Qyuns Therapeutics Co., Ltd. (“Qyuns” or the “Company”, stock code: 2509.HK) announced that on November 5, 2026, it entered into an exclusive license agreement with Caldera Therapeutics, Inc. (“Caldera”) for a preclinical bispecific antibody program targeting TL1A and IL-17.

Under the agreement, Caldera is granted exclusive worldwide rights to research, develop, register, manufacture and commercialize product candidates arising from the licensed program. In return, Qyuns will receive a one-time, non-refundable and non-creditable upfront payment of USD30 million and will be eligible to receive additional payments of up to USD750 million, subject to the achievement of certain clinical development, regulatory and commercial milestones. Qyuns will also be entitled to receive tiered royalties on net sales of products arising from the licensed program during a specified period following their first commercial sale.

Mr. Qiu Jiwan, Founder, Chairman of the Board and General Manager of Qyuns Therapeutics, commented: “Following our collaboration on QX030N, our renewed partnership with Caldera on a new program reflects the strong mutual trust and effective working relationship we have established. Qyuns’ innovation capabilities in the autoimmune field are highly complementary to Caldera’s strengths in financing and clinical development, providing a solid foundation for the global development of the TL1A/IL-17 bispecific antibody program. We look forward to unlocking the value of our innovations in broader markets through this partnership. Leveraging our increasingly robust portfolio of molecules targeting autoimmune diseases, Qyuns will continue to efficiently develop next-generation innovative therapies.”

The bispecific antibodies covered by this collaboration are designed to simultaneously target two key inflammatory pathways: TL1A and IL-17. TL1A is an emerging target in inflammatory bowel disease (IBD), supported by human genetic and clinical evidence, and is implicated in driving chronic inflammation and fibrosis. IL-17 is a well-validated inflammatory target, with multiple therapies targeting this pathway already commercialized. Dual targeting of these pathways may offer synergistic benefits and provide a differentiated therapeutic approach for immune-mediated diseases.

Established in 2015, Qyuns Therapeutics (2509.HK) is a biopharmaceutical company exclusively focused on biological therapies for autoimmune and allergic diseases. Leveraging its integrated capabilities in R&D, manufacturing and commercial collaboration, Qyuns aims to unlock the commercial value of its pipeline while further strengthening its leading position in the autoimmune field through the efficient development of a series of long-acting bispecific antibodies, with the goal of improving treatment outcomes for patients. Guided by its philosophy of “Innovation for the Great Majority”, Qyuns is committed to addressing challenges of drug accessibility and affordability in its focus areas. The Company has established a diversified pipeline of innovative products, including one approved and marketed product, one product under NDA review, three products in Phase III clinical trials, and several long-acting bispecific antibody programs successfully out-licensed internationally. Its pipeline covers four major therapeutic areas - dermatology, rheumatology, respiratory medicine and gastroenterology - with indications including psoriasis, atopic dermatitis, ankylosing spondylitis, asthma, chronic obstructive pulmonary disease and inflammatory bowel disease. Qyuns is one of the leading biopharmaceutical companies in China focused on autoimmune and allergic diseases.

Fangda Partners provided comprehensive legal services to Qyuns Therapeutics in this transaction, including transaction structuring and the negotiation and revision of transaction documents. The Fangda team was led by partners Henry HE, Yiru WANG, Josh SHIN and Bella WANG, with support from associates Essie ZHAO and Yara YANG. Fangda's teams worked closely together to support the signing of the agreement.