A Fully-integrated Biopharmaceutical Company Focused on Fibrosis, Inflammatory Diseases and Cancer May 2026

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. (“Gyre”) and its subsidiaries, including Cullgen Inc. (“Cullgen”), 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 of CG923308 and the potential therapeutic benefit of CG923308. Gyre or Cullgen’s plans, objectives, goals, strategies, future events, or intentions relating to Gyre or Cullgen’s products and markets, the safety, efficacy and clinical benefits of Gyre or Cullgen’s product candidates, the anticipated timing and design of any planned and ongoing preclinical studies and clinical trials, Gyre or Cullgen’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 or Cullgen’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”, “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 synergies that may be achieved between Gyre and Cullgen; the therapeutic potential and utility, efficacy and clinical benefits of the product candidates of the combined company, including for the treatment of fibrosis, pain and solid tumors; the risk/benefit profile of the product candidates of the combined company; expectations regarding Gyre or Cullgen’s research and development efforts, including timing of initiation of Phase 2 trials for the product candidates of the combined company; Gyre or Cullgen’s expectations regarding the advancement of product candidates into IND-enabling studies; and Gyre and Cullgen’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 or Cullgen’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 and Cullgen 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 Cullgen 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 and Cullgen have 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 or Cullgen’s own internal estimates and research. While Gyre and Cullgen believe 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 or Cullgen’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. Forward-looking Statements

Gyre Therapeutics: At-A-Glance Including Recently Announced Acquisition of Cullgen Gyre Therapeutics, Inc. (Nasdaq: GYRE) Pipeline ranges from discovery stage to marketed products with programs covering multiple therapeutic areas including fibrosis, inflammatory diseases and cancer; ~740 Employees WW ~170 R&D ~85 Manufacturing ~370 Sales & Marketing ~115 G&A Combined entity intends to leverage established and cost-efficient China operations for accelerated discovery, early validation, and development of next generation therapeutics based on degraders and DACs San Diego, CA Corporate HQ - G&A, Clinical Development Shanghai, China Drug Discovery, Clinical Development Beijing, China Manufacturing, Clinical Development and Commercialization

Key Value Drivers Robust and balanced therapeutic pipeline including assets from discovery to marketed products, with established manufacturing and commercialization operations 1 Utilization of highly efficient and cost-effective drug discovery and innovation capabilities in China to advance risk-mitigated products to the United States 2 Strong foundation in protein degrader development provides distinct advantage for the development of DACs as next generation ADC therapeutics 3 Accomplished management team in the United States and China with extensive international business operations experience 4

China Innovation & Validation Engine: Driving Strategic Value and Efficiency Robust Portfolio: Fibrosis, Inflammatory Diseases, Cancer and China Innovation F528 Chronic Obstructive Pulmonary Disease (COPD) CG923308 CDK2/Cyclin E Degrader for Solid Cancers IND Enabling Phase 1 Phase 2 Phase 3 NDA Filed Marketed ETUARYTM (pirfenidone) Radiation Induced Lung InjuryLine Extension CG620953 TYK2/JAK1 Degrader for Inflammatory Diseases F351 (hydronidone) CHB-associated Liver Fibrosis F351 (hydronidone) MASH-Associated Liver Fibrosis + CHB ETUARYTM (pirfenidone) Idiopathic Pulmonary Fibrosis (IPF) ETUARYTM (pirfenidone) Pneumoconiosis Line Extension Degrader Efficient & cost-effective operation accelerates new pipeline development and indication expansion Inflammatory Diseases Cancer Pain Others New Molecule Discovery & Optimization Target Validation Clinical Validation

