Vicore Pharma Holding Ab · OMXSTO:VICO

Vicore Pharma Holding Ab — Investor Presentation (February 2025)

34 slides from Vicore Pharma Holding Ab's investor presentation, February 2025

  1. Slide 1: Vicore Pharma

    VICORE PHARMA Unlocking the potential of a new class of drugs – Angiotensin II type 2 receptor agonists (ATRAGs) February 2025

  2. Slide 2: Disclaimers

    Disclaimers This presentation may contain certain forward-looking statements and forecasts based on uncertainty, since they relate to events and depend on circumstances that will occur in the future and which, by their nature, will have an impact on Vicore Pharma’s business, financial condition and

  3. Slide 3: Vicore at a glance

    Vicore at a glance Unlocking the potential of a new drug class – ATRAGs A powerful, upstream mechanism for idiopathic pulmonary fibrosis (IPF) Unprecedented FVC improvement and excellent safety profile in 36-week Phase 2a IPF trial Capitalizing on buloxibutid, while developing an ATRAG clinical pipe

  4. Slide 4: Company overview

    Company overview Vicore Vision Transform the lives of patients where modulation of the AT2 (angiotensin II type 2) receptor can play a central role in halting and reversing disease pathology Financials Publicly listed on Nasdaq Stockholm (VICO) and funded well past Phase 2b data $185m As of February

  5. Slide 5: Advancing a diversified pipeline

    Advancing a diversified pipeline Molecular Therapies Compound Indication Preclinical Phase 1 Phase 2 Phase 3 Comments Rights Global ex-Japan rights Buloxibutid Phase 2b ongoing IPF Japan: (C21) (NCT06588686) Multiple New ATRAGs Preclinical studies Fully-owned Indications Digital Therapies Compound I

  6. Slide 6: IPF: A large and growing commercial opportunity

    IPF: A large and growing commercial opportunity Large commercial market despite SoC shortcomings Majority of the market is not adequately addressed $6.2B+ Population in US and Europe Healthy lung Lung with $4.6B fibrosis ~250,000 $2.0B Only ~26% of US patients High discontinuation rate and initiate

  7. Slide 7: Buloxibutid is a first-in-class AT2 receptor agonist

    Buloxibutid is a first-in-class AT2 receptor agonist with the potential to transform the IPF landscape Phase 2b ASPIRE: confirming the Upstream MoA Exceptional clinical data clinical activity in a randomized, with strong preclinical data in the Phase 2a AIR trial placebo-controlled trial AT2 recepto

  8. Slide 8: AT2R agonism is an upstream intervention driving tissue repair

    AT2R agonism is an upstream intervention driving tissue repair • AT2R is constitutively expressed in the lung, primarily on alveolar epithelial type 2 cells – the “alveolar repair cell” Buloxibutid • AT2R activates tissue protective mechanisms via AEC2s, including anti-fibrotic effects ATRAGs • Bulo

  9. Slide 9: AT2R is highly expressed in human lungs and on precursor AEC2s

    AT2R is highly expressed in human lungs and specifically on precursor AEC2s AT2R—but not AT1R—is expressed in the human lung1 AT2R is selectively expressed on AEC2s2 (AT1R blocker) + buloxibutid Single cell analysis shows AT2 AT2R expression receptor selectively on AEC2 in the lung buloxibutid AEC2

  10. Slide 10: Alveolar epithelial cells are critical for healthy lung function

    Alveolar epithelial cells are critical for healthy lung function Healthy alveolus • The alveolar epithelium is constantly exposed to damaging irritants in inhaled air AEC2 • AEC1 is the predominant alveolar cell type and is responsible for gas exchange Proliferation • AEC2 is a progenitor cell that

  11. Slide 11: Buloxibutid drives tissue repair via AEC2 precursor epithelial cells

    Buloxibutid is an oral, selective AT2R agonist that drives tissue repair via AEC2 precursor epithelial cells Alveolar compartment in IPF Effects of buloxibutid Repeated Micro-injury Buloxibutid AEC2 dysfunction leads to reduced surfactant production, no generation Increased AEC2 viability 1 & surfac

  12. Slide 12: Buloxibutid protects AEC2s and drives increased surfactant production

    Increased AEC2 viability & surfactant 1 production Buloxibutid protects AEC2s and drives increased surfactant production Surfactant protein expression increased by buloxibutid in Buloxibutid protects AEC2 cells against apoptosis1 ex vivo human IPF precision cut lung slices2 50 42% +120% % Increase v

