Corporate Presentation  April 2025  Developing Anti-Fibrotic Therapeutics for Chronic Organ Diseases 

 Forward Looking Statements  This presentation contains “forward-looking statements” within the meaning of the federal securities laws 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 statements concerning: 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 or ongoing preclinical studies and clinical trials; Gyre’s research and development efforts; timing of expected clinical readouts, including timing of topline data from Gyre Pharmaceuticals’ Phase 3 clinical trial evaluating F351 for the treatment of CHB-associated liver fibrosis in the PRC, initiation of Gyre’s Phase 2 trial in the U.S. for F351 for the treatment of MASH-associated liver fibrosis, timing of completion of Gyre’s Phase 2 clinical trial in the PRC of F573 for ALF/ACLF, initiation of Phase 1 trial of F230 for the treatment of PAH and IND submission of F528 in COPD, the expectations regarding commercial launch of nintedanib and avatrombopag maleate tablets, management’s plans and objectives 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,” “design,” “estimate,” “expect,” “forecast,” “intend,” “may,” “might,” “plan,” “potential,” “predict,” “objective,” “should,” “strategy,” “will,” “would,” or the negative of these terms, and similar expressions intended to identify forward-looking statements. 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, 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, and competition from other therapies or products, as well as those described in “Risk Factors” and “Management’s Discussion and Analysis of Financial Condition” in Gyre’s Annual Report on Form 10-K for the year ended December 31, 2024 filed on March 17, 2025 with the Securities and Exchange Commission (the “SEC”) and elsewhere in such filing and in Gyre’s other 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 expected consequences or affect Gyre or its business in the ways 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 made in this presentation 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. Gyre obtained the data used throughout this presentation from its own internal estimates and research, as well as from research, surveys and studies conducted by third parties. Internal estimates are derived from publicly available information and Gyre’s own internal research and experience, and are based on assumptions made by management based on such data and its knowledge, which it believes to be reasonable. In addition, while Gyre believes the data included in this presentation is reliable and based on reasonable assumptions, Gyre has not independently verified any third-party information, and all such data involve risks and uncertainties and are subject to change based on various factors.  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 

 3  Gyre Therapeutics (Nasdaq: GYRE): At a glance  1ST   to receive IPF1 treatment approval (pirfenidone) in China (2011);  Pioneering fibrosis treatment with a track record of success  #1   IPF market share in China for 10 consecutive years2   (~50% market share, 90% + share in pirfenidone in 2024)  ~ 600   dedicated global employees;  ~ 400 commercial team across China and the U.S.  ~ 70 focused on R&D   150,000 +   IPF patients treated with pirfenidone  3,000+  hospitals and pharmacies covered in China across   870+cities  EBITDA positive  since 20173, while revenue grew at ~32% compounded annual growth rate (CAGR)3 during the same period  2024 Revenue: $105.8M  2   state-of-the-art, GMP compliant manufacturing facilities built for growth in China, currently running at 40% and 18% capacity  1. IPF = Idiopathic Pulmonary Fibrosis.  2. Per IQVIA.  3. Financial data inclusive of pro forma data prior to GNI Group and Catalyst Biosciences business combination for comparison purposes only.  

 4  Investment Thesis: Pioneering anti-fibrotic solutions for unmet global health needs  Strong Pipeline  Our lead asset, F351 (Hydronidone), has the potential to become a first-in-class therapy for CHB-related liver fibrosis, addressing a significant unmet medical need in China.  Robust pipeline spanning various clinical stages focused on treating organ diseases.  Efficient R&D Strategy  China-first validation strategy leveraging faster patient enrollment and cost efficiency, followed by expansion into the U.S. helps mitigate clinical and regulatory risks.   F351 is expected to initiate a Phase 2 trial in the U.S. for the treatment of MASH-associated liver fibrosis  Proven Commercial Execution  Maintaining market leadership since the commercialization of first-in-class pirfenidone in 2014, with extensive and effective nationwide commercial coverage in China across more than 3,000 hospitals and pharmacies.  Fully Integrated Platform  Comprehensive in-house capabilities covering discovery, clinical development, regulatory affairs, manufacturing, and commercialization.   Two GMP-compliant manufacturing facilities are strategically located to support robust expansion. 

