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VICORE PHARMA Unlocking the potential of a new class of drugs – Angiotensin II type 2 receptor agonists (ATRAGs) January 2026
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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 results of operations. The terms “anticipates”, “assumes”, “believes”, “can”, “could”, “estimates”, “expects”, “forecasts”, “intends”, “may”, “might”, “plans”, “should”, “projects”, “will”, “would” or, in each case, their negative, or other variations or comparable terminology are used to identify forward-looking statement. There are a number of factors that could cause actual results and developments to differ materially from those expressed or implied in a forward-looking statement or affect the extent to which a particular projection is realized. Factors that could cause these differences include, but are not limited to, implementation of Vicore Pharma’s strategy and its ability to further grow, risks associated with the development and/or approval of Vicore Pharma’s products candidates, ongoing clinical trials and expected trial results, the ability to commercialize buloxibutid, technology changes and new products in Vicore Pharma’s potential market and industry, the ability to develop new products and enhance existing products, the impact of competition, changes in general economy and industry conditions and legislative, regulatory and political factors. No assurance can be given that such expectations will prove to have been correct. Vicore Pharma disclaims any obligation to update or revise any forward- looking statements, whether as a result of new information, future events or otherwise. 2
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Company overview 3 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 Publicly listed on Nasdaq Stockholm (VICO) and funded well past Phase 2b data Financials Vicore is backed by leading specialist investors in the US and Europe Shareholders $381m As of January 9, 2026 market cap $137m As of September 30, 2025 pro forma financial position incl. recent financing Stockholm, Sweden Cambridge, Massachusetts, USA Copenhagen, Denmark Locations
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Compound Indication Preclinical Phase 1 Phase 2 Phase 3 Comments Rights Buloxibutid IPF Phase 2b ongoing (NCT06588686) Targeting full enrollment by H1 2026 Global ex-Japan rights Japan: New ATRAGs Multiple Indications Preclinical studies Fully-owned Pipeline 4 Unlocking the potential of a new class of drugs - Angiotensin II Type 2 Receptor Agonists (ATRAGs) 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.
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IPF is a progressive, fatal disease with significant unmet need despite available therapies 5 ~150K US IPF Patients ~3M Global IPF Patients Orphan Disease with High Unmet Need Limitations of Available Treatment Options 10 months1 Where only ~1/4 of US patients initiate treatment1 And the high discontinuation rate leads to an average time on treatment of only The majority of the IPF market is not adequately addressed today • Existing therapies offer only modest slowing of disease progression and have not demonstrated quality of life benefit • Significant GI side effects limit uptake, often requiring dose reductions and contributing to high discontinuation rates • Despite available treatments, the 5-year mortality rate is 80%2 • There are no approved disease-modifying therapies today Three FDA approved therapies: (1) Dempsey et al. Ann Am Thorac Soc 2021; (2) IPF Foundation
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IPF is a large and growing market with urgent need for innovation 6 2024 2033e $4.2B $10B+ 20241 2030-2033 (estimate)2 (1) Company reports (note: combined sales of marketed drugs Ofev and Esbriet where Ofev sales include SSc-ILD); (2) Global Data, The Insights Partners CAGR 10-15% Global IPF Market Size Significant market expansion expected over the next decade • New Approvals: Jascayd • Disease Awareness: Rising diagnosis rates and expected broader treatment adoption • Epidemiology: Aging population and increasing disease prevalence Drivers of Market Growth Today White Space for Market-Shifting Innovation • Disease-Modifying Efficacy: Stabilization or improvement in lung function • Well-Tolerated & Combinable Therapies: Expanding treatment pool, extending time on therapy, and reducing discontinuations
