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Gyre Therapeutics guides up to $111M FY26 revenue

Gyre Therapeutics, Inc. (GYRE) filed an 8-K to furnish an updated corporate presentation outlining its strategy as a global development engine combining U.S. leadership with China-based discovery, development and commercialization.

Filing Impact
(High)
Filing Sentiment
(Neutral)
Form Type
8-K

Rhea-AI Filing Summary

Gyre Therapeutics, Inc. (GYRE) filed an 8-K to furnish an updated corporate presentation outlining its strategy as a global development engine combining U.S. leadership with China-based discovery, development and commercialization.

The presentation highlights an established China commercial franchise anchored by pirfenidone for idiopathic pulmonary fibrosis, with FY26 total revenue guidance of $100.5–$111 million, intended to help fund a diversified R&D pipeline. The lead China asset F351 (hydronidone) for CHB-induced liver fibrosis has an NDA accepted by the China NMPA, supported by Phase 3 data showing materially higher fibrosis regression and inflammation improvement versus placebo, with potential launch in early 2027.

Gyre describes a broad pipeline of targeted protein degraders and Degrader Antibody Conjugates across oncology, autoimmune disease and pain, including CDK2/Cyclin E, TYK2/JAK1, pan-TRK and GSPT1 degraders, with multiple preclinical and early clinical catalysts planned around 2027.

Positive

  • FY26 revenue guidance of $100.5–$111 million from China commercial operations provides an internal funding base to support Gyre’s R&D pipeline.
  • F351 Phase 3 in CHB-associated liver fibrosis achieved 52.85% fibrosis regression vs 29.84% on placebo with strong statistical significance, supporting the China NDA.
  • F351 also showed 49.57% inflammation improvement vs 34.82% on placebo, reinforcing its anti-inflammatory and anti-fibrotic profile for liver disease.

Negative

  • None.

Insights

Analyzing...

Item 7.01 Regulation FD Disclosure Disclosure
Material non-public information disclosed under Regulation Fair Disclosure, often investor presentations or guidance.
Item 9.01 Financial Statements and Exhibits Exhibits
Financial statements, pro forma financial information, or exhibit attachments filed with this report.
FY26 Total Revenue Guidance $100.5–$111 million Guidance for total revenue from China commercial portfolio in fiscal year 2026
F351 Fibrosis Regression Rate 52.85% vs 29.84% Patients with ≥1-stage fibrosis regression at Week 52, F351 vs placebo in CHB fibrosis Phase 3
F351 Fibrosis Regression Delta 23.01% Difference in ≥1-stage fibrosis regression between F351 and placebo; p = 0.0002
F351 Inflammation Improvement 49.57% vs 34.82% Patients with ≥1-grade liver inflammation improvement without fibrosis progression at Week 52
China HBV Infected Population 60–70 million Estimated total HBV-infected population in China relevant to CHB fibrosis
Global Cancer Pain Market >$11 billion by 2028 Forecast global market size for cancer pain treatments
MASH Fibrosis Market CAGR 42% Forecast compound annual growth rate for U.S. MASH fibrosis therapies from 2025 to 2032
CHB Significant Fibrosis Population 2.6 million Patients with F2–F4 fibrosis within China’s chronic hepatitis B population
Targeted Protein Degraders (TPDs) medical
"Degrader platform for the development of TPDs & DACs"
Degrader Antibody Conjugates (DACs) medical
"next-gen ADCs, called Degrader Antibody Conjugates (DACs)"
Degrader antibody conjugates (DACs) are engineered molecules that pair an antibody’s ability to find a specific cell or protein with a linked agent that triggers that target’s destruction inside the cell, rather than just blocking it. Like a guided removal crew that locates and disposes of a faulty part, DACs can tackle disease-causing proteins that are hard to drug, which can create significant therapeutic upside and development risk for investors.
Breakthrough Therapy designation regulatory
"It received Breakthrough Therapy designation from PRC’s NMPA in 2021"
A breakthrough therapy designation is a regulatory fast-track given to a drug or treatment that shows early signs of providing a major improvement over existing options for a serious condition. Think of it as a VIP lane that can speed up development and more intensive guidance from regulators, which matters to investors because it can shorten time to market, reduce development risk and potentially increase a company’s value — though it does not guarantee approval.
cancer-induced bone pain medical
"Pan-TRK Degrader: Best-in-Class, Non-Opioid Franchise in Cancer-Induced Bone Pain"
MASH fibrosis medical
"MASH Fibrosis Market Provides Significant Upside Opportunity For F351"
Bayesian Optimal Interval technical
"*BOIN: Bayesian Optimal Interval Target DLT rate 0.25"
A Bayesian optimal interval is a statistical method used in early-stage clinical trials to decide whether a tested drug dose is too toxic, too weak, or acceptable by comparing observed patient outcomes to pre-set probability ranges. It uses Bayesian probability to update beliefs as data arrive and sets simple decision rules for dose escalation or de-escalation. Investors care because these rules affect how quickly and reliably a development program finds a safe, effective dose, which influences trial timelines, costs, and the chance a drug advances—think of it as a recipe that adjusts ingredients as you taste, to reach the right balance faster.

