Beyondspring, Inc. · NASDAQ:BYSI
Beyondspring — Investor Presentation (February 2026)
43 slides from Beyondspring's investor presentation, February 2026
Slide 1: Transforming Cancer Care with Immune-modulating Therapies
Transforming Cancer Care with Immune-modulating Therapies February 2026 NASDAQ: BYSI Non-Confidential
Slide 2: Disclaimer
Disclaimer This presentation has been prepared for informational purposes only. No money or other consideration is being solicited, and if sent in response, will not be accepted. This presentation shall not constitute an offer to sell, or the solicitation of an offer to buy, any securities, nor shal
Slide 3: Investment Highlights
Investment Highlights First-in-class small molecule: a unique, reversible tubulin depolymerizing agent Plinabulin: Unique with MoA of dendritic cell maturation and prevention chemotherapy induced Immune Modulator neutropenia >700 cancer patients treated with good tolerability; Demonstrated overall s
Slide 4: Post-ICI Landscape: Severe Unmet Medical Need
Post-ICI Landscape: Severe Unmet Medical Need Immune Checkpoint Inhibitors (ICIs) Have Transformed Cancer Care Around US$60B/year Success Story with a Critical Gap • Approved in 20+ cancer types • Nearly $60B in global annual sales • Have redefined first-line treatment in NSCLC and other solid tumor
Slide 5: Plinabulin: Unique Dual Mechanism with Immune and Safety Benefits
Plinabulin: Unique Dual Mechanism with Immune and Safety Benefits • Reversible tubulin binder – distinct from taxanes, vincas, or colchicine; does not disrupt microtubule dynamics • Immune modulation – induces dendritic cell maturation and primes T cells by activating GEF-H1 • Neutropenia mitigation
Slide 6: Plinabulin, a Differentiated Late-Stage Oncology Asset with Broad Potential
Plinabulin, a Differentiated Late-Stage Oncology Asset with Broad Potential • Robust clinical foundation: >700 cancer patients treated with good tolerability. • Unique MoA: Brain-penetrating, reversible tubulin binder driving dendritic cell maturation and T cell activation (Chem 2019, Cell Reports 2
Slide 7: Plinabulin Monohydrate is a Brain-Penetrant, Unique Tubulin Depolymerizing Agent
Plinabulin Monohydrate is a Brain-Penetrant, Unique Tubulin Depolymerizing Agent which induces “Dendritic Cell or DC Maturation via GEF-H1 release” Plinabulin Monohydrate is a unique tubulin binder1 Plinabulin release GEF-H1 from microtubule, activates In WT DC cells, plinabulin can induce DC matura
Slide 8: Plinabulin's DC Maturation MoA Could Mitigate Acquired Resistance to ICI
Plinabulin’s DC Maturation MoA has the Potential to Mitigate Acquired Resistance to Immune Checkpoint Inhibitors (ICI) • Plinabulin MoA DC maturation: Dendritic cells (DCs) are the most potent antigen-presenting cells and can prime T cell function to strengthening the cancer- immunity cycle. • Syner
Slide 9: Plinabulin-Responding Patients After ICI Failure Show Rapid DC Maturation
Plinabulin-Responding Patients After ICI Failure Show Immune Activation Evidenced by Rapid DC Maturation in the Peripheral Blood CCR7, CD80 and CD83 are rapidly upregulated at cycle 1 Day 4 in responding (PR + SD) patients1 Dendritic Cell Maturation & Migration 1. Lin et al., Med 6(10):100752 (2025)
Slide 10: Plinabulin Unique MoA in Reducing Chemotherapy-induced Neutropenia
Plinabulin Unique MoA in Reducing Chemotherapy-induced Neutropenia Demonstrated in 6 clinical studies for docetaxel and other chemo with early onset action Plinabulin: non-G-CSF based treatment for CIN1 Different from G-CSF, Plinabulin cause limited bone - Generates HSPC, including LSK cells pain an
Slide 11: Plinabulin Differentiated Profile