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Buloxibutid is positioned to transform the IPF landscape 7 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 therapy in global development. Limited efficacy demonstrated at 26 weeks Inconvenient dosing and administration and difficult tolerability profile Combination of unprecedented efficacy, favorable tolerability profile, and convenient dosing Buloxibutid Jascayd (nerandomilast) Tyvaso (treprostinil) admilparant AT2 receptor agonist PDE4B antagonist prostacyclin analog LPA1 antagonist MOA Novel endogenous upstream and multi-modal mechanism Oral BID Oral BID Nebulized formulation, 48 (12x4) breaths per day Oral BIDDosing & Administration Convenient oral dosing Favorable overall profile; mild-to-moderate hair loss GI-tolerability issues, further exacerbated on top of SoC Cough, throat irritation, headache, nausea and flushing Favorable overall profile; transient reduction in blood pressure Tolerability Favorable and combinable tolerability profile Unprecedented FVC improvement (+216mL vs. baseline at 36 weeks) Incremental efficacy (68.8mL vs. placebo at 52 weeks) Incremental efficacy (95.6mL vs. placebo at 52 weeks) Incremental efficacy (45.5mL vs. placebo at 26 weeks) Efficacy Potential to stabilize and improve lung function Offers only incremental improvement in efficacy and tolerability Key ChallengesValue Proposition
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Buloxibutid is a first-in-class AT2 receptor agonist with the potential to transform the IPF landscape 8 AT2 receptor expressed on alveolar progenitor cell (AEC2) Upstream mechanism drives alveolar repair, resolves fibrosis, and promotes vascular function Upstream MoA with strong preclinical data Mean FVC change from baseline of +216 ml at 36 weeks, with benefit observed across all subgroups Synthetic control arm analysis confirms robust treatment effect observed with buloxibutid Excellent gastrointestinal tolerability and no treatment-related SAEs Biomarker data highly supportive of suggested MoA Exceptional clinical data in the Phase 2a AIR trial Phase 2b ASPIRE: confirming the clinical activity in a randomized, placebo-controlled trial 52-week treatment N=360 (120 per arm) IPF patients on stable nintedanib/SoC or not on SoC1 Global footprint 1. As nerandomilast is now approved in the United States, patients receiving stable background nerandomilast therapy will be eligible for enrollment in the trial, though this is anticipated to represent a small subset of the study population.
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AT2R agonism is an upstream intervention driving tissue repair 9 • AT2R is constitutively expressed in the lung, primarily on alveolar epithelial type 2 cells (AEC2) – the “alveolar repair cell” • AT2R activation engages tissue-protective pathways via AEC2s, promoting inhibition of fibrotic progression and fibrosis resolution, anti-inflammatory effects, vasodilation, and reversal of vascular remodeling • Buloxibutid is an oral, selective AT2R agonist • AT1R effects include increase in blood pressure, a key reason for ACE inhibitor and ARB development ATRAGs ➢ Increase blood pressure ➢ Inflammation ➢ Resolution ➢ Repair ➢ Small vessel vasodilation CONSTITUTIVE INDUCIBLE • Anti-fibrotic • Vasodilatory • Anti-inflammatory • Hypertensive • Pro-inflammatory • Pro-fibrotic “Resolution” “Rescue” Buloxibutid
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AT2R is highly expressed in human IPF lungs and on precursor AEC2s 10Source: Adapted from IPF Cell Atlas (Banovich/Kropski) AGTR2 AT2R Expression is Elevated in IPF Lung AT2R expression is highly upregulated in the IPF lung, particularly on AEC2s, and is also present on fibroblasts, myofibroblasts, and endothelial cells with higher expression in the diseased state compared with healthy tissue Single cell analysis shows high AT2R expression on AEC2 in the lung, the progenitor cell that differentiates into AEC1 gas exchange cells AT2R is Highly Expressed on AEC2s AT2 receptor AEC2 AEC1 Disease Control ILD 0.00 0.02 0.04 0.06 0.08 AEC2 Fibroblast Myofibroblast Endothelial Cells