FAQ

What was the main purpose of GYRE’s latest 8-K filing?
The 8-K reports that Gyre Therapeutics made available an updated corporate presentation on its website, furnished as Exhibit 99.1, outlining its China-based commercial foundation, targeted protein degrader and DAC pipeline, and key clinical and commercial milestones.

What FY26 revenue guidance did GYRE disclose in the presentation?
Gyre disclosed FY26 total revenue guidance of $100.5–$111 million from its China commercial portfolio, led by its pirfenidone brand for idiopathic pulmonary fibrosis, positioning this revenue base to help offset R&D cash burn and support pipeline advancement.

What is the regulatory status of F351 for CHB-associated liver fibrosis at GYRE?
F351 (hydronidone) for CHB-induced liver fibrosis has an NDA filing accepted by China’s NMPA in May 2026, with the company indicating potential launch timing after the NMPA decision in early 2027, subject to regulatory approval.

How effective was F351 in Gyre Therapeutics’ Phase 3 trial?
In CHB-associated liver fibrosis, 52.85% of F351 patients achieved ≥1-stage fibrosis regression at Week 52 versus 29.84% on placebo (delta 23.01%, p=0.0002). A key secondary endpoint showed improved liver inflammation, also favoring F351 over placebo.

What major pipeline platforms does GYRE emphasize in the new presentation?
Gyre emphasizes its Targeted Protein Degraders (TPDs) and Degrader Antibody Conjugates (DACs) platforms, with programs targeting CDK2/Cyclin E, TYK2/JAK1, TRK and GSPT1 across oncology, autoimmune diseases, cancer-induced bone pain and hematologic malignancies.

How large is the target population for CHB fibrosis that GYRE is addressing with F351?
The company cites a total HBV-infected population in China of 60–70 million, with 2.6 million patients progressed to significant fibrosis (F2–F4), framing a substantial unmet-need market for CHB-associated liver fibrosis.

AI-generated analysis. How Rhea-AI works. Not financial advice.

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UNITED STATES
SECURITIES AND EXCHANGE COMMISSION
WASHINGTON, D.C. 20549
FORM 8-K
CURRENT REPORT
Pursuant to Section 13 or 15(d) of the Securities Exchange Act of 1934

Date of report (Date of earliest event reported): August 26, 2026

Gyre Therapeutics, Inc.
(Exact name of registrant as specified in its charter)

Delaware
000-51173
56-2020050
(State or other jurisdiction of incorporation)
(Commission File Number)
(IRS Employer Identification No.)

12730 High Bluff Drive
Suite 250
San Diego, CA
  
92130
(Address of principal executive offices)
  
(Zip Code)

Registrant’s telephone number, including area code: (858) 284-0115

N/A
(Former name or former address, if changed since last report)

Check the appropriate box below if the Form 8-K filing is intended to simultaneously satisfy the filing obligation of the registrant under any of the following provisions (see General Instruction A.2. below):

☐
Written communications pursuant to Rule 425 under the Securities Act (17 CFR 230.425)

☐
Soliciting material pursuant to Rule 14a-12 under the Exchange Act (17 CFR 240.14a-12)

☐
Pre-commencement communications pursuant to Rule 14d-2(b) under the Exchange Act (17 CFR 240.14d-2(b))

