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1 September 2026 A Global Innovator Expanding And Reinventing Protein Degrader Therapeutics
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This presentation contains “forward-looking statements” within the meaning of the federal securities laws, including Section 27A of the United States Securities Act of 1933, as amended, and Section 21E of the Securities Exchange Act of 1934, as amended, regarding the current plans, expectations and strategies of Gyre Therapeutics, Inc. and its subsidiaries (“Gyre”), which statements are subject to substantial risks and uncertainties and are based on management’s estimates and assumptions . All statements, other than statements of historical facts included in this presentation, are forward-looking statements, including Gyre’s ability to leverage China operations for discovery, validation and development of therapeutics, clinical development plans, anticipated timelines and milestones of Gyre’s degrader antibody-conjugate platform, CG923308, CG620953, CG009301, CG001419, F351 and ETUARYTM, including the geographic location and timing of anticipated regulatory submissions and approvals, and the potential therapeutic benefits, efficacy, safety and differentiation of such product candidates, and market size and commercial opportunity estimates, Gyre’s plans, objectives, goals, strategies, future events, or intentions relating to Gyre’s products and markets, the safety, efficacy and clinical benefits of Gyre’s product candidates, the anticipated timing and design of any planned and ongoing preclinical studies and clinical trials, Gyre’s research and development efforts, plans and objectives of management for future operations and future results of anticipated product development efforts, potential addressable market size and Gyre’s liquidity and capital resources and business trends. In some cases, you can identify forward-looking statements by terms such as “believe,” “can,” “could,” “anticipate”, “design,” “estimate,” “expect,” “forecast,” “intend,” “may,” “might,” “plan,” “target”, “seek”, “goal”, “assume”, “milestones”, “potential,” “predict,” “objective,” “should,” “strategy,” “will,” “would,” “forthcoming,” or the negative of these terms, and similar expressions that are predictions of or indicate future events and future trends. These forward-looking statements may include express or implied statements relating to: the estimated future financial performance and financial position of Gyre; the therapeutic potential and utility, efficacy and clinical benefits of the product candidates of Gyre; the risk/benefit profile of Gyre’s product candidates ; expectations regarding Gyre’s research and development efforts, including geographic location and timing of initiation of clinical trials for Gyre’s product candidates ; Gyre’s expectations regarding the advancement of product candidates into IND-enabling studies; and Gyre’s expectations, hopes, beliefs, intentions and strategies ; and other statements that are not historical fact. These statements involve known and unknown risks, uncertainties and other factors that could cause Gyre’s actual results to differ materially from the forward-looking statements expressed or implied in this presentation, in addition to those risks and uncertainties, such as the uncertainties inherent in the clinical drug development process, the regulatory approval process, the timing of any regulatory filings, the potential for substantial delays, the risk that earlier study results may not be predictive of future study results, manufacturing risks, competition from other therapies or products and the impacts of current macroeconomic and geopolitical risks. A discussion of these and other factors, is set forth in Gyre’s Annual Report on Form 