Beyondspring, Inc. · NASDAQ:BYSI
Beyondspring — Investor Presentation (August 2026)
37 slides from Beyondspring's investor presentation, August 2026
Slide 1: Transforming Cancer Care with Immune-modulating Therapies
Transforming Cancer Care with Immune-modulating Therapies Aug 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 Focused on developing transformative medicine for patients with unmet medical needs Plinabulin: Unique immune modulator with durable anti- cancer OS Efficacy and Safety in reducing CIN Plinabulin Dublin-4 Confirmatory Phase 3 study: 2/3L non- squamous EGFR WT NSCLC post-ICI Equ
Slide 4: 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 5: 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 6: 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 releases GEF-H1 from microtubule, activates In WT DC cells, plinabulin can induce DC maturation, Plinabulin Monohydrate is a unique tubulin b
Slide 7: Plinabulin Displays GEF-H1-mediated Mechanism-of-Action
Plinabulin Displays GEF-H1-mediated Mechanism-of-Action • By depolymerizing microtubules, plinabulin activates GEF-H1, a C1 domain-associated RhoA activator, in a highly regulated and spatio- temporal dependent manner.1 • As a GEF-H1 agonist, plinabulin has the following anti-cancer mechanism: a) GE
Slide 8: Plinabulin's Immunomodulation and Neutropenia-Mitigating Activities Position it as a Valuable Addition
Plinabulin’s Immunomodulation and Neutropenia-Mitigating Activities Position it as a Valuable Addition for Combination Regimens Antigen-Presenting Cell (APC) Tumor Vasculature Improves safety* Plinabulin induces Plinabulin targets Plinabulin reduces chemotherapy- DC maturation + tumor vasculature in
Slide 9: Plinabulin: Potential "Pipeline in a Drug"
Plinabulin: Potential “Pipeline in a Drug” 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, PFS, ORR benefit 1 Plinabulin alone or + Studies 105 & 106 2, 3 CIN Preven
Slide 10: Post-ICI EGFR WT NSCLC: A Large, Growing and Unmet Clinical Challenge
Post-ICI EGFR WT NSCLC: A Large, Growing and Unmet Clinical Challenge • Limited treatment options after PD-1/L1 inhibitor progression • Docetaxel remains the main option, with poor outcome and high toxicity • Urgent need for differentiated therapy with immune re-sensitization
Slide 11: 12 Phase 3 Studies with No OS Benefit vs. Docetaxel in Post-ICI EGFR WT NSCLC
12 Phase 3 Studies with No OS Benefit vs. Docetaxel in Post-ICI EGFR WT NSCLC Phase 3 study Patient Population Study Design median OS (M) OS HR P value Non-squamous SAPPHIRE 2/3L，non-squamous Sitravatinib (TKI) + Opdivo (PD-1) vs. docetaxel 12.2 vs. 10.6 p=0.144 HR=0.86 HR=0.98 Lenvima (TKI) + pembr
Slide 12: Dublin-3 Study Design: Docetaxel + Plinabulin vs. Docetaxel + Placebo
2/3L EGFR WT NSCLC post ICI with severe unmet medical needs with docetaxel remains SOC; Dublin-3 study demonstrated OS benefit vs. docetaxel Docetaxel + Plinabulin vs. Docetaxel + Placebo in Patients with EGFR WT NSCLC Study Plan Primary endpoint Secondary endpoints • ORR, PFS • DoR • Global, random
Slide 13: 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 14: Plinabulin + Docetaxel (DP) is Safer Than Docetaxel (D) 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 15: Dublin-3: Post-hoc Analysis in Non-squamous EGFR WT NSCLC Progressed on PD-1/L1
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, progressed on ICI Non-squamous (Plinabulin MoA-enriched population) mOS extension of 2.5 months mOS extension of 4.1 months (DP 11.4 vs. D 8.8 m
Slide 16: Study 303 in 2L/3L Metastatic NSCLC Shows Consistent Data as Dublin-3
Study 303 in 2L/3L Metastatic NSCLC Progressed on PD-1/L1 Inhibitors Shows Consistent Data as Dublin-3 Analysis Plinabulin + Docetaxel + PD-1 Inhibitor (n=47) Best Change (%) in Target Lesions ASCO 2026 Primary endpoint: 18.2% Confirmed ORR（RECIST 1.1） Secondary Endpoint Median PFS（RECIST 1.1） 7.0 m
Slide 17: Plinabulin Clinical Efficacy Supports Dublin-4 Patient Selection
Plinabulin Clinical Efficacy Supports Dublin-4 Patient Selection Dublin-3 efficacy with the post-ICI subgroup signal and Study 303 efficacy provide the clinical rationale for Dublin-4 for Plinabulin-mechanism targeted population: • Non-squamous NSCLC + Progressed on ICI with “acquired resistance” Du
Slide 18: Confirmatory Phase 3 Study Design for Dublin-4
Confirmatory Phase 3 Study Design for Dublin-4 Active Group ✓ Advanced and Metastatic non-squamous EGFR, ALK, ROS1, RET WT NSCLC Docetaxel (75 mg/m2) day 1 + Primary endpoint: OS patients who have progressed after prior immunotherapy (anti-PD-(L)1 antibody) Plinabulin (30 mg/m2) day 1 and 8 with pla
Slide 19: Dublin-3: Plinabulin + Docetaxel with 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 20: 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 - Plinabulin + Docetaxel - Docetaxel Lack of durable response post- Strong immune re-priming and a
Slide 21: Plinabulin Future Development: ADC Combination, IO Combination