☐
Pre-commencement communications pursuant to Rule 13e-4(c) under the Exchange Act (17 CFR 240.13e-4(c))

Securities registered pursuant to Section 12(b) of the Act:

Title of each class
  
Trading Symbol(s)
  
Name of each exchange on which
registered
Common Stock
  
GYRE
  
The Nasdaq Capital Market

Indicate by check mark whether the registrant is an emerging growth company as defined in Rule 405 of the Securities Act of 1933 (§230.405 of this chapter) or Rule 12b-2 of the Securities Exchange Act of 1934 (§240.12b-2 of this chapter).

Emerging growth company ☐

If an emerging growth company, indicate by check mark if the registrant has elected not to use the extended transition period for complying with any new or revised financial accounting standards provided pursuant to Section 13(a) of the Exchange Act. ☐

Item 7.01
Regulation FD Disclosure.

On August 26, 2026, Gyre Therapeutics, Inc. (the “Company”) made available an updated corporate presentation on the Company’s website.

A copy of the corporate presentation is furnished as Exhibit 99.1 to this Current Report on Form 8-K and is incorporated by reference herein. The exhibit furnished under Item 7.01 of this Current Report on Form 8-K shall not be deemed to be “filed” for purposes of Section 18 of the Securities Exchange Act of 1934, as amended (the “Exchange Act”), or otherwise subject to the liabilities of that section, nor shall it be deemed incorporated by reference in any filing under the Exchange Act or the Securities Act of 1933, as amended, regardless of any general incorporation language in such filing.


Item 9.01
Financial Statements and Exhibits.

(d) Exhibits.

Exhibit
Number
  
Exhibit Title or Description
     
99.1
  
Corporate Presentation, dated August 2026
     
104
  
Cover page interactive data file (embedded within the Inline XBRL document)

SIGNATURE

Pursuant to the requirements of the Securities Exchange Act of 1934, the registrant has duly caused this report to be signed on its behalf by the undersigned hereunto duly authorized.

 
GYRE THERAPEUTICS, INC.
   
Date: August 26, 2026
By:
/s/ Thomas Eastling
 
Name:
Thomas Eastling
 
Title:
Chief Financial Officer


Exhibit 99.1

 1  August 2026  Building A New Protein Degrader Company For Unmet Medical Needs 
 
 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 
 
 3  Gyre Is A Global Development Engine Fueled by China Discovery and Commercialization Platform  Value Drivers  Key Features  Details  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   Support our next-generation targeted protein degrader (TPD) and Degrader Antibody-Conjugate (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); FY26 ETUARYTM Total Revenue Guidance of $100.5-$111MM  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  Established market for ETUARYTM  F351 potential launch in early 27’ post-NMPA decision for CHB-induced liver fibrosis  San Diego: HQ   Shanghai: Discovery  Beijing: Manufacturing & Sales 
 
 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 for multiple shots-on-goal.  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. 
 
 Priority Pipeline and Upcoming Catalysts  Program and Description  Indication  Pre-IND Studies  Phase 1  Phase 2  Phase 3  Regulatory  Catalyst  DAC Platform /   Next-Gen Degrader Technologies  Oncology / Inflammatory Disease Discovery Platform  Lead DAC selection / IND-enabling advancement  CDK2 / Cyclin E DegraderCG923308  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 / Fibrosis  Cancer  Degrader  DAC  China R&D incubator programs in cancer, pain, immunology & inflammatory (I&I) diseases and others   enables the company to continue shifting new promising clinical programs to global development  5  Discovery & lead selection in China  IND-enabling development in China   IND-enabling development in China   Phase 1 dose escalation ongoing in China  Phase 1 in healthy volunteers completed 
 
 Targeted Protein Degraders (TPDs) 
 
 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 
 
 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  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  Fibrosis  GSPT1 
 
 CG923308 Demonstrates Anti-Cancer Efficacy in Resistant Preclinical Models  9  Minimum Effective Dose is 5~30 mg/kg QD (Human Equivalent Dose: 25~160 mg/day) Estimated therapeutic Window: >20-fold (based on dosage); >10-fold (based on exposure)  MKN1 Gastric CDX  HCC1599 TNBC CDX  OVCAR3 Ovarian CDX  Chemo-resistant TNBC PDX  CDK4/6i-resistant MCF7 CDX  CDK4/6i-resistant breast PDX  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  CDK2 / Cyclin E  TYK2 / JAK1  TRK  DAC  Fibrosis  GSPT1 
 
