Belite Bio, Inc. · NASDAQ:BLTE
Belite Bio — IPO Roadshow (April 2022)
31 slides from Belite Bio's IPO roadshow presentation, Apr 25, 2022
Slide 1: Slowing the Progression of Macular Degeneration
Issuer Free Writing Prospectus dated April 25, 2022 Pursuant to Rule 433 of the Securities Act of 1933, as amended Registration Statement No. 333-264134 Slowing the Progression of Macular Degeneration Mission for Vision Tom Lin, CEO Email / [email protected] BELITE BIO / 1
Slide 2: Disclaimer
Disclaimer This presentation has been prepared by Belite Bio, Inc (the “Company”) solely for information purposes. This presentation does not constitute an offer to sell or issue or the solicitation of an offer to buy or acquire securities of the Company in any jurisdiction or an inducement to enter
Slide 3: Offering Summary
Offering Summary Issuer Belite Bio, Inc Headquarters San Diego, California USA Transaction Type Initial Public Offering of American Depositary Shares (“ADS”) Exchange/Ticker Nasdaq Capital Market / BLTE ADSs Offered 6,000,000 (100% Primary) Price Range $5.50-$6.50 Offering Size $36.0 million Overall
Slide 4: Key Investment Highlights
Key Investment Highlights • Targeting an unmet market for macular degeneration; • Significant support from our controlling shareholder Lin BioScience International Ltd.: • Indicated an interest for up to US$15.0 million of the offering; • Wholly-owned subsidiary of Lin BioScience, Inc., which is pub
Slide 5: Leadership
Leadership Management Tom Lin, MMED, PhD, MBA Nathan Mata, PhD Jane Chiu, MS H.Y. Chuang, CFA, MBA, FRM (Chairman, CEO) (CSO) (VP, Clinical Operations) (CFO) • 10 years of executive management role • 15+ years of ophthalmic drug • 25 years clinical operations experience • 11 years of capital market
Slide 6: Belite Bio Opportunity
Belite Bio Opportunity • Belite Bio’s lead asset LBS-008 is a novel, orally administered, Retinol Binding Protein 4 (“RBP4”) antagonist intended to slow or halt progression of vision loss in Stargardt disease (STGD1) and dry AMD. A Phase 3 trial has been initiated in adolescent STGD1 patients and a
Slide 7: Board of Directors
Board of Directors Board Clinical Advisory Board Tom Lin, MMED, PhD, MBA John M. Longo, PhD Gary C. Biddle, PhD, CPA Ita Lu Dr. Frank Holz Dr. Michel Michaelides Dr. Quan Nguyen (Chairman, CEO) (Independent Director) (Independent Director) (Independent Director) • Prof. of Rutgers Business • Prof. o
Slide 8: Zero Approved Treatments
LBS LIGHT TO INCURABLE BLINDESS 008 For Dry Age-Related Macular Degeneration & Stargardt Disease DISCOVERY PRE-CLINICAL KEY OPPORTUNITY Dry AMD MARKET STGD1 MARKET Zero Approved 11M 1 in 10,000 PHASE I PHASE II Treatments PHASE III dry AMD patients in inherited juvenile onset MARKET the US (90% AMD
Slide 9: Clear Clinical Development Pathway
Clear Clinical Development Pathway LBS 008 Reduction in Lesion Growth Rate as Measured by Retinal Imaging is an FDA Accepted Primary Endpoint in STGD1 and dry AMD completed ongoing planned Phase 1b/2 Phase 3 STGD Phase 2/3 Dry AMD Phase 1 Adolescent Adolescent NDA Dry AMD NDA STGD STGD PRV • Complet
Slide 10: Overview of Stargardt Disease & Dry AMD
