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VICORE PHARMA Unlocking the potential of a new class of drugs – Angiotensin II type 2 receptor agonists (ATRAGs) August 2026
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Forward-Looking Statements This presentation contains "forward-looking statements" within the meaning of the Private Securities Litigation Reform Act of 1995, as amended, that are based on the beliefs and assumptions and on information currently available to management of Vicore Pharma Holding AB (the "Company"). All statements other than statements of historical fact contained in this presentation are forward-looking statements. Forward-looking statements include, but are not limited to, statements concerning: the Company's planned and ongoing preclinical and clinical studies for buloxibutid and other product candidates, including the Phase 2b ASPIRE trial, and the potential advantages of those product candidates, including tolerability and efficacy; the initiation, enrollment, timing, progress, and release of data from, and results of those, clinical studies, including the expected timing of topline data from the ASPIRE trial and the pre-planned futility analysis; the Company's goals with respect to the development, regulatory pathway, and potential use, if approved, of its product candidates; the utility of prior preclinical, clinical, and synthetic control arm data in determining future clinical results; the timing or likelihood of regulatory filings and approvals; the Company's intellectual property position; the ability to commercialize buloxibutid; market opportunity estimates and competitive positioning; the Company's partnership with Nippon Shinyaku; and the sufficiency of the Company's cash position and financial resources to fund planned operations. In some cases, you can identify forward-looking statements by terminology such as "anticipates," "assumes," "believes," "can," "could," "estimates," "expects," "forecasts," "intends," "may," "might," "plans," "potential," "projects," "should," "targets," "will," "would," or in each case their negative, or other variations or comparable terminology. Forward-looking statements involve known and unknown risks, uncertainties, and other factors that may cause the Company's actual results, performance, or achievements to be materially different from any future results, performance, or achievements expressed or implied by the forward-looking statements. These risks and uncertainties include, but are not limited to, the risks and uncertainties set forth in the "Risk Factors" section of the Company's Registration Statement on Form 20-F, as amended, filed with the Securities and Exchange Commission (the "SEC"), and any subsequent reports that the Company files with or furnishes to the SEC. Forward-looking statements represent the Company's beliefs and assumptions only as of the date of this presentation. Although the Company believes that the expectations reflected in the forward -looking statements are reasonable, it cannot guarantee future results, levels of activity, performance, or achievements. Except as requi red by law, the Company assumes no obligation to publicly update any forward-looking statements for any reason after the date of this presentation to conform any of these statements to actual results or to chan ges in its expectations. Non-GAAP Financial Measures and Industry Data This presentation may contain industry and market data obtained from third-party sources. Neither the Company nor any of its affiliates has independently verified this data. Market opportunity estimates are subject to significant uncertainty and are not guarantees of future performance. Trademarks Vicore, the Vicore Pharma logo, and other trademarks or service marks of Vicore Pharma, as well as copyrights, appearing in this presentation are the property of the Company and its affiliates. Trade names, trademarks, and service marks of other companies appearing in this presentation are the property of their respective owners. Solely for convenience, some of the trademarks, service marks, trade names and copyrights referred to in this presentation may be listed without the TM, SM © or ® symbols, but the Company will assert, to the fullest extent under a pplicable law, the rights of the applicable owners, if any, to these trademarks, service marks, trade names and copyrights. 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 may play a central role in halting and reversing disease pathology Dual listing on Nasdaq Stockholm (VICO) and Nasdaq US (VCRE), and funded well past Phase 2b data Financials Vicore is backed by leading specialist investors in the US and Europe Shareholders $328m As of August 20, 2026 market cap $93m As of June 30, 2026 financial positionStockholm, 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) Enrollment complete; targeting topline readout in mid-2027 Global ex-Japan rights Japan: Pipeline 4 Unlocking the potential of a new class of drugs - Angiotensin II Type 2 Receptor Agonists (ATRAGs) Vicore’s lead program, buloxibutid, is an 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 New ATRAGs are in early-stage discovery
