Lin Bioscience, Inc. · TPEX:6696
Lin Bioscience — Investor Presentation (July 2026)
44 slides from Lin Bioscience's investor presentation, July 2026
Slide 1: Bringing Hope to Incurable Diseases
Bringing Hope to Incurable Diseases 2026/07 1
Slide 2: Disclaimer
Disclaimer This presentation is provided by Lin Bioscience, Inc. (“LBS”). The information contained within is not reviewed or reviewed by any accountant or any independent third party. Users should read this material in conjunction with all other public financial and operational information filed to
Slide 3: Novel Treatment for Unmet Medical Need
Novel Treatment for Unmet Medical Need Lin BioScience, Inc. (TW TPEx: 6696) is a drug development company established in 2016 focusing on advancing novel therapies and first- in-class treatments for unmet medical needs in various therapeutic areas such as ophthalmology, oncology, and metabolic disea
Slide 4: Pipeline
Pre- Discovery Phase 1 Phase 2 Phase 3 MARKET Pipeline Clinical Developed by Lin BioScience FDA ODD (AML, ALL), FDA fast track (AML) Acute Leukemia (FDA ODD) Multiple Solid Tumors Oncology Sponsored by Taiwan Industrial Development Programs Bureau’s Innovation Platform Program Glioblastoma / Brain M
Slide 5: Chairman
Chairman • PhD in Medicine - University of Sydney; Specialization: Neurology & Immunology Tom Lin, MMED, PhD, MBA o Treatment Strategies for Autoimmune Neuropathies (Chairman) • Specialist Certificate in Clinical Neuroscience - University of Melbourne; Specialization: Neurology o Neurological Disord
Slide 6: Management Team
Management Team Irene Wang, PhD, MBA (President & CSO) • PhD in Biochemical Sciences, National Taiwan University, Trained at Scripps Research (TSRI), EMBA from University of California San Diego • Co-invented and applied 125 patents and published 6 papers • Extensive Drug development from preclinica
Slide 7: Management Team
Management Team Serena Chen Tzung-Ju Wu, PhD (CFO) (Director, R&D) • Certified Public Accountant & master in • Ph.D. in Cellular and Molecular Pharmacology accounting from National Taipei University. from Rutgers University • Finance manager in a Taiwan biotech company • 10-years of global Pharma/Bi
Slide 8: LBS-007 for Acute Leukemia & Solid Tumor
LBS-007 FOR ACUTE LEUKEMIA & SOLID TUMOR 8
Slide 9: Therapeutic Options For Cancer
Therapeutic Options For Cancer Unmet Medical Needs for Cancer Treatment – Next Generation Therapies • Cancer treatments are like a pyramid— higher levels have fewer side effects but are more costly and less applicable. Genetic Therapy • Chemotherapies form the basis of all cancer treatments. Targete
Slide 10: Non-ATP CDC7 Inhibitor
Non-ATP CDC7 Inhibitor For Treatment of Broad Variety of Cancer types DISCOVERY PRE-CLINICAL ✓ PHASE I/II Novel Anti-Cancer MARKET Target Therapy PHASE II/III 1.7 in 100k (1) $5B 4.1 in 100K MARKET (2) Expected 2026 market (1) ALL incidence (2016) Orphan Drug Designation size of AML & ALL (2) AML in
Slide 11: Inhibits CDC7 in Cell Cycle Regulation
Inhibits CDC7 in Cell Cycle Regulation LBS-007 1 TARGETS 2 INHIBITS 3 PREVENTS S Phase Progression CDC7’s role in Cell Division DNA Replication 11
Slide 12: Potently Inhibits Multiple Cancer Cell Lines & Primary Patient Samples of Blood Cancers