10-K for the year ended December 31, 2025 filed with the Securities and Exchange Commission (the “SEC”) on March 13, 2026 and elsewhere in such other filings and in Gyre’s periodic reports and subsequent disclosure documents filed with the SEC. Gyre cannot assure you that it will realize the results, benefits or developments that it expects or anticipates or, even if substantially realized, that they will result in the consequences or affect Gyre or its business in the way expected. Forward-looking statements are not historical facts and reflect management’s current views with respect to future events. Given the significant uncertainties, you should evaluate all forward-looking statements in the context of these risks and uncertainties and not place undue reliance on these forward-looking statements as predictions of future events. All forward-looking statements in this presentation apply only as of the date made and are expressly qualified in their entirety by the cautionary statements included in this presentation . Gyre has no intention to publicly update or revise any forward-looking statements to reflect subsequent events or circumstances, except as required by law. Certain information contained in this presentation and statements made orally during this presentation relate to or is based on studies, publications, surveys and other data obtained from third -party sources and Gyre’s own internal estimates and research . While Gyre believes these third-party studies, publications, surveys and other data to be reliable as of the date of this presentation, it has not independently verified, and makes no representation as to the adequacy, fairness, accuracy or completeness of, any information obtained from third -party sources . In addition, no independent sources have evaluated the reasonableness or accuracy of Gyre’s internal estimates or research, and no reliance should be made on any information or statements made in this presentation relating to or based on such internal estimates and research . This presentation contains trademarks, trade names and service marks of other companies which are the property of their respective owners . This presentation concerns a discussion of investigational drugs that are under preclinical and/or clinical investigation, and which have not yet been approved for marketing by the U.S. Food and Drug Administration . They are currently limited by Federal law to investigational use, and no representations are made as to their safety or effectiveness for the purposes for which they are being investigated . 2 Forward-looking Statements
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3 Gyre Is A Global Development Engine Fueled by its China Discovery and Commercialization Platform Value Drivers Key FeaturesDetails A Commercial Foundation and Integrated U.S. – China R&D Engine Support Capital-Efficient Advancement of a Diversified Pipeline Growth Opportunities Established Innovation Engine Global Infrastructure Commercial Footprint • Diversified R&D programs spanning across multiple indications • Both early- and late-stage pipeline assets provide near- and long-term catalysts • Supports next-generation TPD and DAC platform development • Fully-integrated R&D capabilities • Leveraging cost-efficient China operations for accelerated discovery, preclinical validation, and early clinical-stage development • ETUARYTM has been the market-leading pirfenidone brand in China for treatment of idiopathic pulmonary fibrosis (IPF) • F351 adds a near-term revenue growth catalyst for the China commercial portfolio Degrader platform for the development of TPDs & DACs Dual degraders for oncology/I&I DACs in pre-IND studies ETUARYTM FY26 Total Revenue Guidance $100.5M-$111M F351 potential launch in early 27’ San Diego: Headquarters Shanghai: Discovery Beijing: Manufacturing & Sales *TPDs = targeted protein degraders; DACs = degrader antibody conjugates
