Science

Learn how we are advancing our pipeline.

Pipeline

Braveheart is advancing BHB-1893 through global late-stage clinical development across multiple cardiovascular indications with significant unmet need.

Program
Phase 1
Phase 2
Phase 3

LIONHEART-HCM is a global, randomized, double-blind, active-comparator-controlled Phase 3 trial evaluating the efficacy and safety of BHB-1893 compared to metoprolol in approximately 210 adults with symptomatic obstructive hypertrophic cardiomyopathy (oHCM). Patients are randomized 2:1 and treated for 24 weeks. The primary endpoint is change in peak oxygen uptake (pVO2) from baseline to Week 24; secondary endpoints include LVOT gradient, NT-proBNP, NYHA class and KCCQ.

BHB-1893 is administered at a fixed dose or with a single titration step, and the trial incorporates symptom-directed, blinded echocardiographic monitoring, designed to evaluate a simpler treatment paradigm than first-generation CMIs.

Results from an interim analysis of LVOT gradient at Week 12 are planned in the second half of 2027.

TRUEHEART-HCM is Braveheart’s planned Phase 2b trial evaluating the efficacy and safety of a fixed 40 mg twice-daily dose of BHB-1893 in adults with symptomatic obstructive hypertrophic cardiomyopathy (oHCM) on background standard of care.

Trial initiation is planned in the first half of 2027.

NOBLEHEART-HCM is Braveheart's planned global, randomized, double-blind, placebo-controlled Phase 3 trial evaluating BHB-1893 in approximately 600 adults with symptomatic non-obstructive hypertrophic cardiomyopathy (nHCM). Patients will be randomized 1:1 and treated for 36 weeks. The dual primary endpoints are change from baseline in KCCQ-CSS and peak oxygen uptake (pVO2) at Week 36; secondary endpoints include NT-proBNP, NYHA class and measures of cardiac structure.

Note: Hengrui is conducting an ongoing Phase 3 oHCM clinical trial (HRS-1893-301) and an ongoing Phase 2 heart failure with preserved ejection fraction (HFpEF) clinical trial of HRS-1893 in China.

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NCT06516068
n=42

In this Phase 2 study of patients with oHCM, BHB-1893 produced rapid, deep reductions in LVOT gradient at all doses studied, with 86% of patients in Group 2, who received 40mg twice daily, achieving a Valsalva LVOT gradient below 30 mmHg at Week 12. More than 80% of patients achieved normal N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels.

All 42 patients continued into the open-label extension, where 90% of patients achieved a Valsalva LVOT-G <30 mmHg during 52 weeks of treatment. BHB-1893 treatment was generally well-tolerated with no on-treatment severe or serious adverse events in the open-label extension.

NCT06816251
n=84
placebo-controlled

In this Phase 2 study of patients with nHCM, BHB-1893 produced rapid, statistically significant reductions in clinically relevant biomarkers (NT-proBNP and cardiac troponin I (hs-cTnI)), and dose-dependent improvements in important echocardiographic domains, including myocardial relaxation, left atrial volume, and left ventricular mass and wall thickness versus placebo.

Patients reported improvements in symptoms and exercise capacity, and patients in the high-dose group showed a placebo-adjusted improvement of 5.5 points in KCCQ-CSS. No adverse events led to permanent discontinuation.

Precise measures and approach icon.

About BHB-1893

BHB-1893 is a next-generation, oral, small-molecule cardiac myosin inhibitor (CMI) being developed for the treatment of HCM and other serious cardiovascular diseases. More than 300 people have received BHB-1893 in clinical studies to date, including randomized Phase 2 trials in both oHCM and nHCM, and an ongoing Phase 3 trial in oHCM.

BHB-1893 is designed to address limitations of first-generation CMIs through:

Rapid and deep gradient reduction without prolonged titration

Patients may experience faster, more pronounced relief and avoid a lengthy and complex dose adjustment process. In a Phase 2 trial in oHCM, 86% of patients in Group 2 achieved a Valsalva LVOT gradient below 30 mmHg by Week 12, and 89% of patients in the twice-daily cohorts were managed on 40 or 60 mg.

Wide therapeutic index that preserves systolic function

Patients may achieve relief without clinically meaningful reductions in systolic function.

Rapid reversibility and predictable pharmacokinetics

Effects may clear quickly and reliably, giving physicians greater confidence and flexibility in managing therapy. Balanced hepatic and renal clearance demonstrated, with no major drug-drug interactions identified.

Simplified dosing and potentially reduced monitoring burden

A simpler treatment regimen may enable fewer clinic visits and less disruption to patients' daily lives. LIONHEART-HCM is evaluating a fixed-dose or single-step dose adjustment with symptom-directed echocardiographic monitoring while TRUEHEART-HCM is evaluating a simple fixed-dose.

Disease modifying potential

Addressing the underlying disease process may offer patients meaningful, long-term outcomes. Compared to placebo, Phase 2 nHCM patients saw decreases in key biomarkers of disease (NT-proBNP and hs-cTnI) as well as reductions in left ventricular mass and wall thickness.

Anatomically correct heart icon

Our Focus

Hypertrophic cardiomyopathy (HCM) is the most common inherited heart disease, estimated to affect more than 700,000 people in the United States. It is driven by excess cardiac myosin activity, which causes the heart muscle to contract too forcefully, relax poorly, and thicken over time. HCM is a leading cause of sudden cardiac death in young people, including competitive athletes, and is associated with an increased risk of atrial fibrillation, heart failure, and stroke. Approximately 38% of patients are hospitalized each year.

Diagnosed U.S. prevalence is growing as awareness and identification improve, and total prevalence, including undiagnosed patients, is projected to approach 1.1 million by 2040, split roughly evenly between oHCM and nHCM.

oHCM is characterized by obstruction in the left ventricular outflow tract (LVOT), the channel through which blood is pumped from the left ventricle to the rest of the body. oHCM patients may experience progressive symptoms, recurrent hospitalizations, and an elevated risk of heart failure, arrhythmia, and premature mortality.
Two cardiac myosin inhibitors are now approved for oHCM, validating the mechanism. Despite this, many oHCM patients continue to experience persistent symptoms and significant treatment burden, highlighting a meaningful unmet medical need. Both approved CMIs are available with REMS programs that require ongoing echocardiographic monitoring on top of multi-step dose titration.
The majority of oHCM patients treated with CMIs are managed in academic centers due to the burden of safety monitoring and dose adjustments. A treatment option with a reduced monitoring and titration burden could enable broader adoption in community practice settings.
Diagnosed prevalence of oHCM in the U.S. is projected to be approximately
196,000
patients in 2026.
Growing disease awareness and improved identification of patients could continue to expand this population.
Fewer than
20%
of eligible oHCM patients have been treated to date with targeted therapies.
nHCM is characterized by unexplained thickening of the left ventricle without the obstruction present in oHCM, resulting in impaired filling of the heart and elevated cardiac biomarkers. nHCM patients may experience a comparable symptom burden to oHCM patients, with symptoms including shortness of breath, fatigue, and exercise intolerance.
There are currently no FDA-approved therapies specifically indicated for nHCM, and current nHCM patient management relies on off-label use of beta blockers, calcium channel blockers, and other supportive measures that address symptoms only. There is a significant need for therapies that can improve symptoms and function and potentially address the underlying disease process.
Diagnosed prevalence of nHCM in the U.S. is projected to be approximately
145,000
patients in 2026.
Growing disease awareness and improved identification of patients could continue to expand this population.
nHCM represents roughly
43%
of diagnosed HCM patients today and is projected to account for about half of all U.S. HCM patients over time, with no approved targeted therapy.

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