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Alveolar epithelial cells are critical for healthy lung function 11 Healthy alveolus AEC – Alveolar Epithelial Cell AEC1 AEC2 CO2 O2 Proliferation DifferentiationSurfactant Gas exchange • The alveolar epithelium is exposed to damaging irritants in inhaled air • AEC1 is the predominant alveolar cell type and is responsible for gas exchange • AEC2 is a progenitor cell that is critical for alveolar integrity and function: • Proliferates to form new AEC2 • Differentiates to AEC1 that need to be replaced • Produces surfactant to maintain alveolar integrity • AT2R is expressed on AEC2
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Click to edit Master title style Buloxibutid is an oral, selective AT2R agonist that drives tissue repair via AEC2 precursor epithelial cells 12 Alveolar compartment in IPF Effects of buloxibutid 1 Increased AEC2 viability & surfactant production 3 Upregulation of collagenase MMPs 2 TGFβ1 release, EMT & excess collagen 1 AEC2 dysfunction 3 MMP dysregulation TGFβ1 AEC2 AEC1 O2 CO2 Normal gas exchange Surfactants Buloxibutid MMPs MMPs Collagen Myofibroblasts Fibroblast Dysfunctional AEC2 Repeated Micro-injury TGFβ1 TGFβ1 Proliferation & differentiation Arteriole Endothelial Cells Anti-remodeling & Vasodilatation (NO release)4 Vascular remodeling & Endothelial dysfunction4 EMT = Epithelial–mesenchymal transition; MMPs = Matrix metalloproteinases 2 Normalization of TGFβ1 and inhibition of EMT and collagen
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Click to edit Master title style Buloxibutid addresses all main disease drivers in IPF and disease modification through tissue repair EMT = Epithelial–mesenchymal transition 13 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 release of pro-inflammatory cytokines through inhibition of NF-κB signaling Anti-Fibrotic Buloxibutid restores dysfunctional AEC2 and surfactant production, normalizes TGFβ1 levels, inhibits EMT and collagen deposition, as well as breaks down existing collagen build up Reverses Vascular Remodeling Buloxibutid reverses vascular remodeling and drives vasodilation through NO release
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SP-B SP-C % Increase vs Control Buloxibutid protects AEC2s and drives increased surfactant production 14 control C21 0.001 µM C21 0.005 µM C21 0.01 µM C21 0.05 µM C21 0.1 µM 0 10 20 30 40 50 9% 14%16% 29%31% 42% %Cell death • Human precision cut IPF lung slices ± 1 µM buloxibutid • One patient, 5 pooled lung slices +70% +120% Surfactant protein expression increased by buloxibutid in ex vivo human IPF precision cut lung slices2Buloxibutid protects AEC2 cells against apoptosis1 • Cultured A549 cells (human AEC2 cell line) • Bleomycin (10µg/ml) induced apoptosis Treatment with buloxibutid protects AEC2s, driving increased surfactant production to address alveolar collapse (1) Adapted from Nalbandyan et al. FASEB 2018; (2) Vicore data on file % Cell death buloxibutid buloxibutid buloxibutid buloxibutid buloxibutid
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Human precision cut lung slices (PCLuS) • Lung tissue collected from IPF patients undergoing transplant • Intrinsic fibrosis, no stimuli added Buloxibutid reduces TGF1 and collagen in human IPF lung slices 15 Collagen protein levels in PCLuSTGFβ1 protein levels in PCLuS Dose-dependent reduction of TGFβ1 and Collagen-1a1 protein Data represent averages +/- SEM of Plus 5 separate tissue slices at each concentration, sampled after 144h exposure to buloxibutid or vehicle Source: Vicore data on file *p<0.05, **p<0.01, ***p<0.001; t-test versus vehicle Vehicle 0.01μM C21 0.1μM C21 1μM C21 0 1000 2000 3000 4000 Collagen-1a1 (pg/ml) ✱ -44% Vehicle C21 0.01M C21 0.1M C21 1M C21 10M 0 50 100 150 TGF- 1(pg/mL) ✱✱ ✱✱ -61% TGF1 (pg/mL) Collagen-1a1 (pg/mL)