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4 Gyre’s Flexible, Capital-Efficient Global Development Strategy China Revenue Builds & De-Risks the Early Pipeline U.S. Capital Advances Priority Assets Globally • Cash-flow Generation: Established commercial operations in China to help offset cash burn. • Reinvestment to R&D Engine: China-generated cash funds preclinical development quickly, at scale, and cost-efficiently, leveraging Gyre’s already-established China infrastructure. • Translational De-risking: Conduct broader preclinical and translational studies to select strongest candidates and build IND-enabling packages. • Focused Capital Allocation: U.S.-raised capital invests into the highest- priority U.S. and global clinical programs. • Flexible Clinical Routing: Initiate studies in the U.S., China or both based on the most efficient development path. • Pivotal Development and Launch: Advance selected assets through U.S. and global clinical studies, pivotal trials, regulatory approvals and launch.
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Global Development Programs and Upcoming Catalysts Program and Description Indication Pre -IND Studies Phase 1 Phase 2 Phase 3 NDA Submitted Catalyst DAC Platform / Next-Gen Degrader Technologies Oncology / Inflammatory Disease Discovery Platform Lead DAC selection / IND- enabling advancement CDK2 / Cyclin E Degrader CG923308 CDK4/6i-resistant Breast Cancer and Other Solid Tumors Q1’27 IND-application submission in U.S. and/or China; Phase 1 start in 2027 TYK2 / JAK 1 Degrader CG620953 Systemic Lupus Erythematosus (SLE) & Rheumatoid Arthritis (RA) Q1’27 IND-application submission in U.S. and/or China; Phase 1 start in 2027 GSPT1 Degrader CG009301 R/R AML, HR-MDS, R/R ALL; Solid Tumor Cancers Phase 1 data in patients with high-risk hematologic malignancies expected at trial completion TRK Degrader CG001419 Cancer-induced Bone Pain (CIBP) Planning Phase 2 initiation in U.S. or China Hydronidone F351 Chronic Hepatitis B (CHB)-induced Liver Fibrosis NDA-filing accepted by China NMPA in May 2026; Potential launch post-NMPA decision in early 2027 Inflammation / FibrosisCancer Degrader DAC China R&D incubator provides new promising clinical assets for global development in cancer, immunology & inflammatory (I&I) diseases, and pain 5 Discovery & lead selection in China IND-enabling development in China; Phase 1 in U.S. and/or China IND-enabling development in China; Phase 1 in U.S. and/or China Phase 1 dose escalation ongoing in China Phase 1 in healthy volunteers completed in Australia; Phase 2 in U.S. or China
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Targeted Protein Degraders (TPDs)
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7 A Modular Degrader Platform: From Discovery to Clinic One Platform. Multiple Degraders. Built for Broad Impact Across Oncology and Immunology. Gyre’s Proprietary Targeted Protein Degraders’ Catalytic Mechanism of Action Enables: High Potency Access to Undruggable Targets Modular Design to Create Multiple Degraders Our expertise also translates well into implementing TPD technology into Antibody-drug conjugates (ADCs) to make next-gen ADCs, called Degrader Antibody Conjugates (DACs). Ubiquitin Proteasome System (UPS) – Our Engine for Targeted Protein Degradation Disease causing protein Lys E3 ligase Degrader Disease causing protein Lys E3 ligase RING Ub Ub Ub Ub Ub E2 Gyre’s Targeted Protein Degrader Molecule Identifying & Binding Tagging Disease Protein Disease-Causing protein being degraded by the proteasome Degraded protein Proteasome Ubiquitin Chain Disease- causing protein