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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 potentially 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. Buloxibutid Jascayd (nerandomilast) Tyvaso (treprostinil) Admilparant AT2 receptor agonist Novel endogenous upstream and multi-modal mechanism PDE4B antagonist prostacyclin analog LPA1 antagonistMOA Oral BID Convenient oral dosing Oral BID Nebulized formulation, 48 (12x4) breaths per day Oral BIDDosing & Administration Favorable and combinable tolerability 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 Tolerability1 Mean FVC improvement Observed +216mL vs. baseline at 36 weeks Potential to stabilize and improve lung function Incremental efficacy +68.8mL vs. placebo at 52 weeks Pooled efficacy: TETON-1&2 +111.8mL vs. placebo at 52 weeks Incremental efficacy +45.5mL vs. placebo at 26 weeks Efficacy2 Limited efficacy demonstrated at 26 weeks Inconvenient dosing and administration and difficult tolerability profile Combination of improved efficacy, favorable tolerability profile, and convenient dosing Offers only incremental improvement in efficacy and tolerability Key ChallengesValue Proposition (1) Tolerability based on clinical data generated to date; (2) Efficacy data observed in the Phase 2a AIR trial Graphic is not meant to represent head-to-head study. Cross-trial comparisons are challenging due to differences in trial design, patient selection, and analysis method.
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Buloxibutid is an AT2 receptor agonist with the potential to offer a differentiated treatment standard in IPF 8 AT2 receptor expressed on alveolar progenitor cell (AEC2) Upstream mechanism is believed to drive alveolar repair, resolve fibrosis, and promote vascular function Upstream MoA with strong preclinical data Observed mean FVC change from baseline of +216 mL at 36 weeks, with benefit observed across all subgroups1 Synthetic control arm analysis reinforces the meaningful treatment effect observed with buloxibutid Good gastrointestinal tolerability and no treatment-related SAEs Biomarker data highly supportive of suggested MoA Encouraging clinical data observed in the Phase 2a AIR trial Phase 2b ASPIRE: confirming clinical activity in a randomized, placebo- controlled trial 52-week treatment Fully enrolled (n=378) IPF patients on stable nintedanib/SoC or not on SoC2 Global footprint (1) Mean FVC change observed in patients that completed the Phase 2a clinical trial; (2) As nerandomilast is approved in the United States, patients receiving stable background nerandomilast therapy were 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 10(1) Adapted from IPF Cell Atlas (Banovich/Kropski) AGTR2 AT2R Expression is Elevated in IPF Lung1 AT2R expression is highly upregulated in IPF lungs, 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 is associated with tissue repair via AEC2 precursor epithelial cells 12 Alveolar compartment in IPF Observed effects of buloxibutid1 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 & Vasodilation (NO release)4 Vascular remodeling & Endothelial dysfunction 4 EMT = Epithelial–mesenchymal transition; MMPs = Matrix metalloproteinases 2 Normalization of TGFβ1 and inhibition of EMT and collagen (1) According to preclinical and clinical data generated to date
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Click to edit Master title style Buloxibutid is designed to target key disease drivers in IPF, with a potentially disease-modifying mechanism through tissue repair EMT = Epithelial–mesenchymal transition 13 Tissue repair and regeneration Buloxibutid designed to target precursor epithelial cells (AEC2) to drive tissue repair, offering a potentially disease-modifying mechanism of action Anti-inflammatory Buloxibutid associated with inhibition of pro-inflammatory cytokine release through inhibition of NF-κB signaling Anti-fibrotic Buloxibutid associated with restoration of dysfunctional AEC2 and surfactant production, normalization of TGFβ1 levels, inhibition of EMT and collagen deposition, as well as break down of existing collagen build up Reverses vascular remodeling Buloxibutid associated with vasodilation and reversal of vascular remodeling through NO release Effects Observed in Preclinical Studies