 JAK2/3 Sparing and Improved Safety Profile  Chronic Inflammation and Autoimmune Diseases  10  TYK2-JAK1 Dual Degrader: Next-Generation Therapy for Autoimmune Diseases  Notes:  https://www.psoriasis.org/psoriasis-statistics/;   https://www.who.int/news-room/fact-sheets/detail/rheumatoid-arthritis;   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  Advantages of Dual Targeting TYK2 and JAK1 with a Degrader  Broader Cytokine Coverage  Higher and Broader Efficacy Potential  Best-in-Class Opportunity  TYK2  JAK1  +  (Heterodimer)  CDK2 / Cyclin E  TYK2 / JAK1  TRK  DAC  Fibrosis  GSPT1 
 
 CG620953 Demonstrates Efficacy in Lupus and RA Preclinical Models  11  Lupus  RA  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  Dorsal skin lesion score  Kidney injury histopathology  Joint inflammation & cartilage destruction  Sotyktu   (10 mpk, qd, po)  Disease model  10 mpk  Control  30 mpk  60 mpk  CG620953 (qd, po)  Dorsal lesion score  Kidney histopathological Score  Disease model  10 mpk  Control  30 mpk  60 mpk  CG620953 (qd, po)  Vehicle  Sotyktu   (10 mpk, qd, po)  Hind paw edema  Days since dosing  Plantar thickness (mm)  Control  Disease model  CG620953 (30 mpk, qd, po)  Tofacitinib (10 mpk, qd, po)  Joint thickness (mm)  Days since dosing  Control  Disease model  CG620953 (30 mpk, qd, po)  Tofacitinib (10 mpk, qd, po)  CG620953 exhibit consistent or improved efficacy outcomes to standard-of-care in preclinical models  CDK2 / Cyclin E  TYK2 / JAK1  TRK  DAC  Fibrosis  GSPT1 
 
 Pan-TRK Degrader: Best-in-Class, Non-Opioid Franchise in Cancer-Induced Bone Pain  1. https://pubmed.ncbi.nlm.nih.gov/30627511  2. https://pubmed.ncbi.nlm.nih.gov/37343145  3. https://pubmed.ncbi.nlm.nih.gov/22570568  4. https://pubmed.ncbi.nlm.nih.gov/26229504  4. https://pubmed.ncbi.nlm.nih.gov/23344095  6. https://pubmed.ncbi.nlm.nih.gov/25919474  7. https://pubmed.ncbi.nlm.nih.gov/37343145  8. Estimates based on treatment pricing of $10 / day  CG001419  First-in-class 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 (8)  U.S.‒China clinical development enables parallel execution and faster timelines  Differentiated Mechanism   Early Clinical Validation   Speed Advantage  Our Differentiated Approach  12  New cases of malignant bone metastasis in the U.S. annually 3,4  280K – 330K  Cancer-Induced Bone Pain U.S. Market Opportunity  70-90% develop symptomatic pain with limited current treatment options 5  Significant Unmet Need  Average treatment duration for cancer-induced bone pain 6,7  193-225 Days  CDK2 / Cyclin E  TYK2 / JAK1  TRK  DAC  Fibrosis  GSPT1 
 
 13  CG001419 Phase 1 Results: PD Target Engagement and Safety  Source: Company data; CG001419-101 (NCT06636500).  Pharmacodynamics: Potential Target Engagement  Multiple Ascending Dose (MAD) PK – Day 7  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.  GFP  TRKA  Patient Plasma  Reporter 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  Fibrosis  GSPT1 
 
 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 to develop a therapeutic showed insufficient therapeutic index. CG009301 demonstrated encouraging safety profile in our preclinical studies and early clinical development.  Notes:  2024 by American Cancer Society estimates  The Cancer Genome Atlas (TCGA) estimates  Schaub et al (2018) Cell Syst PMID: 295967830  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)  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  Fibrosis  GSPT1 
 