Potently Inhibits Multiple Cancer Cell Lines & Primary Patient Samples of Blood Cancers EC50 (nanoM) 5 1000 Acute Leukemia Lymphoma Lung Cancer Breast Cancer Hematopoietic Primary Patient Solid Tumor Cell Line Sample Cell Line 12 Data courtesy of Columbia University
Slide 13: Superior Efficacy at Nanomolar Potency
Superior Efficacy at Nanomolar Potency Approx. 150 nanomolar of LBS-007 can achieve therapeutic effect on cancer cells AML Pancreatic cancer Lung cancer 1.5 LBS-007 (HL-60) LBS-007 LBS-007 (MV4-11) 1.0 Relative Viability 1.0 Etoposide Relative Viability Relative Viability 1.0 LBS-007 (THP-1) LBS-007
Slide 14: In Vivo Efficacy Demonstrated in Animal Models
In Vivo Efficacy Demonstrated in Animal Models Potent tumor reduction in ALL and solid tumor mouse models Acute Lymphoblastic Leukemia (ALL) Ovarian Cancer VENTRAL DORSAL Ctrl 0.3 0.6 1.2 2.4 Ctrl 0.3 0.6 1.2 2.4 (mg/kg/day) Ctrl 0.3 1 3 (mg/kg) ✓ In vivo dose responsive efficacy ✓ In vivo dose resp
Slide 15: In Vivo Efficacy Demonstrated in Animal Models
In Vivo Efficacy Demonstrated in Animal Models Potent tumor reduction in AML mouse models Aggressive AML mouse model (MLL-AF9) AML patient-derived xenograft in mice Bone Marrow Spleen hCD45+ cells (%) Vehicle LBS-007 Vehicle LBS-007 ✓ Disease burden reduced in aggressive AML mouse model at 3 mg/kg ✓
Slide 16: Clinical Development Summary
Clinical Development Summary Discovery Pre - Clinical Phase 1 Phase 2 Phase 3 LBS-007-CT01 Phase 1/2 (Phase 2 dose expansion after determining optimal dose in Phase 1) Enrollment Estimated to enroll 90 patients Sites Australia, Taiwan, US, China Masking Open Label Treatment duration 7 consecutive da
Slide 17: Major Milestones
MAJOR MILESTONES Opening a New Era in Cancer Treatment ✓ 2023/02/10 - We announced that our new drug, LBS-007, has been approved by the Central Adelaide Local Health Network Human Research Ethics Committee (CALHN HREC) to conduct Phase I/II clinical trials for acute leukemia (including AML and ALL)
Slide 18: Tinlarebant (LBS-008) for Geographic Atrophy & Stargardt Disease
TINLAREBANT (LBS-008) FOR GEOGRAPHIC ATROPHY & STARGARDT DISEASE 18
Slide 19: Belite Bio Pipeline Overview
BELITE BIO PIPELINE OVERVIEW PRECLINICAL PHASE 1 PHASE 2 PHASE 3 NDA Stargardt Disease (STGD1) • Ph2, 2-year treatment, completed (13 subjects) • Ph3, 2-year treatment, global trial (“DRAGON” Study) completed (104 subjects) • Ph2/3, 2-year treatment, global trial (“DRAGON II” Study) is ongoing (comp
Slide 20: Tinlarebant Market Opportunity
Tinlarebant MARKET OPPORTUNITY (LBS-008) STARGARDT GEOGRAPHIC ATROPHY DISCOVERY PRE-CLINICAL 1 in 8,800(1,2) The most common PHASE I inherited retinal dystrophy PHASE II PHASE III Patient population with Stargardt Disease: MARKET 53k US (2) 109k China (2) Columbia University + NIH Blueprint “a promi
Slide 21: Mechanism of Tinlarebant Action
Tinlarebant Induced Enzymes MECHANISM OF TINLAREBANT ACTION Down-Regulation Visual Pigment Retinoids Visual Chromophore Rhodopsin 11c-Ral at-Ral STARGARDT Gene PHOTORECEPTORS A2E mutation (PR) causes loss of ABCA4 ABCA4 transporter Mutation of ABCA4 causes at-RDH function accumulation of vitamin A 1
Slide 22: Similar Pathophysiology in STGD1 & GA