Plinabulin Differentiated Profile Mechanism Supported | Clinically Validated | Favorable Safety | Scalable Opportunity Dual Mechanism Superior Safety Profile 1 6 Significantly Lower Neutropenia and Binds Tubulin & Matures Dendritic Cells (vs. standard mitotic arrest) Bone Marrow Toxicity Microenviro
Slide 12: Plinabulin Clinical Studies in Multiple Cancers
Plinabulin Clinical Studies in Multiple Cancers >700 cancer patients treated with Plinabulin with good tolerability Indication/Target Program Preclinical Phase 1 Phase 2 Phase 3 Registration Trial Name / Collaborator NSCLC Study 103 (DUBLIN-3) Plinabulin + Docetaxel Late stage (2nd/3rd line) - OS, P
Slide 13: Post-ICI NSCLC: A Large, Growing and Unmet Clinical Challenge
Post-ICI NSCLC: A Large, Growing and Unmet Clinical Challenge • Limited treatment options after PD-1/L1 inhibitor progression • Chemotherapy remains the main option, with poor outcome and high toxicity • Urgent need for differentiated therapy with immune re-sensitization
Slide 14: Docetaxel Remains a Global Standard of Care in Post-ICI NSCLC
Docetaxel Remains a Global Standard of Care (SOC) in Post-ICI NSCLC, EGFR WT, Despite Limited Benefit and Substantial Toxicity Industry-wide Phase 3 Trials Summary Current Standard of Care 11 Phase 3 Studies with no OS Benefit vs. Docetaxel Docetaxel Overview • 7 global trials including ADCs and ant
Slide 15: Plinabulin and Docetaxel Demonstrated Significant OS Benefit in Dublin-3
“Plinabulin and Docetaxel” Demonstrated Significant OS benefit vs. Docetaxel in a Global Phase 3 Study with Stage IIIb/IV NSCLC EGFR WT Patients (Dublin-3, n=559) Docetaxel + Plinabulin vs. Docetaxel + Placebo in Patients with EGFR Wild-Type NSCLC Study Plan Primary endpoint Secondary endpoints • OR
Slide 16: Plinabulin + Docetaxel Met Primary Endpoint of OS and Secondary Endpoints
Plinabulin + Docetaxel vs. Docetaxel (n=559) Met its Primary Endpoint of OS and Secondary Endpoints of PFS, ORR, and Grade 4 Neutropenia Reduction Plinabulin Significantly Reduced Plinabulin and Docetaxel Showed Significant Grade 4 neutropenia of Docetaxel Improvement in Long-term OS Rate - Double 2
Slide 17: Plinabulin + Docetaxel is Safer Than Docetaxel Adjusted by Exposure
Plinabulin + Docetaxel (DP) is Safer Than Docetaxel (D) Adjusted by Exposure The combination has Significant lower Grade 3 or 4 exposure-adjusted event rates vs. Docetaxel Grade 3 or 4 Event Rates Grade 4 Only Event Rates Adjusted by Exposure Adjusted by Exposure DP (n=274) D (n=278) DP (n=274) D (n
Slide 18: Dublin-3: Post-hoc Analysis in Mechanism-Based Population
Dublin-3: Post-hoc Analysis in Plinabulin Mechanism-Based Population in 2L/3L Non-squamous EGFR WT NSCLC and Progressed on PD-1/L1 Inhibitors Non-squamous Non-squamous, progressed on ICI mOS extension of 2.5 months (Plinabulin MoA-enriched population) (DP 11.4 vs. D 8.8 months, HR 0.72) mOS extensio
Slide 19: Study 303 in 2L/3L Metastatic NSCLC Progressed on PD-1/L1
Study 303 (Plinabulin + Docetaxel + PD-1) in 2L/3L Metastatic NSCLC Progressed on PD-1/L1 Inhibitors Shows Consistent Data as Dublin-3 Analysis Best Change (%) in Target Lesions Primary Endpoint (n=47) Confirmed ORR（RECIST 1.1） 18.2% Secondary Endpoint Median PFS（RECIST 1.1） 7.0 months 16 months+, M
Slide 20: Planned Dublin-4 Study As a Confirmatory Phase 3 Study
Planned Dublin-4 Study As a Confirmatory Phase 3 Study Plinabulin Mechanism-Enriched Patients Dublin-4: “Plinabulin + Docetaxel” vs. “Docetaxel” in 2L/3L non-squamous NSCLC, EGFR/ALK/ROSm/RET Wild Type, progressed on PD-1/L1 with PFS ≥ 3 months ✓ Defined, homogeneous group with clear unmet need and
Slide 21: Confirmatory Phase 3 Study Design for Dublin-4
Confirmatory Phase 3 Study Design for Dublin-4 Active Group ✓ Advanced and Metastatic non-squamous Primary endpoint: OS EGFR, ALK, ROS, RET WT NSCLC Docetaxel (75 mg/m2) day 1 + patients who have progressed after prior immunotherapy (anti-PD-(L)1 antibody) Plinabulin (30 mg/m2) day 1 and 8 Secondary