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8 CDK2-Cyclin E Dual Degrader: Novel Strategy for Multiple Solid Cancer Types Cyclin E Is Functionally Amplified or Overexpressed Across Multiple Cancer Types :[1] Lee et al (2026) Clin Cancer Res. PMID:41870274 [1] Turner NC (2019) J Clin Oncol. PMID: 30807234; [2] Herrera-Abreu MT (2016) Cancer Res. PMID: 27020857; [3] Costa C (2020) Cancer Discov. PMID: 31594766 [4] Freeman-Cook (2021) Cancer Cell. PMID: 34520734; [5] Wander SA (2020) Cancer Discov. PMID: 32404308; [6] Al-Qasem AJ(2022) NPJ Precis Oncol. 2022 PMID: 36153348 [7] Josefine B (2012) Breast Cancer Res Treat. PMID: 23242584; [8] Caldon CE (2012) Mol. Cancer Ther. PMID: 22564725 Diverse CDK4/6i or Endocrine Therapy Resistance Converge on Activation of CDK2/Cyclin E 0% 5% 10% 15% Pan-tumor Ovary Uterus/endometrial Gallbladder GE Urinary Bladder Unknown Primary Gi-neuro Small Cell Breast N = 486,340 CDK2-Cyclin E Dual Degrader Cyclin E overexpression CCNE amplification Rb loss PTEN loss PI3K upregulation MYC overexpression Erα alterations ET Resistance CDK2/ cyclin E CDK4/6i Resistance [1, 4, 5] [6] [2,4] [2,5] [3] [2] [7] [4] [8] CCNE1 Amplification Prevalence (%) [1] Market Opportunity & Unmet Medical Need Verzenio, Kisqali, and Ibrance ~$14.6B Total Global Revenues in 2025 Projected total global revenues between $25.8B - $35.7B by early 2030s ~50% of patients develop resistance to CDK4/6 inhibitors within 2 years of starting therapy Strategic Market Research, July 2026 CDK2 / Cyclin E TYK2 / JAK1 TRK DAC FibrosisGSPT1
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CG923308 Demonstrates Anti-Cancer Efficacy in Resistant Preclinical Models 9 CG923308 produces meaningful anti-cancer efficacy in multiple solid tumor preclinical mouse models, including CDK4/6i-resistant models MKN1 Gastric CDX HCC1599 TNBC CDX 0 3 6 9 12 15 18 21 0 100 200 300 400 Days after treatment initiation Tumor Growth (%) INCB123667, 30 mpk/po/bid Vehicle, n=8 CG923308, 10 mpk/po/qd CG923308, 5 mpk/po/qd 0 3 6 9 12 15 18 21 0 100 200 300 400 500 600 Days after treatment initiation Tumor Volume (mm3) Vehicle, n=5 CG923308, 5 mpk/po/qd CG923308, 10 mpk/po/qd CG923308, 20 mpk/po/qd INCB123667, 30 mpk/po/qd OVCAR3 Ovarian CDX 0 3 6 9 12 15 18 21 24 27 30 0 250 500 750 1000 1250 1500 Days after treatment initiation Tumor Volume (mm3) INCB123667, 30 mpk/po/qd CG923308, 50 mpk/po/qd Vehicle, n=8 CG923308, 10 mpk/po/qd CG923308, 25 mpk/po/qd 0 3 6 9 12 15 18 21 24 27 30 0 200 400 600 800 Degrader, 30 mpk/po/qd Vehicle, n=4 Days after treatment initiation Tumor Volume (mm3) INCB123667, 30 mpk/po/qd CDK4/6i-resistant MCF7 CDX CDK4/6i-resistant breast PDX 0 3 6 9 12 15 18 21 24 27 30 33 36 0 200 400 600 800 Days after the start of treatment Tumor volume (mm3) Vehicle, n=5 CG923308, 30 mpk/po/qd CG923308+Palbo, 30 mpk+50 mpk/po/qd TQB3616, 30 mpk/po/qd 0 3 6 9 12 15 18 21 24 27 30 33 36 0 200 400 600 800 Days after the start of treatment Tumor volume (mm3) Vehicle, n=6 CG923308, 30 mpk/po/qd CG923308+Palbo, 30 mpk+50 mpk/po/qd INCB123667: A phase 2/3 CDK2 inhibitor by Incyte; Palbo: Palbociclib (Ibrance), CDK4/6 inhibitor developed by Pfizer; TQB3616: CDK2/4/6 inhibitor developed by Chia Tai Tianqing; TNBC: triple-negative breast cancer CDK2 / Cyclin E TYK2 / JAK1 TRK DAC FibrosisGSPT1 A. Ovarian Cancer CDX C. Gastric Cancer CDX D. TNBC CDXB. Chemo-resistant TNBC PDX E. CDK4/6i-resistant breast cancer CDX F. CDK4/6i-resistant breast cancer PDX