SIMILAR PATHOPHYSIOLOGY IN STGD1 & GA • STGD1 and GA show a very similar phenotype, where loss of RPE and photoreceptors in the center of the retina, the macula, leads to loss of vision • Fundus autofluorescence imaging, visualizing bisretinoid content in the RPE, shows loss of signal in degenerated
Slide 23: DRAGON Clinical Trial
DRAGON CLINICAL TRIAL 23
Slide 24: DRAGON & DRAGON II Clinical Trial Design in STGD1
DRAGON & DRAGON II CLINICAL TRIAL DESIGN IN STGD1 Reduction in Lesion Growth Rate (DDAF) as Measured by Retinal Imaging is an FDA Accepted Primary Endpoint in STGD1 and GA STGD1 “DRAGON” Phase 3(1) STGD1 “DRAGON II” Phase 1b/2/3 Enrollment 104 subjects (have DDAF) 60 subjects (have DDAF) Sites Globa
Slide 25: Tinlarebant Treatment Led to 80% Reduction in RBP4
TINLAREBANT TREATMENT LED TO 80% REDUCTION IN RPB4, WELL ABOVE GOAL OF 70%* Biomarker: RBP4 - Percent Reduction from Baseline PD Set N=92 70% Reduction Target * In a prior study of a surrogate RBP4 antagonist (fenretinide) in patients with Geographic Atrophy, an RBP4 reduction of ≥70% was associated
Slide 26: DDAF Represents Well-Demarcated Areas of Complete RPE Loss
DDAF REPRESENTS WELL-DEMARCATED AREAS OF COMPLETE RPE LOSS & GROWS PREDICTABLY, MAKING IT AN APPROVABLE PRIMARY ENDPOINT • DDAF (definitely decreased autofluorescence): level of darkness close to 100% (at least 90%) in reference to the ONH • QDAF (questionably decreased autofluorescence): between 50
Slide 27: DDAF Progression Rate in Stargardt
DDAF PROGRESSION RATE IN STARGARDT Natural History of the Progression of Atrophy Secondary to Stargardt Disease (ProgStar) study Strauss RW, Ho A, Jha A, Fujinami K, Michaelides M, Cideciyan AV, Audo I, Birch DG, Sadda S, Ip M, West S, Schönbach EM, Kong X, Scholl HPN; ProgStar Study Group (2023) Th
Slide 28: Primary Endpoint: DDAF in the Study Eye
PRIMARY ENDPOINT: DDAF IN THE STUDY EYE (CHANGE FROM BASELINE) • Annualized rate of lesion growth in the aggregate area of atrophy (DDAF) from baseline as assessed by fundus autofluorescence imaging at Month 25. • Data is shown for the modified full analysis set (mFAS) which consists of all subjects
Slide 29: Primary Endpoint Showed a Statistically Significant & Clinically Meaningful Outcome
PRIMARY ENDPOINT SHOWED A STATISTICALLY SIGNIFICANT & CLINICALLY MEANINGFUL OUTCOME Primary Endpoint: DDAF Change from Baseline (Study Eye) mFAS N = 96 Applying an unstructured covariance matrix, the treatment effect size was 35.7% compared to placebo and yielded a p-value of P = 0.0033 With a first
Slide 30: Statistically Significant Treatment Effect Also Observed in Fellow Eye
A STATISTICALLY SIGNIFICANT TREATMENT EFFECT WAS ALSO OBSERVED IN THE FELLOW EYE FOR THE PRIMARY ENDPOINT Primary Endpoint: DDAF Change from Baseline (Fellow Eye) mFAS N = 95 Tinlarebant slowed DDAF lesion growth in the fellow eye by 33.6% compared to placebo (P = 0.041) 30
Slide 31: Tinlarebant Slowed DAF Lesion Growth in the Study Eye by 33.7%
TINLAREBANT SLOWED DAF LESION GROWTH, THE KEY SECONDARY ENDPOINT, IN THE STUDY EYE BY 33.7% Key Secondary Endpoint: DAF Change from Baseline (Study Eye) mFAS N = 96 Tinlarebant slowed DAF lesion growth by 33.7% compared to placebo (P = 0.027) 31
Slide 32: Tinlarebant Slowed DAF Lesion Growth in the Fellow Eye by 32.7%
