Beyondspring, Inc. · NASDAQ:BYSI
Beyondspring — Investor Presentation (April 2026)
38 slides from Beyondspring's investor presentation, April 2026
Slide 1: Transforming Cancer Care with Immune-modulating Therapies
Transforming Cancer Care with Immune-modulating Therapies April 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-Responding Patients After ICI Failure Show Immune Activation
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 9: 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 10: Plinabulin's Immunomodulation and Neutropenia-Mitigating Activities
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 reduces Plinabulin targets DC maturation + chemotherapy-induced tumor vascula
Slide 11: 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 12: 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 13: 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 14: Plinabulin and Docetaxel Demonstrated Significant OS Benefit in Phase 3 (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 15: Plinabulin + Docetaxel Met Primary Endpoint of OS
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 16: 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 17: Dublin-3: Post-hoc Analysis in Plinabulin 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 18: 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 Primary Endpoint (n=47) – SITC 2025 Best Change (%) in Target Lesions Confirmed ORR（RECIST 1.1） 18.2% Secondary Endpoint Median PFS（RECIST 1.1） 7.0 months 1
Slide 19: 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 20: 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 21: 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 22: 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 23: 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 24: 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 25: 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 26: SEED Is Led By The Scientists Who Discovered Targeted Protein Degradation
SEED Is Led By The Scientists Who Discovered Targeted Protein Degradation ⬢ Combined leadership record of 40 INDs and 12 NDAs ⬢ Balanced by an experienced Nobel Laureate board across finance, risk, legal, Avram Hershko, MD Lan Huang, Ph.D. Co-Founder and SAB Member Co-Founder, CEO and Chairman and d
Slide 27: SEED Built The TPD 2.0 Engine
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 28: SEED's Platform Is Already Generating Clinical Assets Alongside Partners
SEED’s Platform Is Already Generating Clinical Assets Alongside World-class Partners SEED Therapeutics has been validated through deep diligence, long-term capital, and active R&D partnerships with Eli Lilly and Eisai, while building a broad, multi-indication internal pipeline with 6 active programs
Slide 29: 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 30: Ewing Sarcoma Is A Fusion-driven Disease with No New Drugs
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 The cleanest biological proof cancer designation by US FDA 1500 1000 point for RBM39 degradation. 500 0 0 5 10 1
Slide 31: 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 32: 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 33: Leading Oncologists Guiding Development of ST-01156
Leading Oncologists Guiding Development of ST-01156 Dr. George D. Demetri Dr. Robert Maki Dr. Daneng Li Dr. Jordi Rodón Dr. Monica Mita Dana Farber MSK City of Hope MD Anderson Hoag Cancer Institute Associate Professor at Harvard Globally recognized sarcoma expert Associate Professor of Medical Medi
Slide 34: ST-01156: Phase 1a Clinical Development Plan for Dose Escalation
ST-01156: Phase 1a Clinical Development Plan for Dose Escalation 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 (Ewin
Slide 35: ST-01156: Phase 1b Clinical Development Plan for Dose Expansion
ST-01156: Phase 1b Clinical Development Plan for Dose Expansion Presence and quantification of relevant antitumor activity Priority indications Ewing sarcoma (Age 12+) Single-group open-label Hepatocellular carcinoma Cohorts at RP2D Colon cancer N for each cohort = Biliary tract cancer, uterine canc
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 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 37: SEED Therapeutics — Creating Significant Value in 2026–2028
SEED Therapeutics — Creating 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: Science built
Slide 38: Thank You
Thank You General Inquiries: GENERAL@beyondspringpharma.com Investor: IR@beyondspringpharma.com Media: PR@beyondspringpharma.com www.beyondspringpharma.com