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Buloxibutid downregulates expression of EMT transcription factors in AEC2 Vehicle 0.1µM 1µM Vehicle 0.1µM 1µM Vehicle 0.1µM 1µM Vehicle 0.1µM 1µM SNAIL1 SNAIL2 • Primary AEC2 cultures established from normal surgically resected human lung • Buloxibutid treatment under baseline conditions with no stimuli added Source: Conforti et al. 2023, manuscript (Vicore collaboration with U Southampton) 16 buloxibutid buloxibutid buloxibutid buloxibutid
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17 Impact on type III collagen biomarker PRO-C3 Human lung fibroblast assay methodology Buloxibutid potently and dose-dependently inhibited PRO-C3, reflecting inhibition of type III collagen formation and fibrotic activity. The superior in vitro performance of buloxibutid vs. nintedanib and nerandomilast on the IPF biomarker PRO-C3 reflecting fibrotic progression underscores its robust anti-fibrotic mechanism of action Mean±SEM (n=4) ****p<0.0001 (one-way ANOVA) Buloxibutid potently inhibits fibrosis in a human lung fibroblast assay
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MMP-13 demonstrates antifibrotic activity and is crucial for lung repair in IPF 18 • MMP-13 is an enzyme able to cleave fibrillar collagens and plays a significant role in the degradation of the ECM • In mouse models, MMP-13 deficiency has been shown to1,2: 1. Decrease collagenolytic activity 2. Promote lung fibrosis 3. Attenuate fibrosis resolution ECM = Extracellular Matrix; MMP = Matrix Metalloproteases (1) Cabrera et al., 2019; (2) Nkyimbeng et al., 2013 Collagenase MMP dysregulation contributes to IPF pathogenesis Buloxibutid increased plasma MMP-13 in the Phase 2a AIR trial Baseline n=37 Week 12 n=36 Week 24 n=28 Week 36 n=23 0 50 100 150 200 250 Plasma MMP-13 (% of baseline) ** ** *** Buloxibutid significantly increased plasma levels of the fibrolytic collagenase MMP-13, indicating that buloxibutid has the potential to degrade fibrosis
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Buloxibutid’s vascular effects are clinically validated Buloxibutid’s vascular effects (vasodilation) are clinically validated in a forearm blood flow trial in healthy volunteers • Buloxibutid shows dose-dependent increase in local blood flow • Blood flow increased by 63% (p=0.026), without reducing systemic blood pressure or causing other side effects • Local blood concentrations of buloxibutid in line with those reached with oral treatment • No severe or serious TEAEs were reported Source: Vicore data on file 0 10 20 30 40 50 60 70 Buloxibutid 200 µg/min Buloxibutid 3 µg/min +63% +20% +40% Buloxibutid 30 µg/min p=0.026Mean change, n=5 19 Increase in forearm blood flow (%) Buloxibutid addresses endothelial dysfunction and increases local blood flow, mediated by nitric oxide (NO) released from the endothelium
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Buloxibutid shows greater reduction in key hemodynamic and vascular remodeling parameters compared to inhaled treprostinil in preclinical Sugen-Hypoxia rat model 20 -3% -10% -12% -10% -8% -6% -4% -2% 0% Inhaled Treprostinil Buloxibutid Fulton's Index Reduction vs. SuHx control -5% -13%-14% -12% -10% -8% -6% -4% -2% 0% Inhaled Treprostinil Buloxibutid Wall Thickness Reduction vs. SuHx control Inhaled treprostinil and buloxibutid were evaluated in separate studies using the same study protocol Inhaled treprostinil: adapted from Corboz, et al., J. Pharmacol. Exp. Ther. 2022 – Dose: 65 µg/kg Buloxibutid: adapted from Tornling, et al., Int. J. Mol. Sci. 2023 – Dose: average result of 2µM and 20µM dose Clinically relevant doses of buloxibutid shows greater reduction compared to the Sugen-Hypoxia control than clinically relevant dose of inhaled treprostinil across key readouts, including RVSP , mPAP (data not shown), Fulton’s index, wall thickness and muscularization (data not shown) SuHx = Sugen-Hypoxia; mPAP = mean pulmonary artery pressure ; RVSP = right ventricular systolic pressure -10% -20% -25% -20% -15% -10% -5% 0% Inhaled Treprostinil Buloxibutid RVSP Reduction in RVSP from SuHx control Hemodynamic Parameters Right Ventricular Remodeling Pulmonary Vascular Remodeling