Overview of Stargardt Disease & Dry AMD LBS 008 Stargardt Disease (STGD1) • The most common inherited retinal dystrophy (blurring or loss of central vision) in both adults and children • Caused by a dysfunctional retina-specific gene (ABCA4) which causes massive accumulation of toxic vitamin A bypro
Slide 11: Similar Pathophysiology in STGD1 & Dry AMD
LBS Similar Pathophysiology in STGD1 & Dry AMD 008 • STGD1 and dry AMD share STGD1: LATE-ONSET (61-YEAR OLD FEMALE) a similar pathophysiology characterized by excessive accumulation of cytotoxic bisretinoids, retinal cell death, and loss of vision • Vision loss occurs slowly, despite peripheral Dry
Slide 12: Proof of Concept in a STGD1 Mouse Model: Preservation of the Retina
Proof of Concept in a STGD1 Mouse Model: LBS 008 Preservation of the Retina Data Summary Control LBS-008 treated mice Untreated mice • Like STGD1 patients, STGD1 mice harbor a mutated ABCA4 gene and protein and show pronounced accumulation of bisretinoids and retinal degeneration (reduced thickness
Slide 13: Proof-of-Concept from Phase 2 Fenretinide Study in Advanced Dry AMD
Development Pathway: Proof-of-Concept from Phase LBS 008 2 Fenretinide Study in Advanced Dry AMD • Fenretinide is a synthetic derivative of vitamin A (retinol). Fenretinide is able to compete with retinol for binding to RBP4 and reduce delivery of retinol to the eye. • Fenretinide was used in a 2-ye
Slide 14: Clinical Data
Clinical Data BELITE BIO / 14
Slide 15: Phase 1b Daily Dosing in Adolescent STGD1: Mean change of RBP4
Phase 1b Daily Dosing in Adolescent STGD1: LBS 008 Mean change of RBP4 (%) 110 100 90 80 6 Patients RBP4 (%) 70 60 11 Patients 50 40 70% Reduction 30 20 10 Dosing Period 0 1.0 1 Day 2.08 Day 3.015 Day 4.022 Day 5.028 Day 14 6.0 days post treatment Note: After Day 15, data were collected from 6 subje
Slide 16: Phase 1b: Summary of Related Adverse Events
Phase 1b: LBS 008 Summary of Related Adverse Events Frequency Adverse Events Severity Relationship to Drug % Recovered % On-going (#patients) Xanthopsia Mild Definitely Related 7/11 7/7 (100%) 0/7 Delayed Dark Adaptation Mild Definitely Related 7/11 7/7 (100%) 0/7 (DDA) Night Vision Impairment Mild
Slide 17: Interim Phase 2 Results: Summary of Related Adverse Events
Interim Phase 2 Results: LBS 008 Summary of Related Adverse Events Relationship to Frequency Adverse Events Severity % Recovered % On-going Drug (#patients) Xanthopsia Mild Definitely Related 6/13 3/6 (50%) 3/6 (50%) Delayed Dark Adaptation Mild Definitely Related 8/13 1/8 (12.5%) 7/8 (87.5%) Night
Slide 18: Interim Phase 2 Data: Change in DDAF in Adolescent STGD1 Subjects
LBSInterim Phase 2 Data: Change in DDAF in Adolescent 008 STGD1 Subjects 92.3% 12 of 13 subjects showed no lesion growth 7.7% DDAF, or lesion (“dead retina”) in 1 of 13 subjects had STGD1 patient as measured by lesion growth of 0.3 retinal imaging. This is the area mm² in both eyes where retinal cel
Slide 19: Interim Phase 2 Data: Change in QDAF in Adolescent STGD1 Subjects
LBSInterim Phase 2 Data: Change in QDAF in Adolescent 008 STGD1 Subjects Distribution of Change in QDAF 23.0% 3/13 in one eye - Reduction or no change in 1 eye - Reduction or no change in both eyes - Increase in both eyes 5/13 5/13 in both eyes Areas of QDAF progressively evolve into ‘dead retina’.
