4-week safety follow-up allowed assessment of pharmacological reversibility. Key endpoints included biomarkers (NT-proBNP, a marker of diastolic wall stress, and cardiac troponin I, a marker of myocardial injury), patient-reported symptoms and exercise capacity (KCCQ-CSS, peak oxygen consumption [pVO₂]), and echocardiographic measures of diastolic function, cardiac structure and LVEF.

 

HRS/BHB-1893 treatment resulted in rapid and sustained improvement in clinically relevant cardiac biomarkers: NT-proBNP (68–69% reduction) and cardiac troponin I (55–60% reduction), with p values less than 0.0001 versus placebo for both.

 

HRS/BHB-1893 also produced improvements across important echocardiographic domains. Early myocardial relaxation velocity improved, with septal and lateral e' values returning toward normal range in the high-dose group. Left atrial volume index fell by 7.12 mL/m² versus essentially no change in placebo, consistent with normalization of left atrial pressure overload. Left ventricular mass index decreased by 17.4 g/m² in the high-dose group versus an increase of 3.2 g/m² in placebo, and left ventricular wall thickness decreased by 3.3 mm versus 0.1 mm in placebo, showing structural reverse remodeling of the left ventricle.

 

Patients treated with HRS/BHB-1893 reported improvements in symptoms and exercise capacity. The high-dose group showed a placebo-adjusted improvement of +5.5 points in KCCQ-CSS. 52% of high-dose patients achieved a ≥20-point improvement, the threshold for a large to very large improvement, compared to 21% in placebo. Among patients titrated to 60 mg twice daily, absolute pVO₂ change was +2.1 mL/kg/min, representing a placebo-adjusted gain of +0.9 mL/kg/min. 55% of high-dose patients achieved a ≥1.5 mL/kg/min increase from baseline.

 

HRS/BHB-1893 was generally well tolerated, with no new safety signals identified. All treatment-emergent adverse events were mild or moderate, with no severe adverse events and no adverse events leading to interruption or permanent discontinuation of HRS/BHB-1893. Serious adverse events, all assessed as unrelated to study drug, were reported in four patients, 2 in the low-dose group (cellulitis, otolithiasis), 1 in the high-dose group (atrial fibrillation), and 1 in the placebo group (atrial tachycardia). Four patients (7% of the treated population) underwent protocol-specified dose reduction for LVEF below 50% (nadir LVEF values of 46% to 49%); all returned to LVEF above 50% with dose reduction.

 

Results of the study were highlighted in a late-breaking featured clinical research presentation at Heart Failure 2026, the annual congress of the Heart Failure Association of the European Society of Cardiology.

 

About Hypertrophic Cardiomyopathy

 

HCM is among the most common rare diseases, affecting approximately 1 in 500 individuals in the United States. HCM can lead to heart failure, stroke or sudden cardiac death, including in young adults and athletes who may often live with the disease undetected.

 

In HCM, overactive myosin can cause excessive contraction of the heart, resulting in the heart muscle becoming abnormally thick, particularly in the left ventricle — the heart's main pumping chamber. This leads to symptoms like shortness of breath, chest pain, fatigue and fainting, which typically worsen with physical activity and can significantly limit patients' ability to exercise, work or perform routine tasks.

 

Approximately one-third of patients with HCM have non-obstructive hypertrophic cardiomyopathy (nHCM), where there is no obstruction but the muscle is thickened, limiting proper heart function. In nHCM, the absence of a left ventricular outflow tract (LVOT) gradient means there is no mechanical target to relieve, making drug development in this population particularly challenging and leaving patients with limited pharmacological treatment options.

 

About HRS-1893/BHB-1893

 

HRS-1893 (also known as BHB-1893) is an investigational selective, reversible, small-molecule cardiac myosin inhibitor engineered for rapid onset of action, minimal impact on left ventricular ejection fraction, and ease of use. By modulating cardiac contractility, HRS-1893 aims to address the underlying pathophysiology of HCM while maintaining cardiac output.

 

HRS-1893 has undergone extensive clinical development, including dose-ranging Phase 2 studies in both symptomatic oHCM and symptomatic nHCM, multiple clinical pharmacology studies including a bridging study in Australia, and an ongoing Phase 3 study in oHCM in China (NCT07021976). Braveheart Bio entered into an exclusive worldwide license agreement with Hengrui Pharma for the development, manufacture, and commercialization of HRS-1893 outside of Mainland China, the Hong Kong SAR, the Macao SAR, and Taiwan Region.

 

About Hengrui Pharma

 

Hengrui Pharma is an innovative, global pharmaceutical company dedicated to the research, development, and commercialization of high-quality medicines to address unmet clinical needs. Its therapeutic areas of focus include oncology, metabolic and cardiovascular diseases, immunological and respiratory diseases, and neuroscience. Driven by a patient-focused philosophy since its founding in 1970, Hengrui Pharma remains committed to advancing human health by striving to conquer diseases, improve health, and extend lives through the power of science and technology.

 

About Braveheart Bio

 

Braveheart Bio is a late clinical-stage biotechnology company developing novel therapeutics for hypertrophic cardiomyopathy and related conditions. The company is backed by experienced life science investors including Andreessen Horowitz (a16z Bio + Health), Forbion, OrbiMed, Enavate Sciences (a platform of Patient Square Capital), and Frazier Life Sciences. Braveheart is advancing BHB-1893 through late-stage clinical development with the goal of establishing a new standard of care. For more information, visit www.braveheart.bio.