Ying Luo, Ph.D. Chief Executive Officer Thomas Eastling Chief Financial Officer Weiguo Ye Chief Operating Officer Yue Xiong, Ph.D. Chief Scientific Officer Jialiang Wang, Ph.D. Executive Vice President, General Manager Joshua Bergmann, J.D. General Counsel and Corporate Secretary Ruoyu Chen Chief Information Officer Seth Goldblum, MBA Senior Vice President - Corporate Development Jing Liu, Ph.D. Senior Vice President - Platform Chemistry US Management Team Mark Marino, M.D. Senior Vice President-Clinical Development Michael Plewe, Ph.D. Senior Vice President - Medicinal Chemistry Leslie Robinson, Ph.D., J.D. Vice President - Intellectual Property and Licensing Liang Zhao VP Corporate Controller

7 Targeted CDK2-Cyclin E Protein Degradation for Cancer Therapy Expanding the drug design paradigm

Hijacking the Ubiquitin Proteasome System to Target Undruggable Disease-causing Proteins

Cullgen Was Founded on Pioneering Research in the Ubiquitin Pathway and Targeted Protein Degradation Field Cullgen Discovery Cullgen co-founders’ discovery TPD field Discovery Promising phase I/II PROTAC clinical trial results reported Discovery of ROC1, ROC2 Discovery of CRL3 assembly mechanism Discovery of DDB1 as CUL4 linker Discovery of CAND1 Cullgen founded ALK degrader MEK degrader 1999 2005 2001 2003 2004 2006 2007 2008 2009 2020 2010 2015 2011 2012 2013 2014 2016 2017 2018 2019 2000 2002 2021 Viral hijacking of Cullin E3 Discovery of CRL4 assembly mechanism PROTAC proposed Thalidomide binding to CRBN Discovery of IMiD mechanism CRBN- and VHL-based PROTAC 1st PROTAC in clinical trail MDM2-recruiting PROTAC BIRC2-recruiting PROTAC First structure of E3-PROTAC-substrate ternary complex 2022-2025 TRK degrader BRAF degrader EZH2 degrader Opto-PROTAC EGFR degrader PRMT5 degrader Folate-PROTAC CDK4/6 degrader TF-PROTAC AKT degrader WDR5 degrader NSD3 degrader JAK degrader KEAP1 E3 ligand P300/CBP degrader Novel E3 ligand AKT PROTAC LDH degrader NSD2 PROTAC EGFR degrader Bridged PROTAC 2026 1st PROTAC approved! Yue Xiong Jian Jin

CDK2-Cyclin E Drives Solid Cancers and Breast Cancer Resistant to CDK4/6 Inhibitors A. CDK2-cyclin E promotes cell proliferation and cancer development B. Cyclin E is frequently amplified across multiple cancer types C. Diverse CDK4/6i resistance converge on activation of CDK2/cyclin E CCNE1 overexpression Rb loss PTEN loss PI3K upregulation MYC overexpression CCNE1/2 amplification CDK2/ cyclin E CDK4/6i Resistance CDK2-cyclin E1 Degraders [1, 4, 5] [2,4] [2,5] [2] [3] [4] [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 Analyzed by cbioportal (TCGA, PanCancer) CDK2-cyclin E degrader blocks feedback induction of cyclin E by CDK2 inhibition and achieves sustained suppression of cell proliferation