 15  CG009301: Ongoing Phase 1 in China for patients with high-risk heme malignancies   RDE (MTD or OBD)  Phase 1a Dose Escalation  For PK/PD, safety, tolerability  Phase 1b Dose Expansion  For CR/CRi, DOR, RFS, OS  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  BOIN Design  Dose level 8 mg, QD n=xx  R2PD  xx mg, n=9~18  xx mg, n=9~18  Dose level 4 mg QD, n=3~6  Dose level 5 mg QD, n=3~6  Dose level 9 mg, QD n=xx  Accelerated Titration  *BOIN: Bayesian Optimal Interval   Target DLT rate: 0.25   Acceptable DLT range [0.197, 0.298]  Subjects: all relapsed/refractory hematological malignancies  CG9301 iv QD 7 days in 28-day cycle  Subjects: relapsed/refractory AML (global prevalence ~130,000) and HR-MDS (global prevalence ~70,000)   CG009301 iv QD for 7 days in 28-day cycle  CDK2 / Cyclin E  TYK2 / JAK1  TRK  DAC  Fibrosis  GSPT1 
 
 Degrader-Antibody Conjugates (DACs)  
 
 17  Leveraging Expertise in TPDs and China ADC Platform to Develop Degrader-Antibody Conjugates (DACs)  Gyre’s DAC Platform for Multiple Cancer Types  24  HIGH POTENCY  IMPROVED pk  Gyre’s DAC Mechanism of Action & Benefits  IMPROVED SAFETY  17  CDK2 / Cyclin E  TYK2 / JAK1  TRK  DAC  Fibrosis  GSPT1 
 
 Gyre’s DACs Demonstrate Broad Efficacy Across Diverse Tumor Types  mAb: monoclonal antibody recognizing a specific antigen; DXd-ADC: HER2-DXd ADC (Enhertu) Developed by Daiichi Sankyo and AstraZenec  18  CDK2 / Cyclin E  TYK2 / JAK1  TRK  DAC  Fibrosis  GSPT1 
 
 DAC for Prostate Cancer and Solid Tumors With An Epigenetic-Targeting Payload  Therapeutic-resistant PDX model  Prostate cancer CDX model  Non-human primate pilot toxicity  Prostate cancer causes 35,000 – 36,500 death each year and is the second-leading cause of cancer death in the US. The Androgen Receptor (AR) acts as a critical oncogenic engine, driving prostate tumor growth, survival, and therapy resistance even after castration.  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  Fibrosis  GSPT1 
 
 Commercial Foundation and Growth Opportunities with F351 (Hydronidone) 
 
 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 inclusive 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 in 2011 prior to the Reference Listed Drug (RLD) requirement. Without RLD, generic competitors cannot conduct the required bioequivalence studies – creating a market exclusivity beyond patent protection.  Funds the Innovation Pipeline  ETUARYTM’s recurring commercial revenue supports our next-generation degrader / DAC platform without dilution dependence.        ETUARYTM (Pirfenidone) (1)  1  Etorel TM – Launched in 2025  2  F351 (Hydronidone)  3  China’s Leading Pirfenidone Brand For the Treatment of IPF (1)  Complementary PF option that extends the fibrosis toolkit alongside ETUARYTM.  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  Fibrosis  GSPT1 
 
 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 (1) 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  Fibrosis  GSPT1  F351 poised to be the next-generation of fibrosis therapy  
 
 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)  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  Fibrosis  GSPT1 
 
 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. HQ and integrated U.S. and China R&D  Revenues to Support Operations  ETUARYTM and anticipated F351 sales in China expected to cover operation expenses to support early-stage R&D  1  2  3  4 
 
 Thank You! 
 