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Sugen-HypoxiaMonocrotalineBleomycin Strong preclinical in vivo evidence for buloxibutid in pulmonary fibrosis (1) Rathinasabapathy et al. Front Physiol. 2018; (2) Bruce et al. Br J Pharmacol. 2015; (3) Tornling et al. Int. J. Mol. Sci. 2023; RVSP = Right Ventricular Systolic Pressure • Buloxibutid 0.03 mg/kg/day i.p. once daily for 2 weeks • N=14 per treatment group Adapted from (2) Lung collagen staining Control Bleomycin Buloxibutid prevention protocol Buloxibutid treatment protocol Lung collagen staining • Buloxibutid 0.03 mg/kg/day i.p. once daily, 14 days (Treatment). N=5 control and 7-8 in treatment groups Adapted from (1) • Buloxibutid p.o. for 34 days, initiated 21 d. after SuHx- period. N=10-11 per treatment group Adapted from (3) Lung collagen staining Control MCT MCT + C21 0 5 10 15Fibrosis (%) ** • Normalized collagen synthesis and attenuation of disrupted lung architecture • Reversal of pulmonary fibrosis and prevention of right ventricular fibrosis • Reversal of vascular remodeling and improved right heart function • Reversal of fibrosis • Reversal of vascular remodeling • Reduced RVSP and right ventricular hypertrophy Control BLEO C21 Prevention C21 Treatement 0 2 4 6Hydroxy proline (nM) ** * Control SuHx vehicle C21 20 mg/kg 3 4 5 6 7Fibrosis (%) **** 21 buloxibutid prevention buloxibutid treatment MCT + buloxibutid MCT buloxibutid 20 mg/kg SuHx vehicle Normoxia Su/Hx + Vehicle Su/Hx + buloxibutid 2 mg/kg Su/Hx + buloxibutid 20 mg/kg Control 2 weeks MCT MCT MCT + buloxibutid 200 um
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Click to edit Master title style Buloxibutid has an extensive and robust safety database, with over 350 patients dosed across nine completed clinical trials 22 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 366 trial participants have been exposed to buloxibutid over the course of 9 completed clinical trials • In the recently completed Phase 2a AIR trial, IPF patients were exposed to buloxibutid for 36 weeks No significant safety risks have been identified for buloxibutid • The only identified risk of treatment with buloxibutid is reversible, mild to moderate hair loss, observed in 19% of participants in the Phase 2a AIR trial • Across the robust safety dataset, there have been no treatment-related SAEs
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AIR: An open-label Phase 2a trial of oral buloxibutid 100 mg BID for up to 36 weeks in treatment-naïve IPF patients Screening period (<4 weeks) Follow-up period (2-4 weeks) Patient population Treatment-naïve IPF patients with centrally HRCT-confirmed diagnosis Buloxibutid 100 mg twice daily Risk/Benefit evaluation Risk/Benefit evaluation Clinic visits with FVC measurements 36-week treatment period Week 2 6 18 21 24 28 32 369 12 154 Patient population Primary endpoint Safety and tolerability Secondary endpoint Change in forced vital capacity (FVC) from baseline Exploratory endpoints Effect on selected biomarkers 23
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AIR baseline patient characteristics are in line with other IPF trials 24 AIR (N=52) INPULSIS 1&2 (N=1,061)1 Age (years) - Mean (SD) 67 (9) 67 (8) Gender Males Females 77% 23% 80% 20% Ethnicity White Asian 27% 73% 57% 30% BMI (kg/m2) – Mean (SD) 24.6 (4.1) 28 (4.6) FVC % predicted - Mean (SD) 75.5 (14) 79.7 (17) % SoC Pirfenidone Nintedanib 0% 0% 0% 0% In line with other trials. As with the INPULSIS trials, AIR patients were treatment-naïve. In line with other trials. Enrolled study population has disease progression comparable to global IPF study populations. (1) INPULSIS 1&2 were the Phase 3 studies that led to the approval of nintedanib; Richeldi et al. N Engl J Med 2014; 370:2071-82 Key Characteristics
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Treatment emergent adverse events: buloxibutid shows better tolerability than SoC 25 (1) N Engl J Med 2014;370:2071-82; (2) Hair loss was mild to moderate and reversible. One patient discontinued treatment due to hair loss. Note: Rash, gastroesophageal reflux disease, elevated creatinine, and pyrexia were also reported at 8% in AIR trial. Ph3 INPULSIS-1 52-week treatment1 Ph2a AIR 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% Nausea 23% 6% 4% Acute exacerbation of IPF 10% 10% 6% Cough 15% 13% 8% Vomiting 13% 2% 2% COVID-19 n/a n/a 6% Hair loss2 n/a n/a 19% Fatal AE 4% 5% 4% Severe AE 26% 18% 6% Serious AE 31% 27% 10% Good GI tolerability Low rate of exacerbations and cough worsening No serious, severe, or fatal AEs related to buloxibutid Buloxibutid has a favorable tolerability profile allowing it to be combined with other therapies for IPF Comparison to SoC Buloxibutid