TINLAREBANT SLOWED DAF LESION GROWTH, THE KEY SECONDARY ENDPOINT, ALSO IN THE FELLOW EYE BY 32.7% Key Secondary Endpoint: DAF Change from Baseline (Fellow Eye) mFAS N = 94 Tinlarebant slowed DAF lesion growth in the fellow eye by 32.7% compared to placebo (P = 0.017) 32
Slide 33: BCVA in Study Eye Did Not Show Any Significant Change
AS EXPECTED, BCVA IN STUDY EYE DID NOT SHOW ANY SIGNIFICANT CHANGE Tinlarebant Placebo BCVA at Baseline 39.9 39.4 BCVA at EOS 39.7 40.0 • The overall change of visual acuity was minimal over the period of 24 months in both treatment groups • Test–retest variability for ETDRS change scores in Stargar
Slide 34: ProgStar: Visual Acuity Change Over 24 Months
PROGSTAR: VISUAL ACUITY CHANGE OVER 24 MONTHS PROSPECTIVE COHORT (N=434) • Overall rate of BCVA loss was 0.55 letters/year over two years • BCVA of eyes with baseline BCVA between 20/70 and 20/200 declined at a rate of 0.6 letters/year Kong X, Fujinami K, Strauss RW, Munoz B, West SK, Cideciyan AV,
Slide 35: Safety Results
SAFETY RESULTS Sar Fa |
Slide 36: Tinlarebant Demonstrated a Well Tolerated Safety Profile
TINLAREBANT DEMONSTRATED A WELL TOLERATED SAFETY PROFILE SAFETY SET N = 104 Subjects Who Experienced at Least One Non-Ocular Treatment-Emergent Adverse Events (TEAE), N / (%) Tinlarebant 5mg Placebo Category (N=69) (N=35) TEAE 59 (85.5%) 27 (77.1%) Severe TEAE 2 (2.9%) 1 (2.9%) Serious TEAE 2 (2.9%)
Slide 37: The Majority of Ocular Adverse Events Was Mild
THE MAJORITY OF OCULAR ADVERSE EVENTS WAS MILD SAFETY SET N = 104 Subjects Who Experience at Least One Ocular TEAE, N / (%) Tinlarebant 5mg Placebo Category (N=69) (N=35) TEAE 53 (76.8%) 8 (22.9%) Severe TEAE 2 (2.9%) 0 (0.0%) Serious TEAE 0 (0.0%) 0 (0.0%) Study Drug-Related TEAE 49 (71.0%) 8 (22.9
Slide 38: Phase 3 PHOENIX Trial in Geographic Atrophy
PHASE 3 PHOENIX TRIAL IN GEOGRAPHIC ATROPHY 38
Slide 39: Tinlarebant: ≥70% Reduction of RBP4
TINLAREBANT: ≥ 70% REDUCTION OF RBP4 Phase 1, 5mg Daily Dosing in Healthy Adults: Mean Percent Reduction of RBP4 (excludes placebo) Final dose 70% Reduction Dosing Period 39
Slide 40: Clinical Trial Design Overview in GA
CLINICAL TRIAL DESIGN OVERVIEW IN GA • Established Efficacy Endpoint – Reduction in GA Phase 3 “PHOENIX” (1) atrophic lesion growth rate as measured by retinal imaging is the FDA accepted primary Enrollment 530 subjects endpoint Sites Global • Early Intervention – Targeting patients with Masking Dou
Slide 41: Tinlarebant Summary
TINLAREBANT SUMMARY 41
Slide 42: Summary of Results of the DRAGON Trial
SUMMARY OF RESULTS OF THE DRAGON TRIAL • The DRAGON trial met its primary endpoint: A statistically significant slowing in DDAF lesion growth was observed in subjects treated with 5 mg/day oral Tinlarebant as compared to placebo • The treatment effect was 36% and must be considered clinically meanin
Slide 43: Tinlarebant Has the Potential to Be the First-Ever Approved Treatment for Stargardt Disease
TINLAREBANT HAS THE POTENTIAL TO BE THE FIRST-EVER APPROVED TREATMENT FOR STARGARDT DISEASE • First-ever oral therapy in a retinal degenerative disease to demonstrate a clinically meaningful slowdown of neurodegeneration • 36% reduction in DDAF lesion growth rate, representing a robust and reproduci
Slide 44: Bringing Hope to Incurable Diseases
Bringing Hope to Incurable Diseases info@linbioscience.com 44