Hengrui Pharma and Braveheart Bio Present Data from 52-Week Open-Label Extension of Phase 2 Study of HRS/BHB-1893 in Obstructive Hypertrophic Cardiomyopathy at American Heart Association Scientific Sessions 2026

All 42 patients entered the extension, with no adverse events leading to permanent study drug discontinuation.

Rhea-AI Summary

Braveheart Bio (NASDAQ: BRVE) and Hengrui Pharma presented 52-week extension results for HRS/BHB-1893 in obstructive hypertrophic cardiomyopathy, a heart-muscle disease.

All 42 patients entered the open-label extension. At Week 52, peak oxygen uptake rose by a mean 2.7 mL/kg/min and patient-reported KCCQ-CSS scores rose by 17.3 points from extension baseline. Heart outflow pressure gradients during the Valsalva maneuver were below 30 mmHg in 79% of patients; 57% ended on the starting dose. No on-treatment severe or serious adverse events occurred, but two patients had transient reductions in the heart's pumping fraction below 50%.

A separate post hoc analysis in non-obstructive disease and laboratory findings suggested improved heart relaxation with preserved pumping function. Braveheart plans a fixed-dose Phase 2b obstructive-disease study, TRUEHEART-HCM.

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Hollow bars mark forward-looking points. How the balance works

Positive

• Moderate pointPeak oxygen uptake increased a mean 2.7 mL/kg/min at Week 52 from extension baseline.
• Moderate pointKCCQ-CSS patient-reported scores increased a mean 17.3 points from extension baseline; 45% achieved ≥20-point improvement at Week 52.
• Moderate pointOutflow pressure gradients below 30 mmHg occurred in 79% (33/42) at Week 52 and 90% at one or more visits.
• Minor pointExercise-capacity responses reached ≥1.5 mL/kg/min in 70% and ≥3.0 mL/kg/min in 50% at Week 52.
• Minor pointNYHA Class I, indicating no activity limitation, was achieved by 60% after 52 weeks.

10 minor points

• Minor pointEarly outflow-gradient responses appeared on Day 1; 67% reached below 30 mmHg by Week 1, before first titration.
• Minor pointStarting-dose maintenance reached 57% (24/42) at 40 mg twice daily; another 19% (8/42) ended at 60 mg twice daily.
• Minor pointPost hoc washout analysis showed attenuated rebound in outflow gradients and NT-proBNP, a heart-stress biomarker, after 52 versus 12 weeks.
• Minor pointNo on-treatment severe or serious adverse events occurred; no adverse events caused permanent study drug discontinuation.
• Minor pointPost hoc non-obstructive analysis: 59% exceeded septal relaxation velocity of 7 cm/s versus 20% baseline and 14% control.
• Minor pointPost hoc non-obstructive analysis: 57% exceeded lateral relaxation velocity of 10 cm/s versus 21% baseline and 18% control.
• Minor pointNon-obstructive heart-filling measures improved after 12 weeks: E/e' ratio and left atrial volume index decreased; end-diastolic volume increased.
• Minor pointHeart-muscle deformation measure LVGLS was preserved; 39% treated versus 15% placebo improved by ≥10%.
• Minor pointPreclinical heart-tissue findings showed improved relaxation below concentrations required to meaningfully reduce contraction force.
• Minor point. Forward-looking: it has not happened yet and may not happen.TRUEHEART-HCM is Braveheart's planned fixed-dose Phase 2b study in obstructive hypertrophic cardiomyopathy.

Negative

• Minor pointTwo patients had transient pumping-fraction reductions below 50% (48% and 49%, site-measured); both resumed lower-dose treatment.
• Minor point52-week extension evidence came from an open-label study of 42 patients.
• Minor pointNon-obstructive clinical findings came from a post hoc pooled-dose analysis of 84 patients, rather than a prespecified analysis.