 5  Innovative fibrosis focused development pipeline with sentinel indications in liver and lung  CANDIDATE  INDICATION  PRE-CLINICAL  PHASE 1  PHASE 2  PHASE 3  MARKETED  RIGHTS  TRIAL  F351(Hydronidone)  MASH-associated Liver Fibrosis  Global  Chronic Hepatitis B (CHB) Liver Fibrosis  First  F573  Acute Liver Failure / Acute-on-Chronic Liver Failure  F230  Pulmonary Arterial Hypertension (PAH)  F528  Chronic Obstructive Pulmonary Disease (COPD)  ETUARY(pirfenidone)  Idiopathic Pulmonary Fibrosis (IPF)  China  First  Radiation-induced lung injury (RILI) with or without immune-related pneumonitis (CIP)  Pneumoconiosis (PD)  Diabetic Kidney Disease (DKD)  Q2 2025: Ph2 IND Filing  Q2 2025: Phase 3 Top-line Results  4Q 2025: Complete enrollment  4Q 2025: Start Phase 2/3 Trial  (Adaptive Approach) 

 6  Our lead asset, Hydronidone, targets CHB fibrosis -- a high-need and untapped market in China  The market for CHB-associated liver fibrosis is significantly unmet.  Current standard of treatment, e.g. entecavir, tenofovir, focuses on only reducing liver inflamation.  Patients with F2 - F4 fibrosis are at a high risk of progression to cirrhosis and HCC, major causes of liver-related mortality.  Note: The Fourth National Serological Survey on HBV in China (2020) provided baseline HBV prevalence data. The 60-70M total HBV cases and F2-F4 fibrosis estimates are derived using internal modeling based on this survey’s fibrosis prevalence rates and awareness levels.  Hydronidone, a structural analog of pirfenidone, reverses fibrosis by modulating TGF-β / p38γ / Smad7 signaling pathway — a key driver of fibrosis progression. It received Breakthrough Therapy designation from PRC’s NMPA in 2021, enabling expedited review.  Initial Target  Total HBV Infected Population in China  60 - 70 Million  Chronic Hepatitis B (CHB) Diagnosed Population  14.7 Million  Progressed to Significant Fibrosis Population  5.5 Million  Diagnosed Compensated F-2-F4   2.6 Million 

 7  Hydronidone demonstrates significant fibrosis regression with improved safety profile in previous Phase 2 trial  Trial Overview2  Description  Patient Population  Treatment Groups  Testing Method  Primary Endpoint  Multicenter, double-blinded, placebo-controlled, Phase 2 trial evaluating Hydronidone in CHB-associated liver fibrosis  168 patients with biopsy-confirmed fibrosis (F2-F4)  180mg, 270mg, 360mg Hydronidone + Entecavir vs. placebo  Liver biopsy (histological fibrosis stage)  ≥1 stage fibrosis improvement (Ishak score) at week 52  1. The reported % of fibrosis improvement is based on the Intent-to-Treat (ITT) population. 2. Hydronidone for the Treatment of Liver Fibrosis Related to Chronic Hepatitis B: A Phase 2 Randomized Controlled Trial, Clinical Gastroenterology and Hepatology (2022).  A total of 7 patients (4.2%) experienced SAEs, comparable to placebo (4.6%). Most SAEs were mild/ moderate and resolved after stopping treatment. 

 8  Expanding Hydronidone’s potential: From CHB fibrosis in China to MASH in the U.S.  1. Based on analysis of third-party epidemiological research, published academic studies, and internal modeling.  Compensated F2-F4 MASH diagnosed population: ~650K1  CHB diagnozed population: ~ 90K1  Market Opportunity  The U.S. MASH fibrosis market is 7.2x larger than CHB fibrosis.  Clinical Rationale  Hydronidone modulates TGF-β / p38γ / Smad7 signaling pathway — directly targeting fibrosis progression and offering a differentiated approach from metabolic agents.  Regulatory Pathway  Hydronidone’s CHB data helps to reduce risks in MASH development and potentially supports accelerated regulatory review and fast track.  Competitive Differentiation  Hydronidone’s unique anti-fibrotic approach positions it as a complementary therapy — not a competitor — to metabolic agents like THR-β, GLP-1s, and FGF21. 

 9  CHB and MASH share common fibrotic signaling pathway  CHB- Associated Liver Fibrosis  MASH- Associated Liver Fibrosis  Etiology  Viral (HBV)  Metabolic (Obesity, T2 diabetes)  Fibrosis Driver  Target Cell Type  F351 Mechanism  TGF-β / p38γ / Smad7  Hepatic Stellate Cells  Anti-fibrotic via TGF-β, p38γ & Smad7  Rationale for MASH expansion: Hydronidone targets the same core fibrotic biology - TGF-β, p38γ, and Smad7 - underlying both CHB and MASH, providing a mechanistically de-risked path into MASH. 