CDK2-Cyclin E Degrader for Treating CCNE1-amplified Solid Cancers and Breast Cancer Resistant to CDK4/6 Inhibitors Turner NC (2019) J Clin Oncol. PMID: 30807234; Freeman-Cook (2021) Cancer Cell PMID: 34520734; Herrera-Abreu MT (2016) Cancer Res. PMID: 27020857 Howlader (2014) J Natl Cancer Inst PMID: 24777111; Gehrchen ML et al. BJC Rep. 2024 PMID: 39516670 Indication Solid tumors with CCNE1 amplification (CCNE1amp); HR+/HER2- breast cancer with CDK4/6i resistance; Patient Population Estimated in the US for 2024 by ACS (cancer.org) and cbioportal analysis of TCGA database CCNE1amp solid cancer: >25,000 new cases/year Ovarian cancer (19,680 new cases, 19% CCNE1amp) Endometrial cancer (67,880 new cases, 10.8% CCNE1amp) TNBC (62,144 new cases, 10.7% CCNE1amp) Esophagogastric cancer (49,260 new cases, 10.1% CCNE1amp) Non-small-cell lung cancer (187,664 new cases, 4% CCNE1amp) HR+HER2- metastatic breast cancer with CDK4/6i resistance: ~25,000 patients/year (310,720 new cases of breast cancer, 73% are HR+, 20-30% with metastatic disease; 40-50% progression rate) Current SOC (US) Chemotherapy/ADCs Hormone therapy (ovarian, breast) Immunotherapy (breast, esophagogastric) Targeted therapy (e.g. CDK4/6i, HER2 mAb, PARPi) Unmet Clinical Needs Chemo/ADCs/hormone/targeted therapy: drug resistance, side effects Immunotherapy: low response rate as monotherapy Clinical Position Solid tumors with CCNE1amp Breast cancer with CDK4/6i resistance Biomarker CCNE1amp CDK4/6i resistant Proof-of-concept Study Phase 1a/1b with expansion cohorts in CCNE1amp ovarian, endometrial, TNBC, esophagogastric cancer as monotherapy; Phase 1a/1b with expansion cohorts in CDK4/6i resistant HR+ breast cancer as monotherapy; C. Target Product Profile A. CCNE1 highly correlates with poor patient survival B. Deletion of CDK2/E1 re-sensitizes Palbo-resistant cells to Palbo

CG923308 Induces Potent and Selective CDK2-Cyclin E Degradation in Multiple Cancer Types No degradation against known IMiD neosubstrates (GSPT1, SALL4, IKZF1/3, ZFP91, CK1α, et al) CCNE1-amp Gastric MKN1 CG923308 (nM) 0 1 3 10 30 100 CDK2 CyclinE1 β-actin p-Rb DC50 (nM) CDK2 Cyclin E1 Cyclin E2 MKN1 <0.3 0.5 <0.3 OVCAR3 0.6 30 0.9 HCC1599 0.4 1.4 0.3 MCF7 0.7 8.1 2.6 HEK293T 0.9 6.7 1.6 A. Potent degradation of CDK2 and Cyclin E B. Selective degradation of CDK2 and Cyclin E1 Cyclin E1: not identified in HEK293T Degrader concentration: 100-fold of DC50 CyclinE2

CG923308 Induced CDK2-Cyclin E Degradation Is Mediated Through Cullin, Proteasome and CRBN CDK2 β-actin CG923308 (nM) Parental OVCAR3 cells CRBN KO OVCAR3 cells 0 3 10 30 100 300 0 3 10 30 100 300 CRBN p-Rb 1 Bortezomib: proteasome inhibitor 2 MLN4924: neddylation inhibitor 3 MG132: proteasome inhibitor CDK2 Cyclin E1 CDK1 β-actin MKN1 DMSO CG923308 - BTZ1 MLN2 MG3 - BTZ1 MLN2 MG3 A. POI- and CRBN-dependent Ternary complex formation B. Proteasome and Cullin-dependent degradation C. CRBN-dependent degradation Cyclin E1

CG923308 Induces Senescence, Cell Cycle Arrest and Growth Inhibition of CCNE1-amp Solid Tumors A. CG923308 induces cell senescence and cell cycle arrest at G1 in CCNE1-amp solid tumors B. CG923308 induces potent and selective cell growth inhibition in CCNE1-amp solid tumors CG923308 Gastric MKN1 DMSO β-gal Ovarian OVCAR3 CG923308 DMSO