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Buloxibutid stabilizes and improves lung function over the 36-week AIR trial 26 Note: n=48 patients with 2-week FVC data. Observed values, no imputation. *p<0.05, **p<0.01, ***p<0.001; t-test versus expected untreated decline corresponding to -120 mL/24 weeks Untreated patients1,2 Buloxibutid 1Noble et al. Eur Respir J. 2016 Jan; 47(1): 243–253 2Richeldi et al. Engl J Med 2014; 370:2071-2082 n=48 48 44 40 39 35 34 34 33 32 28 28 28 -200 -100 0 100 200 300 400 0 4 8 12 16 20 24 28 32 36 FVC change (mL) mean +SEM Week ** ** *** *** *
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27 All subgroups show FVC stabilization and improvement over baseline at 36 weeks Mean FVC change at week 36 vs baseline Subgroup (# patients); ∆mL SoC1,2 Untreated patients1,2 Note: Probable UIP and Typical UIP according to HRCT categorization at baseline. n=48 48 44 40 39 35 34 34 33 32 28 28 28 Probable UIP (n=18); 321 Typical UIP (n=10); 27 India (n=20); 277 RoW (n=8); 65 Male (n=23); 230 Female (n=5); 170 All (n=28); 216 -200 -100 0 100 200 300 400 0 4 8 12 16 20 24 28 32 36 FVC change (mL) mean +SEM Week Change at week 36 vs baseline Mean and median; ∆mL Mean FVC change at week 36 vs baseline (all) +216 ml Median FVC change at week 36 vs baseline (all) +63 ml 1Noble et al. Eur Respir J. 2016 Jan; 47(1): 243–253 2Richeldi et al. Engl J Med 2014; 370:2071-2082
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IPF Patient External Control Data Filter IPF Patient Data using Air Trial Inclusion Criteria Efficacy Testing External Control Arm Generation • Over 10,000 patients • Mean 12-month FVC change -170.3 ml • Age >= 40 years • FVC % predicted >= 60% • FEV1/FVC >= 70% • Treatment naïve patients • ~30,000 randomly sampled groups of 48 patients generated from filtered control data • 1:1 treatment-control ratio • Matching on 8 clinical variables at baseline • Univariate and multivariate tests of similarity with control • 408 randomly sampled groups accepted as control arms based on the baseline similarity tests • Mean similarity p-value = 0.23 (SD = 0.05) • Follow-up time – 36 weeks • AIR – mean FVC change +23 ml • Control – mean FVC change -114.8ml Note: Qureight analysis Development of a Synthetic Control Arm analysis to contextualize buloxibutid’s effect in the Phase 2a AIR study 28
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IPF patients selected for the Synthetic Control Arm analysis are highly matched to the Phase 2a AIR patient baseline characteristics Note: Qureight analysis Mean similarity p-value - 0.23 (SD=0.05) 29
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A Synthetic Control Arm analysis demonstrates buloxibutid’s robust treatment effect 30 408 individual matched Synthetic Control Arms (SCAs) generated by Monte Carlo cross validation Change in FVC in the Phase 2a AIR IPF trial compared to the external control arm study The Monte Carlo approach demonstrates that in patients without significant differences in core baseline parameters, buloxibutid showed statistically significant treatment effect compared to control FVC distribution Note: Qureight analysis -150 -100 -50 0 50 +23.2 Mean FVC change of 408 individually matched SCAs -114.8 External Control Arm Study FVC increase (mL) FVC decrease (mL) Phase 2 AIR Study Buloxibutid (imputed data) mean FVC change 99.75% of the SCAs had an FVC trajectory inferior to AIR (corresponds to a p-value of 0.0025) Baseline
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Buloxibutid drives a significant increase in ppFVC, consistent with its impact on absolute FVC 31 Average ppFVC change from baseline at week 36 (1) Average ppFVC at 36 weeks (n=28); (2) 36 week estimated ppFVC for nintedanib and placebo, INPULSIS trial (Richeldi et al. N Engl J Med 2014; 370:2071-82) Average increase of 7.5% precent predicted FVC at 36 weeks from baseline Nintedanib2 -2.0% -6 -4 -2 0 2 4 6 8 % Buloxibutid1 Untreated2 7.5% -4.2% Buloxibutid also demonstrated a median FVC change from baseline at week 36 of +2.2%