 Hydronidone is purpose-built on pirfenidone’s foundation - with enhanced potency and safety  10  Pirfenidone → [Structural Analog + OH] → Hydronidone  ↓ ↓  Modest Liver Activity → Enhanced Smad7 Upregulation + Phase II Metabolism 1  ↑ Hepatotoxicity → ↓ Hepatotoxicity + ↑ Anti-fibrotic Potency  Attribute  Pirfenidone  Hydronidone   Benefit  Structure  Parent compound  Analog with –OH group  ↑ Smad7  MoA  TGF-β  TGF-β + p38γ + Smad7  ↑ Potency  Metabolism  Phase I (oxidation)  Phase II (conjugation)  ↓ Toxicity  Hepatic Safety  Known liver risk  Improved in Ph2 study  ↑ Tolerability  MASH Evidence  Some benefit (PROMETEO, model)2  Stronger effect in a validated preclinical model  ↑ Rationale  1. Phase II metabolism is associated with improved hepatic safety due to faster detoxification.. 2. González-Huezo M, et al. Real-life proof-of-concept trial of prolonged-release pirfenidone in advanced liver fibrosis (PROMETEO study). Hepatol Int. 2021;15(2):377–388.  Hydronidone enhances pirfenidone’s anti-fibrotic effect by also inhibiting p38γ and upregulating Smad7, improving hepatic safety and supporting its expansion into metabolic liver diseases like MASH. 

 Hydronidone reduces fibrosis in a validated MASH mouse model  11  Vehicle  Hydronidone-15mpk  Hydronidone-50mpk  Endpoint  Vehicle  F351 (15 mpk)  F351 (50 mpk)  Fibrosis  Severe  ↓  ↓↓↓  Ballooning  Present  ↓  ↓↓  NASH Score  High  ↓  ↓↓  Hydronidone reduced fibrosis and ballooning in a dose-dependent manner.  Validates anti-fibrotic activity in a metabolic disease setting, supporting MASH expansion.  Note: 100mpk not shown due to plateaued efficacy or potential toxicity. Validated in CCl₄ + HFD-induced NASH model.   Will provide scientific package upon request. 

 12  Hydronidone targets fibrosis specifically for advanced MASH  FIBROSIS STAGING  Risk Staging based on:  Fibrosis Progression  Liver Events  CV Events  Primary Treatment Objectives:  Improve glycemic control  Improve dyslipidemia  Reduce weight  Primary Therapeutic Options  F1  F2  F3  F4  LOW  MEDIUM  HIGH  VERY HIGH  Resolve steatohepatitis  Prevent fibrosis progression  Prevent progression to cirrhosis  Prevent decompensation  Metabolic drugs / obesity drugs  Metabolic + anti-fibrotic drugs  Potent anti-fibrotic + metabolic  Potent anti-fibrotic therapies  Hydronidone Primary Target 1  1. We estimate ~650K compensated F2–F4 MASH patients in the U.S., based on market data and internal modeling. F351 is expected to target the full group, with a core focus of ~450K patients, excluding low-risk F2s and prioritizing the top 15–20% of F2s with progressive fibrosis. 

 13  Positioning Hydronidone in the evolving MASH treatment landscape  ORAL  INJECTABLE        Hydronidone  Rezdiffra  VK2809  EFX   Pegozafermin  Tirzepatide  Semaglutide  Survodutide  Indication  CHB  MASH   MASH   MASH   MASH   MASH   MASH   MASH   Study Phase  Phase 2  Approved  Phase 2b  Phase 2b  Phase 2b  Phase 2b  Phase 2  Phase 2  MOA  TGF-β   THR-β  THR-β  FGF21   FGF21   GIP/GLP-1   GLP-1  GLP-1/glucagon  Population  ITT  ITT  ITT  ITT  ITT  ITT  ITT  Modified ITT  ITT  N (Active/Placebo)  42/43  ~319/~309  44/41  43/43  63/61  81/45  219/219  80/80  77/77  Total ITT  168  966  181  126  181  192  659  320  295  Focus  F2 - F4  F2 - F3  F2 - F3  F2 - F3  F4  F2 - F3  F2 - F3  F2 - F3  F2 - F3  Duration  52 wks  52 wks  52 wks  96 wks  24 wks  52 wks  72 weeks  46 weeks  Fibrosis Improvement  54.8%  ~26%  56.8%  49%  29%  27%  59.1%  43%  36%  Placebo  25.6%  ~10%  34.1%  19%  12%  7%  32.8%  33%  22%  Placebo-Adjusted  +29.2%  +16%  +22.7%  +30%  +17%  +20%  +26.3%  +10%  +14%  Combination Potential  –                       Note: This illustrative comparison includes data from distinct disease settings (CHB and MASH). While fibrosis is a shared endpoint, differences in etiology, pathophysiology, and trial design limit direct comparability. Cross-indication interpretation is hypothetical and does not imply therapeutic equivalence.  Rezdiffra (Madrigal) sets the benchmark as the first FDA-approved therapy for MASH.  Hydronidone offers a fibrosis-first approach, acting directly on fibrotic tissue.  Hydronidone is designed to be complementary, not competitive — potentially used as an add-on alongside metabolic agents.  Our regulatory aim is to establish a new standard for direct fibrosis reversal in MASH patients. 