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Chronic Inflammation and Autoimmune Diseases 10 TYK2-JAK1 Dual Degrader: Next-Generation Therapy for Autoimmune Diseases Notes: 1. https://www.psoriasis.org/psoriasis-statistics/ 2. https://www.who.int/news-room/fact-sheets/detail/rheumatoid-arthritis; 3. https://www.niams.nih.gov/health-topics/lupus/basics/symptoms-causes; Significant Unmet Need and Market Opportunity Across Autoimmune Diseases Cytokine signaling mediated by TYK2 and JAK1 125MM+ Patients Worldwide(1) Psoriasis 18MM Patients Worldwide(2) Rheumatoid Arthritis 204K+ Patients U.S.(3) Systemic Lupus Erythematosus Other Inflammatory and Autoimmune Indications IL-12 Drives Th1 differentiation and activation IL-23 Drives Th17 differentiation and maintenance Type I IFNs Antiviral response and inflammation TYK2 JAK2 TYK2 JAK1 STAT Activation Pro-inflammatory Gene Expression TYK2 TYK2 JAK1+ (Heterodimer) CDK2 / Cyclin E TYK2 / JAK1 TRK DAC FibrosisGSPT1 Efficacy High Broad / key disease-driving cytokines Low Limited relevance to core IMID pathways SafetyHigh Risk (severe immunosuppression, hematologic, infection, others) Low Risk (more favorable safety profile) JAK1 JAK3 JAK2 TYK2 TYK2 & JAK1 ✓ Broad disease coverage ✓ Synergistic activity via dual degradation enhances efficacy ✓ Sparing JAK2 and JAK3 leads to a favorable safety profile Sweet Spot of TYK2/JAK1 Dual Targeting
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CG620953 Demonstrates Efficacy in Lupus and RA Preclinical Models 11 Lupus RA CG620953 exhibit enhanced efficacy signals in preclinical models CDK2 / Cyclin E TYK2 / JAK1 TRK DAC FibrosisGSPT1 CG620953 (qd, po) Nose lesion score Percent of survival Days since dosing Control-vehicle Disease model CG620953 (10 mpk, qd, po) CG620953 (30 mpk, qd, po) CG620953 (60 mpk, qd, po) Deucravacitinib (10 mpk, qd, po) Survival rate Doral skin lesion score Kidney injury histopathology Kidney histopathological Score CG620953 (qd, po) Joint thickness (mm) Control Disease model CG620953 (30 mpk, qd, po) Tofacitinib (10 mpk, qd, po) Days since dosing Joint inflammation & cartilage destruction Days since dosing Plantar thickness (mm) Control Disease model CG620953 (30 mpk, qd, po) Tofacitinib (10 mpk, qd, po) Hind paw edema TYK2/JAK1 degradation & JAK2/3 sparing TYK2 JAK1 JAK2 JAK3 -100 -80 -60 -40 -20 0 -91 -71 -8 -19 -71 -21 -6 -5 -25 -4 -2 protein % change from baseline 0.1nM 1nM 10nM 0
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Pan-TRK Degrader: Potential First-in-Class, Non-Opioid Therapeutic Degrader for Cancer-Induced Bone Pain 1. https://pubmed.ncbi.nlm.nih.gov/22570568 2. https://pubmed.ncbi.nlm.nih.gov/26229504 3. https://pubmed.ncbi.nlm.nih.gov/23344095 4. https://pubmed.ncbi.nlm.nih.gov/25919474 5. https://pubmed.ncbi.nlm.nih.gov/37343145 CG001419 Oral Pan-TRK Degrader Degrades TrkA at the source Phase 1a target engagement in high single-digit / low double- digit nanomolar ranges. Well-tolerated up to highest dose tested. 6 U.S.‒China clinical development enables parallel execution and faster timelines Differentiated Mechanism Early Clinical Validation Speed Advantage 12 New cases of malignant bone metastasis in the U.S. annually 1,2 280K – 330K 70-90% develop symptomatic pain with limited current treatment options 3 Significant Unmet Need Average treatment duration for cancer-induced bone pain 4,5 193-225 Days CDK2 / Cyclin E TYK2 / JAK1 TRK DAC FibrosisGSPT1 Cancer-Induced Bone Pain U.S. Market Opportunity Our Differentiated Approach 6. Company data; CG001419-101 (NCT06636500).
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13 CG001419 Phase 1 Results: PD Target Engagement and Safety Source: Company data; CG001419 -101 (NCT06636500). Safety / Tolerability from Phase 1 Pharmacodynamics: potential target engagement demonstrated • Plasma-to-reporter cell assay showed TRKA degradation, supporting potential target engagement • Potent surrogate PD activity observed: DC50 = 2.1 ng/mL; DC90 = 16 ng/mL Favorable safety / tolerability profile • Single and multiple oral doses were well tolerated up to the highest tested dose levels • Most TEAEs were mild or moderate; no Grade 4 TEAEs reported • Common TEAEs were largely general / administration-site events, likely related to blood collection procedures Predictable exposure profile supports continued development • Single-dose CG001419 exposure increased dose-proportionally • Fed condition increased systemic exposure; 7-day MAD exposure increased less than dose-proportionally for CG001419 and metabolites M2/M8 Surrogate PD Assay Demonstrated Degradation Potency in the Low-nM Range. 