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Buloxibutid outperforms historical standard of care and untreated decline at 36 weeks 32 75% 82% Buloxibutid vs Untreated1 Buloxibutid vs SoC1 100% Buloxibutid outperforms expected change in FVC of untreated patients and those treated with current standard of care at 36 weeks Percentage of patients outperforming expected ∆FVC (1) Based on historical data (Richeldi et al., 2014); (2) Based on historical data (Flaherty et al., 2018) Note: 25% of patients treated with nintedanib over 52 weeks showed improvement or no decline in FVC in the INPULSIS trials, and for untreated patients the number was 9%. Percentage of patients with improved lung function (FVC) vs baseline 65% 25% 9% 0% 10% 20% 30% 40% 50% 60% 70% Buloxibutid SoC2 Untreated2 Most patients treated with buloxibutid experience improved lung function at 36 weeks, outperforming historical SoC and untreated patients
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Plasma TGFβ1 Buloxibutid increases collagenase MMP-13 drives a trend of decreased TGFβ1 33 Plasma MMP-13 Note: data shown as mean ±SEM ** p<0.01, ***p<0.001 paired t-test vs baseline Baseline n=37 Week 12 n=36 Week 24 n=28 Week 36 n=23 0 4 8 12 16 20 Plasma TGFβ1 (ng/mL) Baseline n=37 Week 12 n=36 Week 24 n=28 Week 36 n=23 0 50 100 150 200 250 Plasma MMP-13 (% of baseline) ** ** *** TGFβ1 is a key fibrotic driver in IPF; reduced TGFβ1 is consistent with buloxibutid’s mechanism of action and translational data MMP-13 is an antifibrotic collagenase that plays a key role in fibrotic resolution
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Phase 2b ASPIRE Trial: Robust randomized trial with global footprint 34 ASPIRE is a randomized, double-blind, placebo-controlled, parallel-group, multicenter, dose-finding trial Primary Endpoint: Change from baseline in FVC at 52 weeks Key Secondary Endpoint: Proportion of patients with disease progression at 52 weeks Screening Follow-up Randomization 1:1:1 n=360 Buloxibutid 50mg BID (n=120) Buloxibutid 100mg BID (n=120) Placebo BID (n=120) Baseline Last Dose52-week treatment duration IPF patients stable on nintedanib/SOC or not on SOC1 (no access, refused, intolerant or failed) Trial Design ~120 sites across 14 countries Global Footprint 1. As nerandomilast is now approved in the United States, patients receiving stable background nerandomilast therapy will be eligible for enrollment in the trial, though this is anticipated to represent a small subset of the study population.
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The ASPIRE trial is designed to capture the significant unmet need and commercial opportunity beyond emerging SOC 0 20 40 60 80 100 120 Admilparant Phase 2 26 Weeks Jascayd (nerandomilast) Ph3 FIBRONEER-IPF 52 Weeks Tyvaso (treprostinil) Ph3 TETON-2 52 Weeks 45.5 mL 68.8 mL 95.6 mL 126mL Significant additional value opportunity Emerging Efficacy Benchmark Change in FVC (mL) vs. Placebo Graphic is not meant to represent head-to-head study. Cross-trial comparisons are challenging due to differences in trial design and patient selection. Phase 2b ASPIRE trial Designed to exceed emerging efficacy benchmark Evolving Landscape Recent positive readouts reinforce the opportunity for tolerable therapies that can further reduce the decline in lung function Blockbuster Potential The trial is powered to ensure it can capture a broad efficacy range that would position buloxibutid as the most effective therapy for IPF to date in a multi-billion-dollar market Operational Confidence Enrollment is progressing as planned; full enrollment expected in 1H 2026 35
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Vicore’s partnership with Nippon Shinyaku for buloxibutid in Japan 36 Vicore Pharma and Nippon Shinyaku have entered an exclusive license agreement to develop and commercialize the drug candidate buloxibutid in Japan. Partnership Overview Vicore has received an upfront payment of USD 10 million and is eligible for up to USD 275 million in milestones, plus tiered royalties on net sales in Japan up to the low 20s. In addition, Nippon Shinyaku will cover a portion of global non-clinical, CMC, and late-stage clinical development costs. Financial Terms The partnership leverages Nippon Shinyaku's local expertise to address IPF, a condition with limited treatment options in Japan, enhancing Vicore's global IPF strategy. Nippon Shinyaku is a leader in the development of therapies for rare respiratory diseases in Japan, including the discovery and development of Uptravi for PAH. Strategic Benefits