  13. Slide 13: Buloxibutid reduces TGFβ1 and collagen in human IPF lung slices

    Reduction of TGFβ1 and inhibition of 2 EMT and collagen Buloxibutid reduces TGFβ1 and collagen in human IPF lung slices TGFβ1 protein levels in PCLuS Collagen protein levels in PCLuS Human precision cut lung slices (PCLuS) ✱✱ 150 4000 ✱ ✱✱ Collagen-1a1 (pg/mL) (pg/ml) 3000 (pg/mL) TGFβ11(pg/mL) 100

  14. Slide 14: Buloxibutid downregulates expression of EMT transcription factors in AEC2

    Reduction of TGFβ1 and inhibition of 2 EMT and collagen Buloxibutid downregulates expression of EMT transcription factors in AEC2 SNAIL1 SNAIL2 Vehicle 0.1µM 1µM Vehicle 0.1µM 1µM Vehicle 0.1µM 1µM Vehicle 0.1µM 1µM buloxibutid buloxibutid buloxibutid buloxibutid • Primary AEC2 cultures established

  15. Slide 15: MMP-13 demonstrates antifibrotic activity and is crucial for lung repair

    3 Upregulation of collagenase MMPs MMP-13 demonstrates antifibrotic activity and is crucial for lung repair in IPF Collagenase MMP dysregulation contributes to IPF Buloxibutid increased plasma MMP-13 in the pathogenesis Phase 2a AIR trial • MMP-13 is an enzyme able to cleave fibrillar collagens 250

  16. Slide 16: Strong preclinical in vivo evidence for buloxibutid in pulmonary fibrosis

    Strong preclinical in vivo evidence for buloxibutid in pulmonary fibrosis Bleomycin Monocrotaline Sugen-Hypoxia 6 15 * * 7 ** ** * * * Hydroxy proline (nM) 6 4 10 Fibrosis (%) Fibrosis (%) 5 2 5 4 0 0 3 Control BLEO buloxibutid C21 buloxibutid C21 Control MCT MCT MCT + + C21 Control SuHx SuHx buloxi

  17. Slide 17: Buloxibutid's upstream mechanism is differentiated from other IPF mechanisms

    Buloxibutid’s upstream tissue repair mechanism is fundamentally differentiated from other mechanisms in development for IPF Most IPF mechanisms systemically block components of the aberrant wound healing process. In contrast, AT2R agonism activates an upstream endogenous system locally in the lung t

  18. Slide 18: AT2R is selectively and constitutively expressed in the lung

    AT2R is selectively and constitutively expressed in the lung, in contrast to the broader tissue expression of other IPF targets in development Target is upregulated in the lung in the IPF disease state IPF Target Expression in Healthy Tissue AGT2R LPAR1 αv β1 β6 SHH PDE4B IP-R Buloxibutid Admilparan

  19. Slide 19: Buloxibutid has an extensive and robust safety database

    Buloxibutid has an extensive and robust safety database, with over 350 patients dosed across nine completed clinical trials Buloxibutid has been tested extensively in the clinic, generating a robust safety database • Not including patients enrolled in the ongoing Phase 2b ASPIRE trial, a total of 36

  20. Slide 20: AIR: open-label Phase 2a trial of buloxibutid in treatment-naïve IPF patients

    AIR: An open-label Phase 2a trial of oral buloxibutid 100 mg BID for up to 36 weeks in treatment-naïve IPF patients Patient Patient population population Clinic visits with FVC measurements Treatment-naïve IPF Week 2 4 6 9 12 15 18 21 24 28 32 36 patients with Screening period Follow-up period centr

  21. Slide 21: AIR baseline patient characteristics are in line with other IPF trials

    AIR baseline patient characteristics are in line with other IPF trials Key Characteristics AIR INPULSIS 1&2 (N=52) (N=1,061)1 Age (years) - Mean (SD) 67 (9) 67 (8) Males 77% 80% In line with other trials. Gender Females 23% 20% White 27% 57% Enrolled study population has disease progression comparab

  22. Slide 22: Treatment emergent adverse events: better tolerability than SoC

    Treatment emergent adverse events: buloxibutid shows better tolerability than SoC INPULSIS 1 AIR 52-week treatment1 36-week treatment Nintedanib Placebo Buloxibutid n=309 n=204 n=52 Any AE 96% 89% 71% Common AEs (Non-exhaustive) Diarrhea 62% 19% 6% Good GI tolerability Nausea 23% 6% 4% Acute exacerb

  23. Slide 23: Buloxibutid stabilizes and improves lung function over the AIR study

    Buloxibutid stabilizes and improves lung function over the 36-week AIR study 400 *** 300 ** *** Buloxibutid 200 FVC change (mL) 28 ** mean +SEM 28 100 * 28 33 40 34 0 32 n=48 44 35 34 48 39 -100 Untreated patients1,2 -200 0 4 8 12 16 20 24 28 32 36 Week 1Noble et al. Eur Respir J. 2016 Jan; 47(1): 2