Key Figures

Peak oxygen uptake change: 2.7 mL/kg/min KCCQ-CSS change: 17.3 points Week 52 LVOT-G response: 79% (33/42) below 30 mmHg +3 more

Peak oxygen uptake change

2.7 mL/kg/min

Mean increase at Week 52 from OLE baseline

KCCQ-CSS change

17.3 points

Mean increase at Week 52 from OLE baseline

Week 52 LVOT-G response

79% (33/42) below 30 mmHg

Valsalva gradient at Week 52

LVOT-G response during treatment

90%

Achieved a Valsalva gradient below 30 mmHg at one or more visits

LVGLS improvement

39% treated vs. 15% placebo

Patients with improvement of at least 10%

Transient LVEF reductions

2 patients; 48% and 49%

LVEF fell below 50%; both resumed treatment at a lower dose

Key Terms

open-label extension, left ventricular ejection fraction, nt-probnp, placebo-controlled, +1 more

5 terms

open-label extension medical

"a 52-week open-label extension (OLE) of the Phase 2 study"

An open-label extension is a continuation of a clinical trial where all participants and researchers know which treatment is being given, often after an initial blinded phase. It allows further study of a drug's long-term safety and effectiveness. For investors, it can indicate ongoing interest and confidence in a product's potential, influencing perceptions of its future value.

left ventricular ejection fraction medical

"based on Valsalva LVOT-G and left ventricular ejection fraction (LVEF) criteria"

Left ventricular ejection fraction (LVEF) is the percentage of blood the heart’s main pumping chamber pushes out with each beat, measured by comparing the volume before and after contraction. Think of it as how much water a pump empties from a tank each cycle — higher percentages mean stronger pumping. Investors care because LVEF is a common clinical measure that affects patient outcomes, market size for treatments, trial success, reimbursement and regulatory decisions in healthcare-related investments.

nt-probnp medical

"LVOT-G and N-terminal pro-B-type natriuretic peptide (NT-proBNP)"

A blood test marker released when the heart is under strain; higher NT‑proBNP levels indicate the heart is working harder or may be failing, similar to a dashboard warning light that signals engine stress. Investors watch NT‑proBNP because changes in the marker can drive clinical trial results, treatment approvals, hospital use, and insurance decisions for heart drugs and devices, all of which affect revenue, adoption and valuation in healthcare companies.

placebo-controlled medical

"from the completed, placebo-controlled Phase 2 HRS-1893-202 study"

"Placebo-controlled" describes a testing method where one group receives the actual treatment or intervention, while another group receives a harmless, inactive version called a placebo. This approach helps determine whether the real treatment has genuine effects beyond psychological expectations. For investors, understanding this ensures confidence that reported benefits are real and not influenced by bias or false perceptions.

left ventricular global longitudinal strain medical

"Left ventricular global longitudinal strain (LVGLS) was preserved"

A measure of how much the left ventricle muscle shortens along its long axis during contraction, expressed as a percentage obtained from echocardiography (speckle-tracking) or cardiac MRI; more negative values mean greater shortening (for example, −20% is more contraction than −15%). It quantifies longitudinal fiber function and can detect subtle systolic dysfunction even when ejection fraction appears normal, but values vary with imaging modality, vendor software, image quality, heart rate and loading conditions, so comparisons should use the same technique and reference ranges.

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HRS/BHB-1893 demonstrated meaningful improvements in exercise capacity and patient-reported outcomes, with rapid, deep, and durable left ventricular outflow tract (LVOT) gradient reduction at 52 weeks

Data support a highly simplified dosing regimen, with a majority of patients potentially served by the starting dose

HRS/BHB-1893 data across both forms of hypertrophic cardiomyopathy (HCM) and preclinical models suggest potential to address underlying pathophysiology of disease, findings consistent with reverse-remodeling and diastolic benefits

Braveheart Bio to host Investor Event and Webcast today at 3:35 p.m. CT (4:35 p.m. ET), including discussion of a planned fixed-dose oHCM study, TRUEHEART-HCM

SHANGHAI and SAN FRANCISCO, Nov. 06, 2026 (GLOBE NEWSWIRE) -- Hengrui Pharma (SSE: 600276; HKEX: 1276) and Braveheart Bio (NASDAQ: BRVE) today presented data from a 52-week open-label extension (OLE) of the Phase 2 study of the investigational, next-generation cardiac myosin inhibitor HRS/BHB-1893 in patients with obstructive hypertrophic cardiomyopathy (oHCM). The data were presented at the American Heart Association (AHA) Scientific Sessions 2026.