 Strategic moves to strengthen our pirfenidone franchise and prepare for potential future hydronidone launch  14  ETUARY® (pirfenidone)1  Nintedanib - Acquired in 2024   Avatrombopag – Acquired in 2024  2017  2024  $15.3m  $105.8m  32% CAGR1  Expanding Our IPF Market:   Gyre’s ETUARY has dominated China’s IPF market. Through the strategic acquisition of a generic Nintedanib, we further strengthen our leadership by offering physicians a full spectrum of IPF treatments.  Securing a Foothold in Liver Disease  We acquired rights to a generic Avatrombopag as a strategic entry point into the liver physician network—paving the way for the future launch of Hydronidone.  ETUARY was approved in 2011 before the Reference Listed Drug (RLD) requirement. Without RLD, generic competitors can not conduct the required bioequivalence (BE) studies. This creates a market exclusivity beyond patent protection.   Financial data inclusive of proforma data prior to GNI Group and Catalyst Science merger for comparison purposes only.  Note: 2017 sales number is audited (China) and 2024 is audited (U.S. GAAP). See Note 2 above for further clarification.   2025 Sales Forecast: $118m-$128m 

 15  Transitioning into a fully integrated global biopharma company  Beijing Office  Shanghai Office  Shunyi Manufacturing Facility  CangZhou Manufacturing Facility  Dual Global Headquarters  San Diego, CA   Beijing, China   Integrated Manufacturing Infrastructure  Shunyi Facility (Beijing): State-of-the-art R&D and manufacturing center - adding annual capacity of 700 million capsules.  Cangzhou Facility: Robust API production center with 50 tons annual capacity.  Rigorous Quality Systems  Integrated Quality Management System to ensure consistent product identity, safety, and efficacy.  San Diego Headquarters 

 Expected milestones for Hydronidone  16  1H 2025  2H 2025  1H 2026  Gyre plans to advance additional pipeline compounds including pirfenidone, F573, F528, and F230in a variety of fibrotic and inflammatory diseases  Submission of New Drug Approval   2Q 2025  NMPA Approval   2026  Initiate Phase 2 in MASH-Associated liver Fibrosis  FDA Meeting  Q2/3 2025  2H 2026 

 Market leader in IPF with ETUARY® in China.  China-first, U.S.-second development strategy.  De-risked approach with efficient resource allocation.  Integrated platform: R&D, regulatory, manufacturing, commercial.  17  Gyre: Building on proven success with a measured, de-risked approach to drive sustainable growth  Scientific Innovation  Demonstrated fibrosis reversal in CHB Phase 2 trial, Phase 3 read-out expected in 2Q25.  Breakthrough Therapy designation in China.  Distinct anti-fibrotic MoA; complementary to metabolic agents.  U.S. Phase 2 in MASH expected in 2025.  Proven Execution  Strategic Growth  Hydronidone currently planned for dual-market success (CHB + MASH).  Positioned to become a category leader in fibrosis care.  Significant unmet global markets with multi-billion potential.  Backed by long-term parent GNI Group . 