  24. Slide 24: All subgroups show FVC stabilization and improvement at 36 weeks

    All subgroups show FVC stabilization and improvement over baseline at 36 weeks 400 Change at week 36 vs baseline Mean FVC change at week 36 vs baseline Mean and median; ∆mL Subgroup (# patients); ∆mL Mean FVC change at +216 ml week 36 vs baseline (all) Probable UIP (n=18); 321 300 Median FVC change

  25. Slide 25: Significant increase in ppFVC, consistent with absolute FVC

    Buloxibutid drives a significant increase in ppFVC, consistent with its impact on absolute FVC Average ppFVC change from baseline at week 36 8 7.5% Buloxibutid also demonstrated a 6 median FVC change from baseline at week 36 of +2.2% 4 2 % 0 -2 -2.0% -4 Nintedanib2 -4.2% -6 Buloxibutid1 Untreated2 A

  26. Slide 26: Buloxibutid outperforms historical standard of care and untreated decline

    Buloxibutid outperforms historical standard of care and untreated decline at 36 weeks Percentage of patients Percentage of patients with improved outperforming expected ∆FVC lung function (FVC) vs baseline 100% 70% 60% 50% 40% 30% 65% 75% 82% 20% 10% 25% 9% 0% Buloxibutid Buloxibutid vs Buloxibutid

  27. Slide 27: Buloxibutid increases MMP-13 and drives a trend of decreased TGFβ1

    Buloxibutid increases collagenase MMP-13 drives a trend of decreased TGFβ1 Plasma TGFβ1 Plasma MMP-13 20 250 ** 16 200 *** Plasma MMP-13 (% of baseline) Plasma TGFβ1 ** 12 150 (ng/mL) 8 100 4 50 0 0 Baseline Week 12 Week 24 Week 36 Baseline Week 12 Week 24 Week 36 n=37 n=36 n=28 n=23 n=37 n=36 n=28

  28. Slide 28: Phase 2b ASPIRE trial design

    Phase 2b ASPIRE trial design A randomized, double-blind, placebo-controlled, parallel-group, multicenter, dose-finding trial​ IPF patients on stable nintedanib/SoC or not on SoC (no access, refused, intolerant or failed) 52-week treatment duration; N=270 (90 per arm) Study Assessment of efficacy, sa

  29. Slide 29: Partnership with Nippon Shinyaku for buloxibutid in Japan

    Vicore’s partnership with Nippon Shinyaku for buloxibutid in Japan Partnership Overview Vicore Pharma and Nippon Shinyaku have entered an exclusive license agreement to develop and commercialize the drug candidate buloxibutid in Japan. Financial Terms Vicore has received an upfront payment of USD 10

  30. Slide 30: Almee is a digital therapy for anxiety in pulmonary fibrosis

    Almee is a digital therapy for anxiety in pulmonary fibrosis with the potential to increase commercial sales of molecular therapies Product AlmeeTM is a digital companion to personalize pulmonary fibrosis treatment. description COMPANION study demonstrated clinical validation. Clinically Behavior mo

  31. Slide 31: Almee provides multiple benefits for molecular assets

    Almee provides multiple benefits for molecular assets Treats the psychological impact of living with PF Designed to improve QoL for patients which current SoCs don't address True patient engagement – designed to create trust and empowerment Increased Label & IP adherence, initiation, Data access Dif

  32. Slide 32: Vicore has a platform of proprietary ATRAGs

    Vicore has a platform of proprietary ATRAGs Buloxibutid – a first-in-class drug for rare lung diseases • Orphan drug status in IPF granted – Market exclusivity for 7 years in the US and 10 years in the EU. • Vicore has formulation and method-of-use IP granted in the US and EU covering buloxibutid, w

  33. Slide 33: Strong leadership team with extensive industry experience

    Strong leadership team with extensive industry experience Board of Directors AHMED MOUSA CHIEF EXECUTIVE OFFICER HANS SCHIKAN, PharmD – CHAIRMAN Experienced biotech executive with a background in 25 years management experience in global pharmaceuticals (e.g. molecular biology, law, and business deve

  34. Slide 34: Vicore is well positioned to unlock the potential of a new class of drugs

    Vicore is well positioned to unlock the potential of a new class of drugs - in rare lung diseases and beyond Contact us Visiting addresses IR contacts www.vicorepharma.com Stockholm Copenhagen Boston AHMED MOUSA, CEO, ahmed.mousa@vicorepharma.com Kornhamnstorg 53 Agern Allé 5A One Broadway, 14th Flo

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