 1  Appendix 
 
 CG923308: CDK2-Cyclin E Dual Degrader On-Target Activity Promotes Growth Inhibition  Potent and Selective Degradation Profile  Overcome Feedback Induction of Cyclin E1  Induced Potent Growth Inhibition  A next-generation CDK2 targeted strategy designed to overcome CDK4/6i or ET resistance in breast cancer 
 
 CG923308 Demonstrates Anti-Cancer Efficacy in Resistant Preclinical Models  Minimum Effective Dose is 5~30 mg/kg QD (Human Equivalent Dose: 25~160 mg/day)  HR+HER2- breast CDX  CCNE1-Amplified Solid Tumors  A  CDK4/6i-Resistant HR+HER2- Breast Cancers  B  HR+HER2- breast PDX  4/5 CR  All doses were well tolerated in animals, with no significant body weight loss observed during the studies   TGI (%) = [1-(Ti-T0)/ (Vi-V0)] ×100% (If Ti>T0); TGI (%) = [1-(Ti-T0)/ (T0)] ×100% (If Ti<T0)  Ti is the tumor volume of treatment group, T0 is the tumor volume of the treatment group on the first day of treatment; Vi is the tumor volume of vehicle control group, V0 is the tumor volume of the vehicle group on the first day of treatment.  INCB: INCB123667 at 30 mg/kg, a CDK2 inhibitor at Phase III  CG923308：5-50 mg/kg  TQB3616: a CDK2/4/6 inhibitor approved by NMPA  TGI (%) = [1-(Ti-T0)/ (Vi-V0)] ×100% (If Ti>T0); TGI (%) = [1-(Ti-T0)/ (T0)] ×100% (If Ti<T0) 
 
 CDK2-Cyclin E Protein Degradation in Preclinical Model Tumors  Orally administrated CG923308 induces CDK2-cyclin E degradation in tumors 
 
 CG620953 Demonstrates Favorable Safety and PK  30  FAVORABLE SAFETY PROFILE  FAVORABLE PK PROPERTIES  Favorable Safety Signals  No genotoxicity, no hERG inhibition, and no cardiotoxicity in in vitro and in vivo studies  No Off-target Liabilities Identified  Clean KinomeScan and proteomics profile with No neosubstrate degradation  Low CNS Liability  Minimal brain penetration   Preliminary safety data from 4 species (rodent and non-rodent) reveal a wide safety margin.  Species  Dose  (mg/kg)  AUC(last)  (hr*ng/mL)  F (%)  Mouse  30  27,232  ~100  Rat  10  2,754  31.9  Dog  10  2,536  37.2  Monkey  25  8,826  25.4  Oral Administration  Moderate-to-high oral bioavailability  Low-to-moderate clearance rate  No CYP inhibition  Non-human primates 
 
 31  Non-Opioid Franchise in Cancer Pain  Notes:  Custom Market Insights, 2024  Gyre/Cullgen 8-K, Jun 2, 2026  Nexalis Investor Announcement, Apr 19, 2026  Dogwood 10-K, Mar 18, 2026  Cocco, Scaltriti & Dri/on, Nat Rev Clin Oncol, 2018  Gyre/Cullgen 8-K, Jun 2, 2026  Pfizer tanezumab Phase III cancer bone pain trials  Gyre/Cullgen 8-K, Mar 2, 2026  >$11Bn  Global Cancer Pain Market by 2028 (1)  The NGF / TrkA Pathway is a Key Driver of Cancer Pain  of patients treated with opioids for cancer-induced bone pain report continued bone pain (2)  70%  of cancer patients experience breakthrough cancer pain (3)  40‒80%  new cases of chemotherapy-induced neuropathic pain annually worldwide (4)  ~3MM  Tanezumab (anti-NGF antibody) Showed Pain Reduction in Phase III Cancer Bone Pain Trials (7)  Cancer cells produce NGF,  activating TrkA on sensory nerves in bone  TrkA mutations cause congenital insensitivity to pain (CIPA) - genetic validation (5)  Blocking the NGF / TrkA pathway reduces cancer bone pain (6)  1  2  3  Large, Underserved Market  Validated Target In Cancer Pain 
 