 18  APPENDIX: F351 - Mechanism of Action  

 19  Comparison of Hydronidone and Pirfenidone metabolism  Hepatic cell  Hepatic stellate cell  Myofibroblasts  Liver fibrosis  Activation  As a key profibrotic cytokine, TGF-β drives hepatic stellate cell (HSC) activation, promotes extracellular matrix (ECM) deposition, and triggers fibrogenesis.  The p38γ isoform plays a pivotal role in TGF-β-stimulated collagen production. F351 attenuates fibrosis, at least in part, by targeting the p38 MAPK transduction pathway.  During hepatic injury, TGF-β upregulation triggers hepatic stellate cell (HSC) activation and differentiation into myofibroblasts. This phenotypic transformation is characterized by cytoskeletal remodeling, including α-smooth muscle actin (α-SMA) expression, which serves as a specific marker for myofibroblasts and the onset of fibrogenesis.  Extensive preclinical and clinical studies indicate that activated myofibroblasts with elevated α-smooth muscle actin (α-SMA) expression serve as the dominant producers of fibrillar collagen and key ECM proteins, thereby driving hepatic fibrogenesis.  Liver Injury → TGF-β ↑ triggers multiple fibrosis pathways: 1. → p38γ → HSC Activation → α-SMA ↑ → ECM Accumulation → Fibrosis 2. → Smad2/3 (phosphorylation) → Fibrosis 3. ⊣ Smad7 (inhibitory) → Upregulation of TGF-beta signaling → Activation of both p38gamma and SMAD2/3 cascades 

 Smad7 is a negative regulator of TGF-β signaling.  Smad7 knockdown can promote HSC activation and liver fibrosis.  Smad7 overexpression can prevent liver fibrosis.  Hydronidone is believed to effectively target this pathway.  Inhibiting HSC activation is believed to be one of the most effective therapeutic strategies to fight liver fibrosis  20  Xu, Xianjun et al. “Hydronidone ameliorates liver fibrosis by inhibiting activation of hepatic stellate cells via Smad7-mediated degradation of TGFβRI.” Liver international : official journal of the International Association for the Study of the Liver vol. 43,11 (2023): 2523-2537. doi:10.1111/liv.15715  TGF-β plays important role in liver fibrosis by activating HSCs 

 Smad7 is a known negative regulator of liver fibrosis, suggesting clinical potential in a recognized cascade   Xu, Xianjun et al. “Hydronidone ameliorates liver fibrosis by inhibiting activation of hepatic stellate cells via Smad7-mediated degradation of TGFβRI.” Liver international : official journal of the International Association for the Study of the Liver vol. 43,11 (2023): 2523-2537. doi:10.1111/liv.15715  21  Animal studies demonstrated hydronidone upregulated the expression of Smad7 and inhibited phosphorylation of Smad2/3 

 22  Hydronidone vs. Pirfenidone: Mechanistic and safety advantages  The introduction of a hydroxyl group shifts its metabolic profile from pirfenidone's dominant Phase I oxidation to preferential Phase II conjugation (M3/M4 metabolites). Phase II metabolism, known as "detoxification metabolism," can prevent the formation of active metabolites and covalent binding to proteins, suggesting a mechanistic basis for hydronidone's improved hepatic safety profile compared with pirfenidone.  Phase II metabolism  Phase I metabolism  Optimization  Achieve higher P38γ binding affinity  Pirfenidone  Hydronidone  Kinase Inhibition Profile  In vitro kinase assay shows that both hydronidone and pirfenidone effectively inhibit p38γ activity, with hydronidone exhibiting a higher inhibition potency than pirfenidone.  These findings indicate that hydronidone exhibits stronger inhibition of the p38γ pathway, potentially contributing to its enhanced antifibrotic activity. 

 23  Hydronidone shaping up to be Pirfenidone 2.0  Feature  Hydronidone  Pirfenidone  Mechanism of Action  Tri-pathway mechanism: inhibits p38γ, upregulates Smad7, and suppresses TGF-β/Smad2/3 signaling  Broadly downregulates TGF-β levels, with less defined pathway specificity  Metabolism  Undergoes Phase II metabolism, known for safer detoxification and fewer reactive byproducts  Primarily metabolized through Phase I oxidation (CYP1A2), which can generate reactive metabolites  Liver Safety  Designed to reduce hepatotoxicity; favorable liver safety profile in trials  Observed increases in liver enzymes in some patients; rare hepatic events documented  Fibrosis Efficacy (in humans)  Shown to reverse fibrosis in 55% of patients with CHB (270 mg group)1  Exploratory clinical data in liver fibrosis; not approved for fibrotic liver disease  1. Cai et al. Clin Gastroenterol Hepatol. 2023;21(7):1893–1901. doi:10.1016/j.cgh.2022.05.056 

 24  Thank you  Contact:  David Zhang  David.Zhang@Gyretx.com