CG923308 Induces Cell Senescence and Growth Inhibition of HR+/HER2- Breast Cancer Resistant to CDK4/6 Inhibitors Characterization of Abemaciclib-resistant MCF7 clone (by WB): Loss of Rb Cyclin D1 upregulation Cyclin E1 upregulation DMSO Abemaciclib-resistant, Rb-deficient MCF7 Abemaciclib β-gal CG923308 Abemaciclib CG923308 - + - - + - A. Abemaciclib-resistant, Rb-deficient MCF7 clones B. Palbociclib-resistant, Rb-deficient MCF7 clone Palbociclib CG923308 - + - - + - Characterization of Palbociclib-resistant MCF7 clone (by RNAseq): Loss of Rb CDK2 upregulation Cyclin E1 upregulation

CG923308 Shows Superiority Over Phase 2/3 CDK2 Inhibitors In Vitro CG923308 overcomes feedback induction of cyclin E1 CG923308 induces deeper and more sustained pRb suppression CG923308 induces more potent growth inhibition CCNE1-amp Gastric MKN1 (nM) CG923308 INCB123667 0 1 3 10 30 100 0 1 3 10 30 100 CDK2 Cyclin E1 p-Rb GAPDH

CG923308 Is Orally Bioavailable Across Preclinical Species CG923308 is orally bioavailable across preclinical species B. Orally administrated CG923308 induces CDK2-cyclin E degradation in tumors HCC1599 Xenograft Tumor Vehicle Low dose Medium dose High dose CDK2 Cyclin E1 p-Rb β-actin Mouse Rat Dog Monkey F% >60 >60 >20 >15

CDK2-Cyclin E Degrader Shows More Potent In Vivo Anti-cancer Efficacy Over Phase 2/3 CDK2 Inhibitors in CDX Models Vehicle’ and INCB123667 treatment were conducted in a separate experiment B. CCNE1-amp MKN1 Gastric CDX C. CCNE1-amp HCC1599 TNBC CDX A. CCNE1-amp OVCAR3 Ovarian CDX Vehicle’ and INCB123667 treatment were conducted in a separate experiment All doses were well tolerated, with no significant body weight loss observed during the studies

CDK2-Cyclin E Degrader Shows More Potent In Vivo Anti-cancer Efficacy Over Phase 2/3 CDK2 Inhibitors in PDX Models All doses were well tolerated, with no significant body weight loss observed during the studies B. Rb-deficient, CDK4/6i-resistant HR+HER2- Breast PDX PDX was derived from a patient with HR+HER2- breast tumor resistant to Fulvestrant and CDK4/6 inhibitors Vehicle’ and Palbociclib treatment were conducted in a separate experiment A. Chemo-resistant CCNE1-amp TNBC PDX PDX was derived from a patient with CCNE1-amp TNBC tumor resistant to chemo drugs

CDK2-Cyclin E Degrader: A Potential Therapeutic for Multiple Solid Cancers Cullgen has developed CDK2-cyclin E dual degraders that induce highly selective and potent targeted protein degradation CDK2-cyclin E dual degrader induces senescence, cell cycle arrest and growth inhibition of CCNE1-amp solid tumors and HR+/HER2- breast tumor resistant to CDK4/6 inhibitors CDK2-cyclin E dual degrader shows superiority over Phase 2/3 CDK2 inhibitors in vitro: 1) Degrader overcomes feedback induction of cyclin E1; 2) Degrader induces deeper and more sustained pRb suppression; 3) Degrader induces more potent growth inhibition on CCNE1-amp tumors CDK2-cyclin E dual degrader is orally bioavailable across preclinical species CDK2-cyclin E dual degrader shows more potent in vivo anti-cancer efficacy over Phase 2/3 CDK2 inhibitors in CCNE1-amp ovarian, gastric and TNBC CDX/PDX models and CDK4/6i-resistant HR+HER2- breast PDX model CDK2-cyclin E dual degrader is well-tolerated in animals with sufficient therapeutic window CDK2-cyclin E dual degrader has potential for the treatment of solid tumors with CCNE1 amplification and HR+/HER2- breast cancers with CDK4/6i resistance Cullgen anticipates submitting an Investigational New Drug (IND) application for CG923308 in the first quarter of 2027

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