Vicore Pharma Holding Ab · OMXSTO:VICO
Vicore Pharma Holding Ab — Investor Presentation (May 2026)
40 slides from Vicore Pharma Holding Ab's investor presentation, May 2026
Slide 1: Vicore Pharma
VICORE PHARMA Unlocking the potential of a new class of drugs – Angiotensin II type 2 receptor agonists (ATRAGs) May 2026
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
Slide 3: 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 $341m As of May 13,
Slide 4: Pipeline
Pipeline Vicore’s lead program, buloxibutid, is a first-in-class oral small molecule AT2 receptor agonist, which has received Orphan Drug and Fast Track designation from FDA and is currently being investigated in a global 52-week Phase 2b trial in IPF, ASPIRE Compound Indication Preclinical Phase 1
Slide 5: IPF is a progressive, fatal disease with significant unmet need despite available therapies
IPF is a progressive, fatal disease with significant unmet need despite available therapies Orphan disease with high unmet need Limitations of available treatment options Three FDA-approved therapies: ~150K US ~3M Global IPF Patients IPF Patients • Existing therapies offer only modest slowing Where
Slide 6: IPF is a large and growing market with urgent need for innovation
IPF is a large and growing market with urgent need for innovation Global IPF Market Size White Space for Significant market expansion Market-Shifting expected over the next decade Innovation $10B+ Drivers of Market Growth Today • Disease-Modifying CAGR 10-15% Efficacy: Stabilization or $4.2B • New A
Slide 7: Buloxibutid is positioned to transform the IPF landscape
Buloxibutid is positioned to transform the IPF landscape Recently approved and late-stage IPF therapies have demonstrated modest reduction of lung function decline, with many associated with tolerability or administration challenges. Following these programs, buloxibutid is the most advanced IPF the
Slide 8: Buloxibutid is a first-in-class AT2 receptor agonist with the potential to set a new standard in IPF
Buloxibutid is a first-in-class AT2 receptor agonist with the potential to set a new standard in IPF Phase 2b ASPIRE: confirming clinical Upstream MoA Exceptional clinical data activity in a randomized, placebo- with strong preclinical data in the Phase 2a AIR trial controlled trial AT2 receptor exp
Slide 9: 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 (AEC2) – the “alveolar repair cell” Buloxibutid • AT2R activation engages tissue-protective pathways via AEC2s, promoting inhibition of fibroti
Slide 10: AT2R is highly expressed in human IPF lungs and on precursor AEC2s
AT2R is highly expressed in human IPF lungs and on precursor AEC2s AT2R Expression is Elevated in IPF Lung AT2R is Highly Expressed on AEC2s 0.08 Disease 0.06 Control ILD AT2 AGTR2 receptor 0.04 0.02 AEC1 AEC2 0.00 AEC2 Fibroblast Myofibroblast Endothelial Cells AT2R expression is highly upregulated
Slide 11: Alveolar epithelial cells are critical for healthy lung function
Alveolar epithelial cells are critical for healthy lung function Healthy alveolus • The alveolar epithelium is exposed to damaging irritants in inhaled air AEC2 • AEC1 is the predominant alveolar cell type and is responsible for gas exchange • AEC2 is a progenitor cell that is critical for alveolar
Slide 12: Buloxibutid is an oral, selective AT2R agonist that 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 Increased AEC2 viability 1 & surfactant production 1 AEC2 dysfunction AEC2 Dysfunctional AEC2 TGFβ1 releas
Slide 13: Buloxibutid addresses all main disease drivers in IPF and disease modification through tissue repair
Buloxibutid addresses all main disease drivers in IPF and disease modification through tissue repair Tissue repair and regeneration Buloxibutid drives tissue repair by targeting precursor epithelial cells (AEC2), offering a disease-modifying mechanism of action Anti-inflammatory Buloxibutid inhibits
Slide 14: Buloxibutid protects AEC2s and drives increased surfactant 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 vs Control 40 death 31% Cell death 30 29% +70% %%Cel
Slide 15: Buloxibutid reduces TGFβ1 and collagen in human IPF lung slices
Buloxibutid reduces TGF1 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) TGF11(pg/mL) 100 Collagen-1a1 2000 -44% -61% TGF- 50 1000 0 0 • Lung tis
Slide 16: Buloxibutid downregulates expression of EMT transcription factors in AEC2
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 from normal surgically resected human lung • Buloxibutid
Slide 17: Buloxibutid potently inhibits fibrosis in a human lung fibroblast assay
Buloxibutid potently inhibits fibrosis in a human lung fibroblast assay Human lung fibroblast assay methodology Impact on type III collagen biomarker PRO-C3 Mean±SEM (n=4) ****p<0.0001 (one-way ANOVA) Buloxibutid potently and dose-dependently inhibited PRO-C3, reflecting inhibition of type III colla
Slide 18: MMP-13 demonstrates antifibrotic activity and is crucial for lung repair in IPF
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 and plays a significant role in the
Slide 19: Buloxibutid's vascular effects are clinically validated
Buloxibutid’s vascular effects are clinically validated Increase in forearm blood flow (%) 70 p=0.026 Buloxibutid’s vascular effects (vasodilation) are clinically Mean change, n=5 validated in a forearm blood flow trial in healthy volunteers 60 • Buloxibutid shows dose-dependent increase in local bl
