We are a clinical‑stage biopharmaceutical company focused on developing therapies for patients with hypertrophic cardiomyopathy (“HCM”) and other serious cardiovascular diseases. Our lead product candidate, BHB‑1893, is a next-generation oral small‑molecule cardiac myosin inhibitor (“CMI”), that we are developing for the treatment of obstructive HCM (“oHCM”) and non‑obstructive HCM (“nHCM”). Our goal is to improve the treatment options for these patients by enhancing speed of onset, depth of gradient response, systolic safety, and reversibility, and reducing prescribing complexity. BHB-1893 was initially discovered and developed by Jiangsu Hengrui Pharmaceuticals Co., Ltd. (“Hengrui”) in China. We in-licensed BHB-1893 pursuant to an exclusive license agreement with Hengrui (the “Exclusive License Agreement”), and as such, all clinical trials of BHB-1893 completed to date were designed, sponsored, and conducted by Hengrui, primarily in China, with one Phase 1 trial conducted in Australia. We were not involved in the design, conduct, or oversight of these trials. HCM is a chronic, progressive disease characterized by abnormal thickening and impaired relaxation of the heart. HCM is associated with significant morbidity, reduced quality of life, and an increased risk of heart failure and sudden cardiac death. HCM affects more than 700,000 individuals in the United States and remains an area of significant unmet medical need. While the first generation of approved CMIs, mavacamten (marketed as Camzyos) and aficamten (marketed as Myqorzo), marked a notable advance in the treatment paradigm of oHCM, adoption has been constrained by limitations in their therapeutic profile. In pivotal Phase 3 trials of mavacamten and aficamten, a reduction in left ventricular outflow tract gradient (“LVOT-G”) was observed, but with parallel, dose-dependent reduction in left ventricular ejection fraction (“LVEF”). LVOT-G is a measure of heart outflow obstruction and serves as a central measure of therapeutic effect in oHCM, while LVEF measures the percentage of blood ejected with each contraction and is a critical metric for assessing heart health. We refer to the parallel, dose-dependent reductions in LVOT-G and LVEF as the “LVEF cost,” a tradeoff that may prevent patients from achieving a complete gradient response (post-Valsalva or post-exercise LVOT-G <30 mmHg) before reaching low LVEF safety thresholds. In oHCM pivotal trials, complete gradient responses were observed in only 49% of aficamten-treated patients at Week 24 and 57% of mavacamten-treated patients at Week 30, leaving a meaningful proportion with residual obstruction and persistent symptoms. In addition, the potential of both agents to drive systolic dysfunction, as measured by low LVEF, has resulted in a complex multi‑step dose titration, and burdensome echocardiographic (“echo”) monitoring requirements under a Risk Evaluation and Mitigation Strategy (“REMS”). These limitations have hindered real-world uptake, particularly outside of high-volume specialty treatment administration centers. In nHCM pivotal trials, mavacamten failed to show statistically significant improvements on its dual primary endpoints, while aficamten met both of its dual primary endpoints. A reduced LVEF <50% was observed in 21% of participants receiving mavacamten and in 10% of participants receiving aficamten, which required dose reduction and dose interruption for those participants. BHB‑1893 is designed to address these limitations. In clinical trials conducted to date by Hengrui, patients treated with BHB‑1893 were reported to experience a rapid onset of activity, predictable pharmacokinetics, limited drug‑drug interactions (“DDI”), and low LVEF cost. Across the dose ranges evaluated, reductions in LVEF have been limited, which may support initiation of therapy at or near a clinically active dose with less need for prolonged dose titration. In preclinical studies, a greater than proportional improvement in left ventricular end-diastolic volume (“EDV”) was observed relative to the decrease in LVEF in pigs treated with BHB-1893, which may support BHB-1893’s impact on both improved systolic and diastolic function. We believe these attributes collectively have the potential to translate to a differentiated product profile, including improved clinical outcomes and greater ease of use than existing CMIs by reducing the need for frequent intensive titration monitoring, thus mitigating treatment complexity. In a Phase 2 clinical trial of BHB-1893 conducted by Hengrui in 42 symptomatic oHCM patients (“Phase 2 oHCM Study 201”), with a starting dose of 40 mg twice a day (“BID”), rapid and substantial reduction in LVOT-G was observed. Patients in Cohort 2 were observed to experience an 86% complete response rate at Week 12. Patients were observed to experience a rapid onset of pharmacodynamic effect, with the average post-Valsalva LVOT-G dropping below 30 mmHg as early as Day 5. In the BHB-1893 open-label extension (“OLE”) where all 42 patients from the Phase 2 trial received the 40 mg BID regimen for up to 52 weeks, 86% of patients were observed to have a post‑Valsalva LVOT-G <30 mmHg at Week 28. During the 12‑week core treatment period, no BHB-1893 treated patients were observed to experience LVEF less than 50%, the threshold for low heart function and a side effect which has been observed in other CMIs. As of February 2026, in the OLE, with a median 63 weeks of follow-up, no patients had LVEF less than 55% during titration. Two patients experienced transient LVEF measurements below 50% during the extension that resolved following dose modifications. BHB‑1893 has also been evaluated by Hengrui in a randomized, placebo‑controlled Phase 2 trial in patients with nHCM (“Phase 2 nHCM Study 202”), from which results were presented in May 2026. In this trial, BHB-1893-treated patients were observed to have rapid, substantial, and statistically significant reductions in secondary endpoints that are cardiac biomarkers, which were observed to rapidly reverse during trial drug washout. Patients’ functional status and exercise capacity were also higher at the end of the trial compared to baseline. On echo, BHB-1893 treated patients showed statistically significant, dose-dependent improvements in myocardial relaxation, hemodynamic benefit, and cardiac remodeling compared to placebo-treated patients, including observed improvements in diastolic function. Additionally, no patients in the intervention cohorts required trial drug interruption for LVEF reductions, which, together with BHB-1893’s pharmacokinetic profile, supports a generally favorable profile. Our Phase 3 development strategy is informed by clinical data generated to date, including extensive experience from prior studies conducted by Hengrui, which is concurrently developing the same compound, referred to as HRS-1893, in Mainland China, Hong Kong, Macau and Taiwan (collectively, “Greater China”), including an ongoing Phase 3 trial in oHCM (“Phase 3 oHCM Study 301”). We obtained worldwide rights (excluding Greater China) to BHB-1893 in September 2025 through the Exclusive License Agreement. All clinical trials of BHB-1893 completed to date, including the Phase 1 and Phase 2 trials described in this prospectus, were designed, sponsored, and conducted by Hengrui, primarily in China, with one Phase 1 trial conducted in Australia. We were not involved in the design, conduct, or oversight of these trials. We plan to advance BHB‑1893 through global Phase 3 development in both oHCM and nHCM. We expect to initiate LIONHEART-HCM, our global Phase 3 trial in oHCM, in the second half of 2026 and NOBLEHEART-HCM, our global Phase 3 trial in nHCM in the first half of 2027. In addition to our planned global Phase 3 trials in oHCM and nHCM, Hengrui is conducting a Phase 2 trial of HRS-1893 in heart failure with preserved ejection fraction (“HFpEF”), in Greater China, with expected data readouts in the second half of 2027. As of June 9, 2026, more than 300 individuals globally have been dosed with BHB-1893. Our principal executive offices are located in San Francisco, CA.