Slide 22: Dublin-3: Well-tolerated and Manageable Safety Profile
Dublin-3: Plinabulin + Docetaxel with Well-tolerated and Manageable Safety Profile Docetaxel + Placebo Docetaxel + Plinabulin N=278 N=274 n (%) n (%) TEAE All grades Grade 3 Grade 4 All grades Grade 3 Grade 4 Any 276 (99.3) 85 (30.6) 119 (42.8) 273 (99.6) 141 (51.5) 52 (19.0) Hematological Anemia 12
Slide 23: Plinabulin + Docetaxel: Addressing Unmet Needs in 2L/3L NSCLC
Plinabulin + Docetaxel: Addressing Unmet Needs in 2L/3L NSCLC, EGFR WT, Progressed on PD-1/L1 Inhibitor, with Potential Positive Benefit/Risk Ratio Severity of Current SOC Potential Solution Unmet Need - Docetaxel - Plinabulin + Docetaxel Lack of durable response post- Strong immune re-priming and a
Slide 24: First-in-Class Agent Plinabulin: Potentially Transforming Oncology Treatment
First-in-Class Agent Plinabulin: Potentially Transforming Oncology Treatment with Novel Mechanisms and Clinically Meaningful Benefits in NSCLC and Beyond + + SIMPLE SAFE DURABLE Easy to use Safety Benefit Clinical Benefit Day 1 and 8 use in a Reduce AEs including Overall survival and cycle, intraven
Slide 25: De Novo Molecular Glues for Protein Targets Beyond the Reach of Traditional Therapies
De Novo Molecular Glues for Protein Targets Beyond the Reach of Traditional Therapies
Slide 26: SEED: A Clinically Advancing Molecular Glue Company
SEED: A Clinically Advancing Molecular Glue Company with Validated Pharma Partnerships and Near-term Data Targeted protein degradation (TPD) focused on developing novel “molecular glues” TPD Potential ⬢ Addressing 80% of disease-causing proteins considered “undruggable” by traditional methods ⬢ Targ
Slide 27: Experienced Team with Successful Track Record
Experienced Team with Successful Track Record Founders Management Team Board Members • Nobel Prize winner • 40 INDs • Experienced science, • Pioneers in TPD • 12 NDAs business and legal experts • Board members from Lilly and Eisai Non-Confidential 27
Slide 28: Pioneers of E3 Biology as Scientific Foundation for SEED's TPD 2.0 Strategy
Pioneers of E3 Biology as Scientific Foundation for SEED’s TPD 2.0 Strategy Pioneering structural biology solving both major E3 classes – HECT and CRL (RING-based) – enabling rational E3 selection Avram Hershko, MD, PhD Nobel Laureate Co-discovered ubiquitin–mediated protein degradation, establishin
Slide 29: RITE3: A Rational Platform for E3 Selection and Molecular Glue Engineering
RITE3TM : A Rational, Multi-Dimensional Platform for Precise E3 Selection and Molecular Glue Engineering Target-Centric Discovery - Starts with disease-causing protein (POI) - Leverages weak basal interactions of selected E3 and POI, resulting in Higher HTS hit rates Expansive E3 Ligase Coverage and
Slide 30: Integrated Structural, Cellular, and Biophysical Capabilities
Integrated Structural, Cellular, and Biophysical Capabilities to Engineer Potent Molecular Glues LumIDTM: identify the right E3 Quasi-Interface Analyses Basal Affinity Validation near POI in live cell Computational and structural biology Cell biology: real-time monitoring of Biophysics: distinguishi
Slide 31: Advancing Six High-Value TPD Programs with Clinical Readouts Beginning in 2026
Advancing Six High-Value TPD Programs with Clinical Readouts Beginning in 2026 Target Target E3 Ligase Molecular IND Indication Lead ID IND Filing Phase 1 Milestones Protein Selection ID Glue HTS Candidate ✓ IND cleared with US and China FDA in 2H 2025 RBM39 ST-01156 ✓ First patient dosed in Jan. On
Slide 32: RBM39: A clinically validated splicing dependency across multiple cancers