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Vicore has a platform of proprietary ATRAGs 37 Follow-on compounds provide life-cycle-management optionality in IPF and complementary indications, as well as opportunities in a range ofother diseases • Optimized to drive differentiated biology and therapeutic activity in a range of potential diseases where the angiotensin II pathway can play a therapeutic role. • Enable Vicore to significantly extend its AT2R franchise in respiratory diseases beyond buloxibutid, as well provide optionality to pursue a range of other diseases, either fully alone or in partnerships. 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 covering buloxibutid, with expiry in 2042 before considering PTE or SPC*. *PTE = Patent Term Extension; SPC = Supplementary Protection Certificate
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HANS SCHIKAN, PharmD – CHAIRMAN 25 years management experience in global pharmaceuticals (e.g. CEO of Prosensa). Extensive board work experience from US Nasdaq-listed biotech firms. ANN BARBIER, MD, PhD More than 20 years of experience in drug discovery and development in rare diseases, including rare respiratory diseases. MICHAEL BUSCHLE, PhD More than 25 years of experience in basic research as well as biotech and pharma R&D. Extensive board work experience from US Nasdaq-listed biotech firms. ELISABETH BJÖRK, MD, PhD Broad drug development experience, currently leading global late- stage development activities in CVRM at AstraZeneca. Extensive board work experience in small and mid-size international life science companies. JACOB GUNTERBERG Experienced venture capitalist and life science sector financier. HEIDI HUNTER 25 years in senior pharmaceutical development and commercialization positions. YASIR AL-WAKEEL, BM BCH A seasoned executive board member and strategic advisor with focus on strategic finance and business development in biotech companies. Strong leadership team with extensive industry experience 38 Board of Directors AHMED MOUSA CHIEF EXECUTIVE OFFICER Experienced biotech executive with a background in molecular biology, law, and business development. MIKAEL NYGÅRD, PhD CHIEF OPERATING OFFICER Experienced healthcare Business Development executive, has led M&A and Corporate Development functions. JOHAN RAUD, MD, PhD CHIEF SCIENTIFIC OFFICER Ex AstraZeneca: Director of inflammation research. 25 years of experience in drug development. HELEN BARKER VP AND HEAD OF CMC Pharmaceutical scientist and business leader, with over 25 years experience delivering the technical and strategic development of novel compounds, devices, and companies. JIMMIE HOFMAN VP BUSINESS DEVELOPMENT Business Development executive with extensive deal- making experience. PROF. BERTIL LINDMARK, MD, PhD CHIEF MEDICAL OFFICER Extensive industry experience in respiratory and inflammatory diseases. Ex-AstraZeneca: Led the development of global brands like Pulmicort and Symbicort. HANS JEPPSSON, PhD CHIEF FINANCIAL OFFICER Cross-disciplinary background in finance and medicine. Ex Danske Bank: Equity analyst.
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www.vicorepharma.com info@vicorepharma.com www.vicorepharma.com info@vicorepharma.com Stockholm Kornhamnstorg 53 SE-111 27 Stockholm Sweden Copenhagen Agern Allé 5A DK-2970 Hørsholm Denmark Contact Us Addresses: Boston One Broadway, 14th Floor Cambridge, MA 02142 USA ahmed.mousa@vicorepharma.com hans.jeppsson@vicorepharma.com megan.richards@vicorepharma.com ahmed.mousa@vicorepharma.com AHMED MOUSA, CEO, ahmed.mousa@vicorepharma.com hans.jeppsson@vicorepharma.com HANS JEPPSSON, CFO, hans.jeppsson@vicorepharma.com IR Contacts: megan.richards@vicorepharma.com MEGAN RICHARDS, IR, megan.richards@vicorepharma.com