 CG001419 Degrades TRK Proteins in Neurons and Neuron-like Cells  CG001419 (nM)  0  0.6  1.25  2.5  5  10  20  40  80  Lane  1  2  3  4  5  6  7  8  9  CG001419 (nM)  0  2.5  5  10  20  40  80  Ent.  Lane  1  2  3  4  5  6  7  8  TRKB  TRKB  TRKC  TRKC  TRKA  TRKA  Tuj1  CG001419 degrades TRKs in mouse neurons  B. CG001419 degrades TRKs in NT2-derived human neurons  Tubulin  C. CG001419 degrades ectopically expressed dog TRKs in dog MDCK cells  Cell line  MDCK-TRKA  CG001419 (nM)  0  2.1  6.2  18.5  55.6  166.7  500  Lane  1  2  3  4  5  6  7  TRK  Tubulin  MDCK-TRKC  0  2.1  6.2  18.5  55.6  166.7  500  1  2  3  4  5  6  7  MDCK-TRKB  0  2.1  6.2  18.5  55.6  166.7  500  1  2  3  4  5  6  7 
 
 CG001419 Does Not Penetrate Into the Brain  Conc. (ng/ml)  Heart  Liver  Spleen  Lung  Kidney  Muscle  Fat  Brain  Tumor  Plasma  Brain/  Plasma  Tumor/  Plasma   0.5 h  384   1835   443   637   318   40   64   5   32   447   0.011  0.072  4 h  1875   6340   1945   3320   4545   552   635   18   456   1715   0.010  0.266  24 h  124   299   90   295   246   92   73   4   277   58   0.066  4.775 
 
 CG001419 Shows PK-driven Analgesic Activity 
 
 CG001419 Shows Significant Analgesic Activity in Two Rat Models of OA Pain  A. Monoiodoacetate (MIA)-induced OA model, continuous dosing  B. Total medial meniscectomy (TMM)-induced OA model, once per week dosing 
 
 CG001419 Shows Significant and Dose-Dependent Analgesic Activity in a Surgical Pain Model  Baseline  Day 0  Rats get a 1-cm cut at left hind paw   Day 1  Day 1  The 1st dose immediately after surgery  Day 1 qd  The 1st assessment, 4~5 hrs after surgery   Day 2 bid  Assess daily, 4~5 hrs after the morning dose  Day 3  bid  Assess daily, 4~5 hrs after the morning dose  Day 4  bid  Assess daily, 4~5 hrs after the morning dose  Day 5  bid  Assess daily, 4~5 hrs after the morning dose  Day 6 qd  Assess daily, 4~5 hrs after the morning dose 
 
 CG001419 Shows Significant Analgesic Activity in a Rat Neuropathic Pain Model (sciatic nerve incision)  A. Mechanical allodynia   B. Heat stimulus  po/bid  po/bid 
 
 CG001419 Does Not Affect Mouse Mobility in a Balance Beam Test  B. CG1419 does not impair mouse crossing through balance beams of 4 different diameters (0.8-2.0 cm)  Gent.: Gentamycin  (positive control)  Data shown as mean±SD, One-way ANOVA with Turkey’s test; * compared with gentamicin group, *, **, ***: P<0.05, <0.01, <0.001 repectively; ^:compare with vehicle group, P<0.05.  A. TRK inhibition may induce ataxia via impacting on the peripheral nerve system in human  Liu et al., (2020) Ann. Oncol. PMID: 32422171 
 
 IV Administered CG9301 Shows Efficacy in Leukemia CDX and Orthotopic PDX Models  A. CG9301 induces significant regression in subcutaneous leukemia xenograft models  B. CG9301 induces significant reduction of tumor burden in an orthotopic AML PDX model  
 
 CG9301 shows synergistic interaction with SOC venetoclax and azacitidine in AML models 
 
 Epigenetic Factor DAC Demonstrates Potent and TAA-dependent Target Degradation and Cell Killing     Cell Line  TAA Positive Cell Line  Compounds  (nM）  DMSO  Degrader  DAC  DMSO  Linker-degrader  DMSO  0.01  0.1  1  10  100  0.01  0.1  1  10  100  0.01  0.1  1  10  100  Lane  1  2  3  4  5  6  7  8  9  10  11  12  13  14  15  16  17  18  Cell Line  TAA Negative Cell Line  Compounds  (nM）  DMSO  Degrader  DAC  DMSO  Linker- degrader  mAb  DMSO  0.01  0.1  1  10  100  0.01  0.1  1  10  100  0.01  0.1  1  10  100  10  100  Lane  1  2  3  4  5  6  7  8  9  10  11  12  13  14  15  16  17  18  19  20  p300  CBP  Actin  p300  CBP  GAPDH  A. Gyre’s epigenetic factor DAC induces potent protein target degradation in a TAA-dependent manner in vitro  B. Gyre’s epigenetic factor DAC kills cancer cells in a TAA-dependent manner   Linker-degrader (IC50: 24.25 nM)  Naked antibody (IC50: > 1uM)  Degrader (IC50: 0.08nM)  DAC (IC50: 0.08 nM)   TAA Positive Cells  Linker-degrader (IC50: 103 nM)  Naked antibody (IC50: > 1uM)  Degrader (IC50: 0.61 nM)  DAC (IC50: 138 nM)   TAA Negative Cells  Protein 1  Protein 2  Protein 1  Protein 2 
 