RBM39: A clinically validated splicing dependency across multiple cancers BIOLOGY ⬢ Master regulator of oncogenic RNA Why it matters splicing programs essential for tumor survival ⬢ Splicing machinery is non-enzymatic and historically undruggable MECHANISM ⬢ Molecular glue-mediated degradation via W
Slide 33: Ewing Sarcoma: Cleanest Biological Proof Point for RBM39 Degradation
Ewing Sarcoma Is A Fusion-driven Disease with No New Drugs in the Complete tumor 3500 regression in 3000 Tumor volume (mm3) Past 30 Years Ewing Sarcoma 2500 2000 Rare pediatric and orphan 1500 cancer designation by US FDA 1000 500 The cleanest biological proof 0 point for RBM39 degradation. 0 5 10 1
Slide 34: RBM39 Drives Progression in Rare and Large Tumor Indications
RBM39 Drives Progression in Rare and Neuroblastoma Large Tumor Indications Sarcoma Hepatocellular Colorectal Cancer Carcinoma SARC LIHC CRC 1.0 RBM39 1.0 RBM39 1.0 HR = 1.48 (1.17-1.88) Low Low P = 0.0012 0.8 High 0.8 High 0.8 Survival probability Survival probability Probability 0.6 0.6 0.6 0.4 0.4
Slide 35: Strong Anti-tumor Activity in RBM39-dependent Liver & Colon Cancer Models
Strong Anti-tumor Activity in RBM39-dependent Liver & Colon Cancer Models Colon Cancer RBM39 high expression in colon Liver Cancer RBM39 high expression in liver cancer (T), not in normal tissue (N) cancer (T), not in normal tissue (NT) 1 2 3 4 5 N T N T N T N T N T 1 2 3 4 5 6 T NT T NT T NT T NT T
Slide 36: Clear Value Path for ST-01156
Clear Value Path for ST-01156: Target Engagement, Dose Expansion, and Early Efficacy Readouts – First Patient Dosed in January 2026 Focus on MoA-based Indications, Accelerating Clinical Development • Rational clinical indications selection based on RBM39 Target Engagement • Orphan and large cancer i
Slide 37: Breakthrough Investments Highlight the Value of Molecular Glues and Degraders
Breakthrough Investments Highlight the Value of Molecular Glues and Degraders Discovery stage TPD assets Upfront payments of $35 - $60M and Nurix Closes $120 Million Financing to $500M - $5B in potential milestones. Support Protein Degradation Program Pre-IND / IND stage TPD assets $100- $300M in up
Slide 38: SEED Therapeutics: Why We Will Create Significant Value in 2026–2028
SEED Therapeutics — Why We Will Create Significant Value in 2026–2028 Clinically advancing first-in-class • ST-01156 IND cleared in the U.S. and China • First-in-human safety and target engagement data molecular glue degrader expected in 2026 • Solved structural biology of both major E3 classes: Sci
Slide 39: Thank You
Thank You General Inquiries: [email protected] Investor: [email protected] Media: [email protected] www.beyondspringpharma.com
Slide 40: Appendix
BeyondSpring Inc. Appendix
Slide 41: Seasoned Management Team with Deep Global Biopharma Expertise
Seasoned Management Team with Deep Global Biopharma Expertise Lan Huang, PhD June Lu, PhD John Mao, PhD Co-Founder, Chairman & Chief Executive Officer Chief Scientific Officer SVP, Development Biotech entrepreneur with 20+ years across Drug development leader with 25+ years’ Senior biotech developme
Slide 42: Proven Board with Global Biopharma and Financial Expertise
Proven Board with Global Biopharma and Financial Expertise Brendon Delaney Jen Majeti, PhD, MBA Lan Huang, PhD Mathew Kirkby, MA Patrick Fabbio Sihai Xu, MBA Director Director Co-Founder, Chairman and Director Director Director Chief Executive Officer Seasoned commercial leader Biotech investor and
Slide 43: Scientific Advisors with Global Oncology Leadership
Scientific Advisors with Global Oncology Leadership Adam Grippin, MD, PhD John Ruckdeschel, MD Stephen Lin, MD Trevor Feinstein, MD Alfred Zippelius, MD MD Anderson Cancer Center Fox Chase Cancer Center MD Anderson Cancer Center Piedmont Cancer Institute University Hospital Basel Physician-scientist