After the 12-week core period and a washout period, all 42 patients restarted HRS/BHB-1893 for an additional 52 weeks in the OLE. At Week 52, peak oxygen uptake (pVO2) increased by a mean of 2.7 mL/kg/min from OLE baseline; Kansas City Cardiomyopathy Questionnaire Clinical Summary Score (KCCQ-CSS) increased by a mean of 17.3 points over the same period. At Week 52, 79% (33/42) of patients achieved a Valsalva LVOT gradient (LVOT-G) below 30 mmHg, with 90% of patients achieving a Valsalva gradient <30 mmHg at one or more visits during the treatment period. A majority (57%) of patients ended the study on the 40 mg twice-daily (BID) starting dose.

In a separate presentation, Braveheart Bio reported new preclinical mechanistic data and ad hoc analyses of the completed Phase 2 study in non-obstructive HCM (nHCM), suggesting HRS/BHB-1893 improves diastolic function while preserving systolic function.

“These 52-week data suggested the combination of clinical effect, tolerability, and simplicity in dosing of HRS/BHB-1893, which gives us growing confidence to proceed with our clinical development in China,” said Su Zhang, Vice President and Head of Non-Oncology Clinical Development, Hengrui Pharma. “We believe that it indicates HRS/BHB-1893 will be an effective and practical option for HCM patients.”

“These data reinforce the differentiated clinical profile of HRS/BHB-1893, suggesting encouraging efficacy, safety, and ease of use over a longer course of treatment,” said Travis Murdoch, M.D., President and Chief Executive Officer, Braveheart Bio. “The study data also suggest potential reverse-remodeling. Taken together with data presented today on the mechanistic differentiation of HRS/BHB-1893 from preclinical work and the completed nHCM Phase 2 study, we believe that HRS/BHB-1893 could fundamentally address the biology of HCM, including diastolic dysfunction, across both forms of the disease.”

“HCM has long been treated as a disease of obstruction, but the biology is more fundamental, and today's data begin to reflect that reality,” said Theodore Abraham, M.D., Co-director of UCSF HCM Center of Excellence. “These results suggest that it may be possible to engage that biology directly. The evidence of attenuated rebound after 52 weeks points to a treatment that is beginning to modify the structural and biological substrate of the disease. The diastolic findings in non-obstructive patients, consistent across preclinical models and the clinic, show that the same mechanism can improve ventricular relaxation and filling that have historically constrained this class. For patients living with HCM in all its forms, that could represent a meaningfully different kind of progress.”

Long-term efficacy and safety data of HRS/BHB-1893 in patients with obstructive hypertrophic cardiomyopathy: results from the 52-week extension period

The Phase 2 study of HRS/BHB-1893 (NCT06516068) enrolled 42 adults with symptomatic oHCM. During the 12-week core period, patients were randomized across three dosing cohorts. Following the core period and a washout phase, all 42 patients entered the OLE. Patients then resumed treatment with HRS/BHB-1893 at a starting dose of 40 mg BID with opportunity for titration to 60 mg or 80 mg BID based on Valsalva LVOT-G and left ventricular ejection fraction (LVEF) criteria.

Exercise capacity and symptoms improved with extended treatment. Peak oxygen uptake (pVO2) increased by a mean of 2.7 mL/kg/min at Week 52 from OLE baseline, with 70% of patients achieving a ≥1.5 mL/kg/min improvement and 50% achieving a ≥3.0 mL/kg/min improvement. KCCQ-CSS increased by a mean of 17.3 points at Week 52 from OLE baseline, with 45% of patients achieving a ≥20-point improvement. 60% of patients achieved New York Heart Association (NYHA) Class I after 52 weeks of treatment.

HRS/BHB-1893-treated patients showed rapid, deep, and durable reductions in LVOT-G. Responders were observed as early as Day 1. By Week 1 (before the first titration), 67% of patients achieved complete LVOT-G response (Valsalva gradient <30 mmHg). At Week 52, 79% of patients (33/42) achieved Valsalva LVOT-G <30 mmHg, and 90% of patients achieved a Valsalva gradient <30 mmHg at one or more visits during the treatment period. 57% of patients (24/42) were maintained on the 40 mg BID starting dose and an additional 19% (8/42) were maintained on 60 mg BID at end of study.

The OLE washout design enabled a post hoc analysis comparison of gradient and biomarker rebound following 12 weeks versus 52 weeks of treatment with matched drug exposure. Following the 12-week core period, LVOT-G and N-terminal pro-B-type natriuretic peptide (NT-proBNP) returned to or went above pre-treatment levels after washout. Following 52 weeks of OLE treatment, signs of reduced disease burden were observed with attenuated return of NT-proBNP and LVOT-G.