 ETUARY™ Lifecycle Management: Potential to Drive Market Expansion Via Label Expansion  Ref 1. Bai et al. (2025) https://pubmed.ncbi.nlm.nih.gov/39546810/  Ref 2. Hou et al (2025) https://pubmed.ncbi.nlm.nih.gov/41207313/  B. A phase 2 trial demonstrates efficacy of ETUARY™ in treating radiation-induced lung injury (RILI)2  A. Preclinical studies demonstrate efficacy of ETUARY™ in treating pneumoconiosis1  Gross Vital Capacity  Gas Transfer Efficiency  Airway Resistance / Flow  BIBF: nintedanib; DLCO: Diffusing Capacity of the Lung for Carbon Monoxide ; IC: Inspiratory Capacity;   FEV: Forced Expiratory Volume; FVC: Forced Vital Capacity; PFD: Pirfenidone; Si: Silicosis  Operating Lung Volume  Gross Vital Capacity  Airway Resistance / Flow 
 
 F351 / Hydronidone Targets CHB Fibrosis – an Untapped Market in China  Notes: The Fourth National Serological Survey on HBV in China (2020) provided baseline HBV prevalence data. The 60-70MM total HBV cases and F2-F4 fibrosis estimates are derived using internal modeling based on this survey’s fibrosis prevalence rates and awareness levels.  43  Total HBV Infected Population in China  Diagnosed Compensated F-2-F4  Progressed to Significant Fibrosis Population  Chronic Hepatitis B (CHB) Diagnosed Population  60 – 70MM  14.7MM  5.5MM  2.6MM  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  The Market for CHB-associated liver fibrosis is significantly unmet  Current standard of treatment, e.g. entecavir, tenofovir, focuses on only reducing liver inflammation  Patients with F2 – F4 Fibrosis are at a high risk of progression to cirrhosis and HCC, major causes of liver-related mortality 
 
 44  F351: Anti-fibrotic Activity Unlike Existing and Advanced Clinical MASH Therapies  Drug  MOA  Status  MASH Stage  Fibrosis Mechanism  Resmetirom  (Rezdiffra®)  THR-β agonist  FDA/EMA  Approved  F2-F3  Indirect – reduces lipotoxicity and improves mitochondrial function in hepatocytes  Semaglutide  (Wegovy®)  GLP-1 receptor agonist  FDA Approved  F2-F3  Primarily indirectly through systemic weight loss  Tirzepatide  (Zepbound®)  Dual GIP/GLP-1 receptor agonist  Phase 3  F2-F3  Primarily indirectly through systemic weight loss  Efruxifermin  (AKR-001)  FGF21 analog (Fc-fusion protein)  Phase 3  F2-F3; F4 (cirrhosis arm)  Dual direct + indirect antifibrotic  Lanifibranor  Pan-PPAR (α/δ/γ) agonist  Phase 3  F2-F3  Partial direct + indirect antifibrotic  Survodutide  (BI 456906)  Dual glucagon/GLP-1 agonist  Phase 3  F1-F3  Primarily indirectly through systemic weight loss  F351  TGF-β / p38γ / Smad7 modulator  NDA under review by NMPA (CHB-associated liver fibrosis); Phase 1 complete (MASH)  F2-F3 or F4  Direct antifibrotic targets the primary drivers of collagen deposition and fibrotic scarring in the liver.   Source: CapIQ, Company Filings  F351 is the only therapeutic that has met the primary endpoint for reduction of fibrosis in a phase 3 clinical trial 
 

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