0 50 100 0 4 8 12 16 20 24 Concentration (ng/ mL) Nominal Time (Hours) Low Dose 1 (n=6) Dose 2 (n=6) Dose 3 (n=6) High Dose 4 (n=6) 0 50 100Degradation (%) CG001419 (ng/mL) 0 878.70.87 GFP TRKA Patient PlasmaReporter Cell Line DC50 = 2.1 ng/mL DC90 = 16 ng/mL Completed Phase 1 studies in healthy volunteers; currently planning Phase 2 for cancer-induced bone pain to commence in U.S. or China CDK2 / Cyclin E TYK2 / JAK1 TRK DAC FibrosisGSPT1 Multiple Ascending Dose (MAD) PK – Day 7 Pharmacodynamics: Potential Target Engagement
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14 CG009301: Targeting GSPT1 for AML and Solid Tumor Cancers • GSPT1 controls protein translation termination and plays important function for leukemia stem cells and tumor cells with MYC overproduction • GSPT1 lacks an active site and is often considered “undruggable” • Other programs targeting GSPT1 show insufficient therapeutic index. CG009301 demonstrate encouraging safety profile in our preclinical studies and early clinical development. Notes: 1. 2024 by American Cancer Society estimates 2. The Cancer Genome Atlas (TCGA) estimates 3. Schaub et al (2018) Cell Syst PMID: 295967830 4. Volpe et al. (2022) Clin Lymphoa Myelom Leuk, PMID: 34544674 GTP Hydrolysis Peptide Release GTP GSPT1 60S CAG UAA 40S eRF1 GDP GSPT1 60S CAG UAA 40S eRF1 GDP GSPT1 60S CAG UAA 40S eRF1 Global Blood Cancer Treatment Market Size, by Treatment Type, 2023-2033 (USD Bn) U.S. Patient Population ~20,800 new cases ~10,000 new cases ~6,500 new cases 28% 11,220 mortality 1,330 mortality 30-40% MDS progress to AML (4) AML (1) MDS (1) ALL (1) MYC-amplified Solid Tumors (2),(3) 5.9 6.5 7.2 7.9 8.7 9.6 10.6 11.7 12.9 14.3 15.7 0 8 16 2023 2024 2025 2026 2027 2028 2029 2030 2031 2032 2033 Chemotherapy Radiation Therapy Targeted Therapy Others The Market will Grow 10.3% The Forecasted Market 15.7Bn At the CAGR of: size for 2033 in US$: CDK2 / Cyclin E TYK2 / JAK1 TRK DAC FibrosisGSPT1
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15 CG009301: Ongoing Phase 1 in China for patients with high-risk heme malignancies CDK2 / Cyclin E TYK2 / JAK1 TRK DAC FibrosisGSPT1 Dose Escalation Dose Expansion RP2D Dose X：xx mg, n=9~18 Dose X：xx mg, n=9~18 28 days as one cycle R/R-AML, HR-MDS & R/R-ALL Recurrent or refractory haematological malignancies 50-86 subjects BOIN Design Rapid titration Dose level 1 - mg QD, n =1 Dose level 2 - mg QD, n=1 Dose level 3 - mg QD, n=3 Dose level 6 - mg QD,n=6~12 Dose level 7 - mg QD,n=6~12 Dose level 8 - mg QD,n=xx Dose level 4 - mg QD, n=3~6 Dose level 5 - mg QD,n=3~6 Dose level 9 - mg QD,n=xx Dose level 10 - mg QD,n=xx Dose level 2 - mg QD, n=3 Dose level 3a - mg QD,n=3~6 Dose level 2a - mg QD, n=3~6 Dose level 3 - mg QD,n=3~6 D1-7 each cycle iv. administration BOIN Design D1-14 each cycle iv. administration
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Degrader-Antibody Conjugates (DACs)
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Leveraging Expertise in TPDs and China ADC Platform to Develop Degrader-Antibody Conjugates (DACs) Gyre’s DAC Platform for Multiple Cancer Types HIGH POTENCY IMPROVED PK Gyre’s DAC Mechanism of Action & Benefits ENHANCED SAFETY 17 CDK2 / Cyclin E TYK2 / JAK1 TRK DAC FibrosisGSPT1 mAbs – monoclonal antibodies TAAs – Tumor-assisted Antigens