HRS/BHB-1893 was generally well tolerated across the 52-week OLE period, with no on-treatment severe or serious adverse events. All on-treatment treatment-emergent adverse events (TEAEs) were mild or moderate in severity and no adverse events led to permanent study drug discontinuation. Two patients had transient reductions in LVEF below 50% (48% and 49% site-measured) and both resumed treatment at a lower dose.

The data were presented in a late-breaking oral presentation, “Long-Term Efficacy and Safety of HRS/BHB-1893 in Patients With Obstructive Hypertrophic Cardiomyopathy: Results From the 52-Week Extension Period,” by Xueyi Wu, M.D., Fuwai Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, on Friday, November 6, 2026, at 2:15 p.m. CT.

HRS/BHB-1893 improved indices of diastolic function: evidence from in vitro studies and nHCM patients

In a second presentation, Braveheart Bio reported mechanistic and clinical evidence that HRS/BHB-1893 improves indices of diastolic function with minimal effect on systolic performance, suggesting potential to address a therapeutic gap that has limited existing therapies.

The post hoc pooled-dose analysis evaluated effects of HRS/BHB-1893 on cardiac function in HCM engineered heart tissues (EHTs) and echocardiographic parameters for 84 patients with nHCM from the completed, placebo-controlled Phase 2 HRS-1893-202 study (NCT06816251). In preclinical HCM EHTs carrying the R403Q pathogenic myosin mutation, HRS/BHB-1893 was observed to improve relaxation time well below concentrations required to meaningfully reduce systolic force.

In nHCM patients, post hoc pooled-dose analysis showed significant improvements across multiple established indices of diastolic function after 12 weeks of treatment. For septal e', 59% of treated patients exceeded the normal threshold of 7 cm/s, compared to 20% at baseline and 14% in the control group. For lateral e', 57% of treated patients exceeded the 10 cm/s threshold, compared to 21% at baseline and 18% in the control group. E/e' ratio decreased and left ventricular end-diastolic volume increased, which is consistent with a downward shift of the left ventricular pressure-volume relationship and a more compliant, distensible ventricle. Left atrial volume index decreased, reflecting the downstream benefit of improved diastolic filling. Left ventricular global longitudinal strain (LVGLS) was preserved across the treated group, with 39% of HRS/BHB-1893-treated patients versus 15% of placebo patients demonstrating an improvement in LVGLS by ≥10%.

Because patients with nHCM have no obstruction to relieve, these results point to the proposed mechanism of action of HRS/BHB-1893. Across laboratory models and patients, the molecule appears to act on the excess actomyosin cross-bridge activity that drives diastolic dysfunction in HCM, improving ventricular filling while preserving systolic function. Together, the data support the potential of HRS/BHB-1893 as a differentiated, next-generation cardiac myosin inhibitor.

The data were presented in a moderated poster session, “HRS/BHB-1893, a Next-Generation Cardiac Myosin Inhibitor, Improves Indices of Diastolic Function in Non-Obstructive Hypertrophic Cardiomyopathy: Evidence from In Vitro Studies and Patients,” by Carlos L. del Rio, Ph.D., Senior Vice President, Cardiovascular Research & Translational Science, Braveheart Bio, on Friday, November 6, 2026.

Investor Event and Webcast

Braveheart Bio will host an investor event and webcast today, November 6, 2026, at 3:35 p.m. CT (4:35 p.m. ET) to discuss these data and how they inform future clinical plans, including a planned fixed-dose Phase 2b study in oHCM (TRUEHEART-HCM). A live webcast will be available in the Investors section of the Braveheart Bio website at ir.braveheart.bio, and a replay will be archived following the event.

About Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathy (HCM) is a chronic disease estimated to affect more than 700,000 individuals in the United States, and remains an area of significant unmet medical need. 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 can lead 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 two-thirds of patients with HCM have oHCM, where the thickened muscle creates a blockage in the heart's main pumping chamber, making it harder for blood to flow out to the body with each heartbeat. 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.