Slide 20: Interim Phase 2 Results: Change of Vision in Adolescent STGD1 Subjects
Interim Phase 2 Results: Change of Vision in Adolescent LBS 008 STGD1 Subjects Change in BCVA BCVA gain in 8 of 13 Subjects (61.5%) 46.1 % 6/13 - Letter gain in 1 eye in one eye - Letter gain in both eyes - Letter decrease 5/13 2/13 Best-Corrected Visual Acuity (BCVA) Test 38.5% in both Provides let
Slide 21: Capital Structure and Use of Proceeds
Capital Structure and Use of Proceeds Shares* % Primary Purpose Estimated Amount % (in USD millions) Lin Bioscience International 16,428,597 59.0% Dry AMD clinical trials $22.0 68.2% Ltd.** Management Team 5,165,310 18.6% General corporate purposes $9.4 29.3% Pre-Offering Investors 2,732,638 9.8% ST
Slide 22: Investment Highlights
Investment Highlights • LBS-008 is a novel oral treatment intended to slow or halt disease progression in both dry AMD and STGD1. • Clear Clinical Pathway: • LBS-008 continues to be well-tolerated. • Ongoing 2-year Phase 2 trial (6 months of reported interim safety data and preliminary efficacy data
Slide 23: Thank you
Thank you Tom Lin, CEO Email / [email protected] For more info please visit: www.belitebio.com
Slide 24: Appendix
Appendix BELITE BIO / 24
Slide 25: Disease Progression in STGD1
LBS Disease Progression in STGD1 008 ProgStar Case Study: Retinal Imaging at First Observation and 22 months later • A2E and related bisretinoids exhibit a characteristic autofluorescence under retinal imaging allowing the disease to be detected and monitored. First Observation: Central Lesion in Sa
Slide 26: Normal Processing of Vitamin A in the Visual Cycle
Normal Processing of Vitamin A in the LBS LBS-008 Induced Down-Regulation Enzymes 008 Visual Cycle Visual Pigment Retinoids Visual Chromophore Rhodopsin 11c-Ral at-Ral PHOTORECEPTORS (PR) ABCA4 11c-RDH at-RDH RETINAL PIGMENT EPITHELIUM (RPE) 11c-Rol RPE65 at-RE LRAT at-Rol RBP Receptor RBP4 at-Rol B
Slide 27: Toxic Vitamin A Byproducts Accumulate in Patients with STGD1
Toxic Vitamin A Byproducts Accumulate in LBS LBS-008 Induced Down-Regulation Enzymes 008 Patients with STGD1 Visual Pigment Retinoids Visual Chromophore Rhodopsin 11c-Ral at-Ral A2E STARGARDT PHOTORECEPTORS Gene mutation causes loss of (PR) ABCA4 ABCA4 transporter 11c-RDH Mutation of ABCA4 causes ac
Slide 28: LBS-008 Mechanism of Action
LBS-008 Mechanism of Action LBS-008 Induced LBS Down-Regulation Enzymes 008 Visual Pigment Retinoids Visual Chromophore Because bisretinoids are derived from vitamin A (retinol), reducing the delivery of retinol to the eye is expected to reduce bisretinoid levels in the eye leading to preservation o
Slide 29: RBP4 Reduction Reduces A2E Accumulation by 80%
RBP4 Reduction Reduces A2E LBS 008 Accumulation by 80% Effect of LBS-008 on biomarkers in a STGD1 mouse model (ABCA4-/-/RDH8-/-) • Daily dosing at approx. 25mg/kg of LBS-008 for 12 weeks. • A mean RBP4 reduction of ~90% in LBS-008 treated mice led to an ~80% reduction in A2E compared to untreated AB
Slide 30: RBP4 Reduction Preserves Photoreceptor Cells
RBP4 Reduction Preserves Photoreceptor Cells LBS 008 Effect of LBS-008 on retinal pathology in a STGD1 mouse model (ABCA4-/-/RDH8-/-) • Outer Nuclear Layer (ONL) thickness was significantly decreased in untreated ABCA4-/-/RDH8-/- mice, compared to mice treated with LBS-008 • Macular degeneration in
Slide 31: Phase 1 Daily Dosing in Healthy Adults: Mean change of RBP4
Phase 1 Daily Dosing in Healthy Adults: LBS 008 Mean change of RBP4 (exclude PBO) 130 120 110 100 RBP4 (%) 90 80 70 60 50 40 70% Reduction 30 20 10 Dosing Period - 0 4 8 12 14 16 20 24 28 Days BELITE BIO / 31