Slide 20: Buloxibutid shows greater reduction in hemodynamic and vascular remodeling parameters than inhaled treprostinil
Buloxibutid shows greater reduction in key hemodynamic and vascular remodeling parameters compared to inhaled treprostinil in preclinical Sugen-Hypoxia rat model Inhaled treprostinil and buloxibutid were evaluated in separate studies using the same study protocol Hemodynamic Parameters Right Ventric
Slide 21: 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 Fibrosis (%) 10 Fibrosis (%) 5 2 5 4 0 0 3 Control BLEO buloxibutid C21 buloxibutid C21 Control MCT MCT MCT MCT+ C21 + Control SuHx SuHx C21
Slide 22: 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
Slide 23: AIR: An open-label Phase 2a trial of oral buloxibutid
AIR: An open-label Phase 2a trial of oral buloxibutid 100 mg BID for up to 36 weeks in treatment-naïve IPF patients Patient population Patient 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
Slide 24: 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
Slide 25: Treatment emergent adverse events: buloxibutid shows better tolerability than SoC
Treatment emergent adverse events: buloxibutid shows better tolerability than SoC Comparison to SoC Buloxibutid Ph3 INPULSIS-1 Ph2a 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 tole
Slide 26: Buloxibutid stabilizes and improves lung function over the 36-week AIR trial
Buloxibutid stabilizes and improves lung function over the 36-week AIR trial 400 *** 300 ** *** Buloxibutid FVC change (mL) 200 28 ** mean +SEM 28 28 100 * 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
Slide 27: All subgroups show FVC stabilization and improvement over baseline 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
Slide 28: Development of a Synthetic Control Arm analysis to contextualize buloxibutid's effect
Development of a Synthetic Control Arm analysis to contextualize buloxibutid’s effect in the AIR trial • Age >= 40 years IPF Patient • FVC % predicted >= 60% • Follow-up time – 36 weeks External Control • FEV1/FVC >= 70% External Control Arm Generation • AIR – mean FVC change +23 ml Data • Treatment
Slide 29: IPF patients selected for the Synthetic Control Arm analysis are highly matched to AIR patients
IPF patients selected for the Synthetic Control Arm analysis are highly matched to the Phase 2a AIR patient baseline characteristics Mean similarity p-value - 0.23 (SD=0.05) Note: Qureight analysis 29
Slide 30: A Synthetic Control Arm analysis demonstrates buloxibutid's robust treatment effect
A Synthetic Control Arm analysis demonstrates buloxibutid’s robust treatment effect Change in FVC in the Phase 2a AIR IPF trial 408 individual matched Synthetic Control Arms (SCAs) compared to the external control arm study generated by Monte Carlo cross validation 50 Phase 2 AIR Study Buloxibutid (
Slide 31: Buloxibutid drives a significant increase in ppFVC
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
Slide 32: Buloxibutid outperforms historical standard of care and untreated decline at 36 weeks
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
Slide 33: Buloxibutid increases collagenase MMP-13 and drives a trend of decreased TGFβ1
Buloxibutid increases collagenase MMP-13 and drives a trend of decreased TGFβ1 Plasma TGFβ1 Plasma MMP-13 20 250 ** 16 200 *** Plasma MMP-13 (% of baseline) Plasma TGFβ1 ** 150 (ng/mL) 12 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
Slide 34: Phase 2b ASPIRE Trial: Robust randomized trial with global footprint
Phase 2b ASPIRE Trial: Robust randomized trial with global footprint ASPIRE is a randomized, double-blind, placebo-controlled, parallel-group, multicenter, dose-finding trial Trial Design Global Footprint Randomization 1:1:1 ~120 sites across 14 countries n=378 Buloxibutid 50mg BID Follow-up Screeni
Slide 35: ASPIRE includes a pre-planned, independent futility analysis
ASPIRE includes a pre-planned, independent futility analysis An independent Data Monitoring Committee (iDMC) will conduct a pre-specified futility assessment once ~27% of patients have accrued data for the primary endpoint analysis. Timing and Rationale Method Communication Purpose of the futility a
Slide 36: Phase 2b ASPIRE trial: designed to position buloxibutid as a differentiated therapy for IPF
Phase 2b ASPIRE trial: designed to position buloxibutid as a differentiated and highly competitive therapy for IPF in a multi-billion-dollar market Limited clinical Clinically meaningful Transformational impact efficacy efficacy Defining Success in IPF Phase 2b ASPIRE: target efficacy profile buloxi
Slide 37: Vicore's 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
Slide 38: 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 up to 10 years in the EU and Japan. • Vicore has dosage form and method-of-use IP granted in the US and EU coverin
Slide 39: 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
Slide 40: Contact Us
Contact Us Addresses: IR Contacts: www.vicorepharma.com www.vicorepharma.com ahmed.mousa@vicorepharma.com Stockholm Copenhagen Boston AHMED MOUSA, CEO, ahmed.mousa@vicorepharma.com Kornhamnstorg 53 Agern Allé 5A One Broadway, 14th Floor info@vicorepharma.com info@vicorepharma.com hans.jeppsson@vicor