About HRS/BHB-1893

HRS/BHB-1893 (designated HRS-1893 by Hengrui and BHB-1893 by Braveheart) is an investigational next-generation oral small-molecule cardiac myosin inhibitor engineered for rapid onset of action, minimal impact on left ventricular ejection fraction (LVEF) and ease of use. By modulating cardiac contractility, HRS/BHB-1893 aims to address the underlying pathophysiology of hypertrophic cardiomyopathy (HCM) while maintaining cardiac output.

HRS/BHB-1893 has undergone extensive clinical development, including dose-ranging Phase 2 studies in both symptomatic obstructive HCM (oHCM) and symptomatic non-obstructive HCM (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 Chinese mainland, the Hong Kong SAR, the Macao SAR and Taiwan Region.

About Hengrui Pharma

Hengrui Pharma is an innovation-driven, 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 clinical-stage biopharmaceutical company focused on developing therapies for patients with hypertrophic cardiomyopathy (HCM) and other serious cardiovascular diseases. Its lead product candidate, BHB-1893, is a next-generation oral small-molecule cardiac myosin inhibitor (CMI) being developed for the treatment of obstructive HCM (oHCM) and non-obstructive HCM (nHCM). Braveheart's goal is to improve the treatment options for these patients by enhancing speed of onset, depth of gradient response, systolic safety and reversibility, and by reducing prescribing complexity. For more information, visit www.braveheart.bio.

Forward-Looking Statements

This press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995, including, without limitation, statements regarding the therapeutic potential, safety, efficacy, tolerability, and dosing of HRS/BHB-1893, including its potential to support a low-monitoring dosing regime with a majority of patients served by the starting dose and potential reverse-remodeling; the potential of HRS/BHB-1893 to address the underlying biology of HCM, to improve diastolic function or to be a differentiated, next-generation cardiac myosin inhibitor across both forms of HCM; the beneficial characteristics, and the potential therapeutic effects of HRS/BHB-1893; the potential of HRS/BHB-1893 to reach a broad population of patients; and the clinical development of HRS/BHB-1893, including the ongoing Phase 3 study. Words such as “aim,” “anticipate,” “believe,” “expect,” “may,” “potential,” “suggest,” “will” and similar expressions are intended to identify forward-looking statements. These statements are based on current expectations and are subject to risks and uncertainties that could cause actual results to differ materially, including that results of earlier-stage, open-label or nonclinical studies may not be predictive of results of later or controlled clinical trials; risks related to the design, conduct and outcomes of clinical trials; the regulatory review and approval process; dependence on the license arrangement between the companies; and the other risks described in Braveheart’s filings with the U.S. Securities and Exchange Commission, including its most recent Quarterly Report on Form 10-Q and Hengrui’s public disclosures. Forward-looking statements speak only as of the date of this press release, and, except as required by law, Braveheart and Hengrui undertake no obligation to update them.

Contacts

Contact Information for Hengrui

Media
Jill Liu
Associate Branding & PR Manager
jie.liu.jl391@hengrui.com

Investor Relations
Lina Zhang
Head of Capital Markets and Securities Affairs
lina.zhang.lz511@hengrui.com

Contact Information for Braveheart Bio

Media
FGS Global
Braveheart-bio@fgsglobal.com

Investors
Alexander Sharif
New Street Investor Relations
Alexander@NewStreetIR.com

FAQ

AI-generated questions and answers. How Rhea-AI works. Not financial advice.

What did Braveheart Bio's HRS/BHB-1893 show after 52 weeks in obstructive hypertrophic cardiomyopathy?

At Week 52, peak oxygen uptake increased by a mean 2.7 mL/kg/min and KCCQ-CSS patient-reported scores increased by a mean 17.3 points from extension baseline. Valsalva outflow pressure gradients were below 30 mmHg in 79% (33/42) of patients.

What safety findings were reported in Braveheart Bio's HRS/BHB-1893 extension study?

There were no on-treatment severe or serious adverse events, and no adverse events led to permanent study drug discontinuation. All on-treatment treatment-emergent adverse events were mild or moderate. Two patients had transient pumping-fraction reductions below 50% and resumed treatment at a lower dose.

How were HRS/BHB-1893 doses adjusted in Braveheart Bio's extension study?

Patients restarted at 40 mg twice daily, with possible increases to 60 mg or 80 mg twice daily. Adjustments depended on Valsalva outflow pressure gradients and left ventricular ejection fraction, the proportion of blood pumped out with each contraction.