Plinabulin Future Development: ADC Combination, IO Combination Preclinical ADC Combination Data Human Evidence After ICI Failure Dato-DXd ± PD-1 in hTROP2-MC38 / hPD-1 mice 8 cancers failed prior ICI – NSCLC, Head & Neck, Hodgkin lymphoma CR 6/10 Survival ↑ CD8/Treg ↑ DCR 54% C1D4 DC Mature Dato-DXd
Slide 22: First-in-Class Agent Plinabulin: Potentially Transforming Oncology Treatment
First-in-Class Agent Plinabulin: Potentially Transforming Oncology Treatment 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, intravenous chemotherapy-induced durable response infusion of 30-
Slide 23: Create The Glue, Capture The Protein, Eliminate The Disease
Create The Glue Capture The Protein Eliminate The Disease De novo molecular glues for protein targets beyond the reach of traditional therapies
Slide 24: SEED Therapeutics – Category-defining Molecular Glue Company
SEED Therapeutics – Category-defining Molecular Glue Company 1 Molecular glue field with clinical validation + value recognition 4 Clinical proof of mechanism in RBM39 target engagement ST-01156, novel RBM39 degrader: Rapid enrollment with leading US institutions, Molecular glue and TPD validation k
Slide 25: SEED Was Co-founded By Pioneers in Targeted Protein Degradation and Eli Lilly
SEED Was Co-founded By Pioneers in Targeted Protein Degradation and Eli Lilly ⬢ Scientific capability to use >600 E3 ligases, which consists only 2 structural classes of HECT and RING, solved first by co-founders. Nobel Laureate Avram Hershko, MD Lan Huang, Ph.D. ➢ Novel E3s or RITE3 use can increas
Slide 26: SAB with Deep Expertise in Science, Clinical, AI and Business
SAB with Deep Expertise in Science, Clinical, AI and Business George Demetri, MD Avram Hershko MD Ning Zheng, PhD Michele Pagano, MD Mansuo Shannon, PhD Alan Roemer, MBA, MPH Pranam Chatterjee, PhD SAB Chair, clinician with Co-Founder and SAB Co-Founder and SAB Co-Founder and SAB SAB Member, Neuro-e
Slide 27: Highly Experienced Board of Directors
Highly Experienced Board of Directors Lan Huang, PhD James Tonra, PhD Linus Lin, PhD Yoshiharu Mizui, PhD Jackson Tai Ko-Yung Tung, JD Co-Founder, CEO and President, CSO and Director Director Director Director Director Chairman 20+ years of drug discovery AVP of Molecular Discovery Founder and Presi
Slide 28: SEED Built The TPD 2.0 Engine To Find The Optimal Ligase
SEED Built The TPD 2.0 Engine To Find The Optimal Ligase and Degrade Any Disease-causing Protein SEED's RITE3 platform unlocks access to more than 600 ligases encoded in the human genome. Then designs custom molecular glues to bind them. More ligases. Better matches. Higher hit rates. Pathogenic Pro
Slide 29: SEED's Internal Pipeline Spans Three Therapeutic Areas
SEED’s Internal Pipeline Spans Three Therapeutic Areas SEED Therapeutics is advancing 5 wholly-owned programs in oncology, neurodegeneration, and immunology, powered by 4 novel E3 ligases discovered on our proprietary platform. ONCOLOGY ONCOLOGY NEURODEGENERATION NEURODEGENERATION IMMUNOLOGY RBM39 U
Slide 30: 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 31: ST-01156: Total Tumor Regression In Vivo
ST-01156: Total Tumor Regression In Vivo. FDA Orphan + Rare Complete tumor 3500 regression in 3000 Tumor volume (mm3) Pediatric Disease Designation Ewing Sarcoma 2500 2000 Rare pediatric and orphan 1500 The cleanest biological proof cancer designation by US FDA 1000 point for RBM39 degradation. 500
Slide 32: RBM39 Drives Progression For Rare and Large Cancer Indications
RBM39 Drives Progression For Rare and Large Neuroblastoma Cancer Indications with >1 Million Addressable Patients 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 prob
Slide 33: Ewing Sarcoma Proves The Mechanism. Liver and Colon Cancer Are The Market
Ewing Sarcoma Proves The Mechanism. Liver Cancer And Colon Cancer — More Than 700,000 Patients — Are The Market. 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
Slide 34: Quality And Efficient Execution of Phase 1a Clinical Study
Quality And Efficient Execution of Phase 1a Clinical Study Objectives Key Eligibility Safety, tolerability, PK, PD, recommended Age 18+ all solid cancers phase 2 dose (RP2D) and preliminary activity Age 16+ for Ewing sarcoma / signal detection Backfilling of lower doses: Priority cancers (Ewing, hep
Slide 35: Encouraging First-in-human Safety, Pharmacokinetics, And Proof of Mechanism
Encouraging First-in-human Safety, Pharmacokinetics, And Proof of Mechanism ST-01156 CLINICAL PROGRAM Oral, CNS-penetrant RBM39 molecular glue degrader • Phase 1 in advanced solid tumors • Dose escalation ongoing Safety & Tolerability Pharmacokinetics Target Engagement No DLTs On Track RBM39 OBSERVE
Slide 36: 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 Novartis Sticks With Orionis in Second Deal: $500M - $5B in potential milestones. $40 M upfront with total value up to $1.4 B Pre-IND / IND stage TPD assets $10
Slide 37: Thank You
Thank You General Inquiries: [email protected] Investor: [email protected] Media: [email protected] www.beyondspringpharma.com