Gyre Therapeutics, Inc. · NASDAQ:GYRE
Gyre Therapeutics — Investor Presentation (May 2026)
21 slides from Gyre Therapeutics's investor presentation, May 14, 2026
Slide 1: A Fully-integrated Biopharmaceutical Company Focused on Fibrosis, Inflammatory Diseases and Cancer
A Fully-integrated Biopharmaceutical Company Focused on Fibrosis, Inflammatory Diseases and Cancer May 2026
Slide 2: Forward-looking statements
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
Slide 3: Gyre Therapeutics: At-A-Glance Including Recently Announced Acquisition of Cullgen
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 W
Slide 4: Key Value Drivers
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-mi
Slide 5: China Innovation & Validation Engine: Driving Strategic Value and Efficiency
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 Fil
Slide 6: US Management Team
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 In
Slide 7: Targeted CDK2-Cyclin E Protein Degradation for Cancer Therapy
7 Targeted CDK2-Cyclin E Protein Degradation for Cancer Therapy Expanding the drug design paradigm
Slide 8: Hijacking the Ubiquitin Proteasome System to Target Undruggable Disease-causing Proteins
Hijacking the Ubiquitin Proteasome System to Target Undruggable Disease-causing Proteins
Slide 9: Cullgen Was Founded on Pioneering Research in the Ubiquitin Pathway and Targeted Protein Degradation
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 Dis
Slide 10: CDK2-Cyclin E Drives Solid Cancers and Breast Cancer Resistant to CDK4/6 Inhibitors
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 overexp
Slide 11: CDK2-Cyclin E Degrader for Treating CCNE1-amplified Solid Cancers and Breast Cancer
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
Slide 12: CG923308 Induces Potent and Selective CDK2-Cyclin E Degradation in Multiple Cancer Types
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
Slide 13: CG923308 Induced Degradation Is Mediated Through Cullin, Proteasome and CRBN
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 inhib
Slide 14: CG923308 Induces Senescence, Cell Cycle Arrest and Growth Inhibition of CCNE1-amp Solid Tumors
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 DMS
Slide 15: CG923308 Induces Cell Senescence and Growth Inhibition of HR+/HER2- Breast Cancer Resistant to CDK4/6 Inhibitors
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 CG92
Slide 16: CG923308 Shows Superiority Over Phase 2/3 CDK2 Inhibitors In Vitro
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
Slide 17: CG923308 Is Orally Bioavailable Across Preclinical Species
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
Slide 18: CDK2-Cyclin E Degrader Shows More Potent In Vivo Efficacy in CDX Models
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 INCB12
Slide 19: CDK2-Cyclin E Degrader Shows More Potent In Vivo Efficacy in PDX Models
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 wit
Slide 20: CDK2-Cyclin E Degrader: A Potential Therapeutic for Multiple Solid Cancers
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 soli
Slide 21: Nw THERAPEUTICS
e> Nw THERAPEUTICS ‘ey Gyre