TRANSTHERA-B - VOLUNTARY ANNOUNCEMENT

TransThera Sciences (Nanjing), Inc. Presented Lineage Reprogramming as a Resistance Mechanism to Endocrine Therapy in HR+ Breast Cancer, as Well as Preclinical Data for Tiangotinib at the 2026 American Association for Cancer Research (AACR) Annual Meeting

TransThera Sciences (Nanjing), Inc.

藥捷安康 ( 南京 ) 科技股份有限公司

(A joint stock company incorporated in the People's Republic of China with limited liability)

(Stock Code: 2617)

VOLUNTARY ANNOUNCEMENT

TransThera Sciences (Nanjing), Inc. Presented Lineage Reprogramming as a Resistance Mechanism to Endocrine Therapy in HR+ Breast Cancer, as Well as Preclinical Data for Tiangotinib at the 2026 American Association for Cancer

Research (AACR) Annual Meeting

This announcement is made by TransThera Sciences (Nanjing), Inc. (the "Company", together with its subsidiaries, the "Group") on a voluntary basis to inform the shareholders and potential investors of the Company about the latest business advancement of the Group.

The Company announced the poster presentation at the 2026 American Association for Cancer Research (AACR) Annual Meeting to disclose that lineage plasticity serves as an important resistance mechanism to endocrine therapies in HR+ breast cancer and to discuss its clinical translational significance.

Title: Convergent FGFR-JAK signaling reprograms luminal identity and drives endocrine

resistance in HR+ breast cancer

Session Title: Mechanisms of Drug Resistance 2

Presentation Time: 9:00:00 AM-12:00:00 PM on 20 April 2026 (Pacific Daylight Time)

Location: Poster Section 16

Poster Board Number: 6

Presentation Number: 1786

Endocrine therapy improves outcomes in HR+ breast cancer, but resistance remains a major clinical challenge. Using single-cell transcriptomics, the research team identified a luminal-to-basal transition with ER/PR downregulation in resistant tumors – plasticity that emerged in primary lesions and amplified in metastases, especially malignant pleural effusions.

Through serial drug selection and coculture models, the study found that therapy-induced and microenvironment-driven resistance both converge on FGFR and JAK pathway activation, which represses luminal genes (ESR1, PGR). As a dual inhibitor targeting both FGFR and JAK, Tinengotinib (TT-00420) restored luminal identity and resensitized resistant models to endocrine therapy in vitro and in vivo. These findings support dual FGFR-JAK blockade as an effective to overcome lineage plasticity-driven endocrine resistance. A phase II clinical trial of tinengotinib plus endocrine therapy in advanced HR+ breast cancer is ongoing.

About Tinengotinib

Tinengotinib is an internally discovered, NDA stage (NMPA), multi-kinase inhibitor that exerts antitumor effects by targeting FGFRs/VEGFRs, mitotic kinases Aurora A/B and Janus kinases (JAK). Ongoing clinical trials conducted globally have revealed the potential of tinengotinib to be efficacious in various solid tumors, including cholangiocarcinoma (CCA), prostate cancer, breast cancer, and liver cancer. Tinengotinib has been granted the Orphan Drug Designation (ODD) and Fast Track Designation by the FDA for the treatment of CCA, the Orphan Drug Designation (ODD) for the treatment of biliary tract cancer by the European Medicines Agency(EMA), and has been included in both the Priority Review List and the Breakthrough Therapy Designation List by the China NMPA.

Warning under Rule 18A.08(3) of the Listing Rules: There is no assurance that the relevant products will ultimately be successfully developed and marketed by the Company.

By order of the Board

TransThera Sciences (Nanjing), Inc.藥捷安康(南京)科技股份有限公司Dr. Frank Wu

Chairman and Chief Executive Officer

Hong Kong, 21 April, 2026