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Gyre’s DACs Demonstrate Broad Efficacy Across Diverse Tumor Types 0 10 20 30 40 0 500 1000 1500 2000 2500Tumor volume (mm3) VCaP Prostate Cancer CDX model Days after treatment initiation Vehicle mAb1-DAC, 1 mpk/iv/q3w mAb1-DAC, 3 mpk/iv/q3w 0 10 20 30 0 200 400 600 800 1000Tumor volume (mm3) HCC827 NSCLC CDX model Days after treatment initiation mAb7-DAC, 3 mpk single dose Vehicle mAb4-DAC, 3 mpk 0 10 20 30 40 50 60 70 80 0 500 1000 1500 2000Tumor Volume (mm3) MDA-MB-453 Breast Cancer Model Days after treatment initiation Vehicle mAb3-DAC, 1 mpk/iv mAb3-DAC, 3 mpk/iv single dose 0 10 20 30 40 50 60 70 80 90 100 0 500 1000 1500 2000 2500Tumor Volume (mm3) BT474 Breast Cacner CDX model Days after treatment initiation Vehicle Dxd-ADC, 5 mpk/iv mAb3-DAC, 10 mpk/iv single dose 0 10 20 30 40 50 60 70 80 0 500 1000 1500 MV4;11 AML CDX model Days after treatment initiation Tumor Volume (mm3) mAb6-L1-DAC Vehicle mAb6-L2-DAC 10 mpk/single dose 0 4 8 12 16 20 24 28 0 500 1000 1500 2000 2500 3000Tumor Volume (mm3) NOMO-1 AML CDX model Days after treatment initiation Vehicle mAb6-DAC, 1 mpk/iv mAb6-DAC, 3 mpk/iv mAb: monoclonal antibody recognizing a specific antigen; DXd-ADC: HER2-DXd ADC (Enhertu) Developed by Daiichi Sankyo and AstraZeneca 18 CDK2 / Cyclin E TYK2 / JAK1 TRK DAC FibrosisGSPT1 A. AML CDX model B. AML CDX model C. Breast Cancer model D. Breast Cancer model E. Prostate Cancer CDX model F . NSCLC CDX model
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DAC for Prostate Cancer and Solid Tumors With An Epigenetic-Targeting Payload Therapeutic-resistant PDX model Prostate cancer CDX model 0 10 20 30 40 0 300 600 900 1200 1500 1800 Days after treatment initiation Tumor volume (mm3) Vehicle mAb3-DAC, 10 mpk single dose mAb4-DAC, 10 mpk single dose Enzalutamide-resistant CRPC PDX model 0 10 20 30 40 0 500 1000 1500 2000 2500Tumor volume (mm3) VCaP Prostate Cancer CDX model Days after treatment initiation Vehicle mAb1-DAC, 1 mpk/iv/q3w mAb1-DAC, 3 mpk/iv/q3w Non-human primate pilot toxicity 0 5 10 15 0 1 2 3 4 5 Days after treatment initiation Body Weight (kg) mAb1-DAC 5 mpk mAb1-DAC 10 mpk i.v., single dose Prostate cancer causes 35,000 – 36,500 deaths each year and is the second- leading cause of cancer death in the US.1 Epigenetic factors are frequently mutated across human malignancies, including prostate cancer. Prior developments targeting epigenetic factors for prostate cancer has been limited by the toxicity. Protein degradation & cytotoxicity 19 CDK2 / Cyclin E TYK2 / JAK1 TRK DAC FibrosisGSPT1 1. American Cancer Society estimates as of August 2026
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Commercial Foundation and Growth Opportunities with F351 (Hydronidone)
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ETUARYTM: The Commercial Anchor of Our Fibrosis Franchise Since 2011 A Durable Revenue Base that Funds Innovation and Supports Our Next-generation Degrader / DAC Platform Notes: 1. ETUARY market position based on IQVIA CHPA data for pirfenidone in China [2014 -2026]: legal review required. Financial data i nclusive of pro forma data prior to GNI Group and Catalyst Biosciences business combination. 2017 sales in audited China GAAP ; 2025 in audited U.S. GAAP 21 Established Leadership ETUARYTM has anchored our IPF franchise in China through consistent execution and broad physician reach, supported by ῀370 commercial personnel across 3,000+ hospitals and pharmacies. Durable Market Position ETUARYTM was approved by NMPA in 2011 before Esbriet approval by US FDA. GYRE Pharmaceuticals has maintained market leadership positions in China since then, which demonstrated GYRE’s capability to manage the drug life cycle. Funds the Innovation Pipeline ETUARY TM's recurring commercial revenue supports our next-generation degrader / DAC platform without dilution dependence. ETUARYTM (Pirfenidone) (1)1 Etorel TM – Launched in 20252 F351 (Hydronidone)3 China’s Leading Pirfenidone Brand For the Treatment of IPF (1) Complementary PF option that extends the fibrosis toolkit alongside ETUARY TM. NDA accepted for priority review by NMPA in May 2026. A One-stop Shop for Fibrosis – Building Physician Reach Ahead of F351 CDK2 / Cyclin E TYK2 / JAK1 TRK DAC FibrosisGSPT1
