/SINO BIOPHARM - VOLUNTARY ANNOUNCEMENT - APPLICATION FOR CLINICAL TRIAL ON TRD221 "COMPLEMENT PROTEIN MODULATOR" APPROVED BY THE NMPA
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SINO BIOPHARM - VOLUNTARY ANNOUNCEMENT - APPLICATION FOR CLINICAL TRIAL ON TRD221 "COMPLEMENT PROTEIN MODULATOR" APPROVED BY THE NMPA

HKEXnews
2026/03/17[Other - Business Update]

SINO BIOPHARM - VOLUNTARY ANNOUNCEMENT - APPLICATION FOR CLINICAL TRIAL ON TRD221 "COMPLEMENT PROTEIN MODULATOR" APPROVED BY THE NMPA

(Incorporated in the Cayman Islands with limited liability) Website: www.sinobiopharm.com (Stock code: 1177)

VOLUNTARY ANNOUNCEMENT APPLICATION FOR CLINICAL TRIAL ON TRD221 "COMPLEMENT PROTEIN MODULATOR" APPROVED BY THE NMPA

The board of directors (the "Board") of Sino Biopharmaceutical Limited (the "Company", together with its subsidiaries, the "Group") announces that TRD221 "Complement Protein Modulator", a national Category 1 innovative drug developed by Beijing Tide Pharmaceutical Co., Ltd. ("Beijing Tide", a subsidiary of the Group) has obtained the clinical trial approval from China's National Medical Products

Administration (NMPA) for the intended treatment of osteoarthritis.

TRD221 for injection is a first-in-class complex polysaccharide drug jointly developed by Beijing Tide and the Institute of Materia Medica, Chinese Academy of Medical Sciences. Polysaccharides possess

favorable profiles of biocompatibility and safety. However, due to their intricate mechanisms of action, challenges in areas such as pharmaceutical research, quality control, and pharmacological evaluation have long constrained the research and development of innovative polysaccharide drugs. As a key protein modulator in the cascade activation of complement system, TRD221 can inhibit the release of inflammatory factors triggered by the activation of complement system, block its direct damage to

chondrocytes and regulate metabolic homeostasis in chondrocytes, thereby facilitating cartilage repair and delaying disease progression.

Osteoarthritis (OA) is a degenerative disease featuring fibrosis, fissuring, ulceration, and loss of

articular cartilage caused by multiple factors. Its main clinical manifestations include joint pain, deformity, and functional impairment. OA not only affects the quality of living of patients severely but also significantly increases the risk of cardiovascular events, deep vein thrombosis in the lower limbs and hip fractures. In 2020, approximately 595 million people worldwide suffered from OA, who were

predominantly affected in joints of knees, followed by hands, hips and other sites. By 2050, the global patient population is projected to increase to 642 million. In China, the prevalence of primary OA among people aged 40 and above has reached 46.3%. With the intensifying profile of aging population, the prevalence rate shows a persistent uptrend.

Current treatments for OA mainly focus on alleviating pain symptoms, with commonly used medications including non-steroidal anti-inflammatory drugs (oral or topical) and intra-articular injection of

hormone, sodium hyaluronate, and other agents. However, significant unmet clinical needs remain in slowing disease progression and improving joint function. The pathogenesis of OA is complex, which involves multiple factors such as cartilage degradation, inflammatory responses, and immune regulation. In particular, as a crucial component of innate immunity, the complement system plays a key role in the onset and progression of OA.

TRD221 demonstrates dual efficacy in alleviating pain symptoms and improving structural damage across multiple mechanism-induced animal models in respect of OA, while exhibiting favorable safety profile and potential as a novel therapeutic solution for OA. The approval for clinical trial will further

enrich the innovative pipeline in the surgical/analgesic field of the Group, while potentially filling existing treatment gaps and providing new therapeutic options for a broad population of OA patients.

By order of the Board

Sino Biopharmaceutical Limited Tse, Theresa Y Y Chairwoman

Hong Kong, 17 March 2026