SHANGHAI, China, October 15, 2026 – ImmuneOnco Biopharmaceuticals (Shanghai) Inc. ("ImmuneOnco," HKEX: 01541) today announced that the Center for Drug Evaluation ("CDE") under China's National Medical Products Administration ("NMPA") has accepted for review the investigational new drug ("IND") application for IMC-003, an activin receptor type IIA ("ActRIIA")-Fc fusion protein independently developed by its subsidiary ImmuneCare Biopharmaceutical Technology (Shanghai) Co., Ltd. ("ImmuneCare"). The application covers the treatment of combined post- and pre-capillary pulmonary hypertension associated with heart failure with preserved ejection fraction ("CpcPH-HFpEF"), a high-risk phenotype within pulmonary hypertension associated with left heart disease ("PH-LHD").

The move marks IMC-003's second pulmonary hypertension ("PH") indication following pulmonary arterial hypertension ("PAH," WSPH Group 1), and represents the molecule's expansion into PH-LHD (WSPH Group 2).

PH is a major global health burden, estimated to affect approximately 1% of the world's population. PH-LHD is the most common form, accounting for roughly 65% to 80% of all PH cases. In China, the prevalence of heart failure among adults aged 35 and above is approximately 1.3%, corresponding to an estimated 8.9 million patients, with HFpEF accounting for close to half of that population. PH is present in a substantial proportion of HFpEF patients, although reported rates vary widely depending on the population studied, the diagnostic approach used and how PH is defined. A subset of these patients develops CpcPH, which carries a particularly poor prognosis and for which no targeted therapy has been specifically approved, representing an urgent unmet clinical need.

PH-LHD and the Unmet Need

PH-LHD (WSPH Group 2) encompasses pulmonary hypertension associated with both heart failure with reduced ejection fraction and HFpEF. CpcPH-HFpEF is a high-risk subtype characterized by the coexistence of elevated left heart filling pressure (a post-capillary component) and progressive pulmonary vascular remodeling (a pre-capillary component). Because its pathophysiology spans both the left heart and the pulmonary vasculature, vasodilators developed for PAH, such as macitentan and tadalafil, have largely failed to show clear benefit in HFpEF populations, and safety signals have raised concerns about edema and marked fluid retention. As a result, strategies targeting the activin signaling pathway to address pulmonary vascular remodeling and myocardial fibrosis have become a closely watched direction in drug development.

The Phase 2 CADENCE trial of sotatercept in PH-LHD reported positive results at the ACC.26 Scientific Sessions and in Circulation. In 164 patients with HFpEF and severe CpcPH, both the 0.3 mg/kg and 0.7 mg/kg doses significantly reduced pulmonary vascular resistance, the primary endpoint of the trial, at 24 weeks compared with placebo, and both doses improved mean pulmonary artery pressure, pulmonary artery wedge pressure and six-minute walk distance. Time to clinical deterioration was 82% lower in the 0.3 mg/kg group, while no significant reduction was observed in the 0.7 mg/kg group. To the Company's knowledge, CADENCE is among the first trials to report positive results in PH-LHD for an agent already approved for PAH.

Beyond providing proof of concept that inhibiting activin signaling can improve pulmonary vascular and cardiac hemodynamics, CADENCE also showed improvements in left atrial volume and in left heart filling pressure as reflected by pulmonary artery wedge pressure, suggesting that key drivers of adverse outcomes in HFpEF may be modulated. The findings indicate that the potential benefit of sotatercept extends beyond a modest reduction in resting pulmonary vascular resistance, and underscore the importance of targeting inflammation, cell proliferation and endothelial dysfunction in HFpEF. As ligand trap biology advances, this points to the possibility of using signaling networks to reverse fibrosis and cell hypertrophy, and reinforces the principle of treating the underlying biology of disease rather than focusing solely on hemodynamic parameters.

IMC-003: A Differentiated Approach on a Validated Mechanism

The CADENCE results further support the scientific rationale behind IMC-003. As a next-generation ActRIIA-Fc fusion protein, IMC-003 features an engineered ActRIIA extracellular domain designed to enhance binding to and neutralization of the key ligand Activin A, while also improving product consistency. In Sugen5416-hypoxia and monocrotaline-induced pulmonary hypertension animal models, IMC-003 demonstrated favorable efficacy compared with existing agents of the same class. Its high selectivity for Activin A may allow therapeutic benefit at lower exposure and could help reduce the risk of bleeding. These attributes are based on preclinical and in vitro data and have not been evaluated in head-to-head clinical trials.

Dr. Wenzhi Tian, Chairman, CEO and CSO of ImmuneOnco and Founder of ImmuneCare, commented:

"CpcPH-HFpEF remains one of the heart failure phenotypes with the worst prognosis and the fewest targeted treatment options. The CADENCE results bring new hope to this field and support the potential of activin signaling inhibition. Acceptance of the IND for IMC-003 in this indication gives us the opportunity to bring a differentiated molecule to a population with profound unmet needs and to help address the long-standing absence of targeted therapy. Efficacy and safety will ultimately determine whether this approach succeeds, and that has been the starting point of our molecular design. We will advance this clinical program in accordance with regulatory requirements and strive to make innovative therapy available to patients in China and worldwide as early as possible."