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Breakthrough Therapy Designation Priority Review of NDA (China NMPA, 2021, 2026) NDA accepted by NMPA in May 2026 22 F351 Phase 3 Results in CHB-associated Liver Fibrosis Supports Regulatory Filing Primary Endpoint Met with High Statistical Significance ≥1-stage fibrosis regression at Week 52: • F351: 52.85% (n=123) vs. • Placebo: 29.84% (n=124) • Delta: 23.01% • p = 0.0002 (ITT analysis with central blinded pathology review) • Consistent with fibrosis regression rates observed in Phase 2 Key Secondary Endpoint Reduction in Liver Inflammation ≥1-grade inflammation improvement without fibrosis progression at Week 52: • F351: 49.57% (n=123) vs. • Placebo: 34.82% (n=124) • Delta: 14.75% • p = 0.0246 • Reinforces anti-inflammatory activity CDK2 / Cyclin E TYK2 / JAK1 TRK DAC FibrosisGSPT1 F351 poised to be the next-generation of fibrosis therapy
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China-First Strategy Provides Accelerated POC 23 MASH Fibrosis Market Provides Significant Upside Opportunity For F351 Forecasted Market Size of MASH Fibrosis Therapies in the USA ($MM USD) $479 $728 $1,109 $1,740 $2,481 $3,310 $4,247 $5,462 2025 2026 2027 2028 2029 2030 2031 2032 USA MASH Therapeutics Sales forecast from Evaluate Pharma as of 5-13-2026 Assumes 50% of all MASH patients progress to MASH fibrosis (Stage ≥F2) based on Luthra & Sheth (2025). Note: 1. Le et al. (2025) JAMA; AJMC; MASH Awareness; Estes et al. (2018) AASLD; L.E.K. interviews • Current U.S. MASH prevalence is estimated at ~14MM (1) • MASH represents tremendous growth opportunity due to very low current MASH diagnosis rate (5-10%) • Rising obesity and diabetes increase MASH progression via liver inflammation 42% CAGR (2025 – 2032) CDK2 / Cyclin E TYK2 / JAK1 TRK DAC FibrosisGSPT1
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24 Key Value Drivers Lead TPD Assets • Opportunities in cancer and autoimmune diseases with dual degraders • TPD portfolio highly validated for large unmet need indications TPD / DAC R&D Engine • Multiple shots on goal • DACs paint a promising picture as the next-gen to ADCs / TPDs alone Global Exposure • Lean operations to de-risk assets • U.S. headquarters and integrated U.S. and China R&D operations Revenues to Support Operations • ETUARY TM and anticipated F351 sales in China expected to cover operation expenses to support early-stage R&D and proof-of-concepts studies 1 2 3 4
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U.S. Management Team with Cross-Culture Operational Experience Ying Luo, Ph.D. Chief Executive Officer Thomas Eastling Chief Financial Officer Weiguo Ye Chief Operating Officer Yue Xiong, Ph.D. Chief Scientific Officer Ruoyu Chen Chief Information Officer Jialiang Wang, Ph.D. Executive Vice President, General Manager Joshua Bergmann, J.D. General Counsel and Corporate Secretary Seth Goldblum, MBA Senior Vice President – Corporate Development Jing Liu, Ph.D. Senior Vice President – Platform Chemistry Michael Plewe, Ph.D. Senior Vice President - Medicinal Chemistry Mark Marino, M.D. Senior Vice President – Clinical Development Leslie Robinson, Ph.D., J.D. Vice President - Intellectual Property and Licensing Liang Zhao Vice President – Corporate Controller Sudan Loganathan, Ph.D. Vice President – Investor Relations & Finance Strategy Chuck Monahan Senior Vice President – Regulatory Affairs
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Thank You!