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SP-B SP-C % Increase vs Control Buloxibutid is designed to protect AEC2s and drive 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% Increase in surfactant protein expression associated with buloxibutid in ex vivo human IPF precision cut lung slices2Buloxibutid associated with reduced apoptosis of AEC2s1 • Cultured A549 cells (human AEC2 cell line) • Bleomycin (10µg/ml) induced apoptosis Treatment with buloxibutid is associated with protection of AEC2s, driving increased surfactant production to potentially 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 is associated with TGFβ1 and collagen reduction in human IPF lung slices 15 Collagen protein levels in PCLuSTGFβ1 protein levels in PCLuS Dose-dependent reduction of TGFβ1 and Collagen-1a1 protein Source: Vicore data on file *p<0.05, **p<0.01, ***p<0.001; t-test versus vehicle Vehicle 0.01μ M C21 0.1 μM C21 1μM C21 0 1000 2000 3000 4000Collagen-1a1 (pg/ml) ✱ -44% Vehicle C21 0.01 µM C21 0.1 µM C21 1 µM C21 10 µM 0 50 100 150TGF-β1(pg/mL) ✱✱ ✱✱ -61% TGFβ1 (pg/mL) Collagen-1a1 (pg/mL) Data represent averages +/- SEM of 5 separate tissue slices at each concentration, sampled after 144h exposure to buloxibutid or vehicle
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Buloxibutid is associated with downregulated 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. of 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 associated with potent and dose-dependent inhibition of PRO-C3, suggesting inhibition of type III collagen formation and fibrotic activity. In a preclinical in vitro assay, buloxibutid showed potent inhibition of IPF biomarker PRO-C3 compared to nintedanib and nerandomilast, which may be indicative of its anti-fibrotic mechanism. Mean±SEM (n=4) ** p < 0.01 **** p < 0.0001 (one-way ANOVA) Collagen biomarker PRO-C3 inhibited in human lung fibroblast assay treated with buloxibutid, suggesting resolution of fibrosis
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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 Metalloproteinases (1) Cabrera et al., 2019; (2) Nkyimbeng et al., 2013 Collagenase MMP dysregulation contributes to IPF pathogenesis Buloxibutid associated with 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) ** ** *** Patients treated with buloxibutid showed a significant increase in plasma levels of the collagenolytic collagenase MMP-13, suggesting that buloxibutid has the potential to degrade fibrosis ** p < 0.01 *** p < 0.001
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Buloxibutid demonstrated greater reduction in key hemodynamic and vascular remodeling parameters compared to inhaled treprostinil in preclinical Sugen-Hypoxia rat model 19 -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 2 mg/kg and 20 mg/kg dose Clinically relevant concentrations of buloxibutid demonstrated 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 (%) **** 20 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 21 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 to date based on current clinical dataset • The only identified risk of treatment with buloxibutid is mild to moderate hair loss, which was observed to be reversible, 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 22
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AIR baseline patient characteristics are in line with other IPF trials 23 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/m 2) – 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 Key Characteristics
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Treatment emergent adverse events: buloxibutid shows better tolerability than SoC 24 (1) N Engl J Med. 2014; (2) Hair loss was mild to moderate and was observed to be 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 observed serious, severe, or fatal AEs related to buloxibutid Buloxibutid has a favorable tolerability profile allowing it to be potentially combined with other therapies for IPF Comparison to SoC Buloxibutid
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Buloxibutid was observed to stabilize and improve lung function over the 36- week Phase 2a AIR trial 25 Note: n=48 patients with 2-week change from baseline 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 (1) Noble et al. Eur Respir J. 2016; (2) Richeldi et al. N Engl J Med. 2014 Untreated patients1,2 Buloxibutid 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 Observed FVC change (mL) mean +SEM Week ** ** *** *** *
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26 All subgroups show FVC stabilization and improvement over baseline at 36 weeks SoC1,2 Untreated patients1,2 Note: n=48 patients with 2-week change from baseline FVC data. Observed values, no imputation. Note: Probable UIP and Typical UIP according to HRCT categorization at baseline. (1) Noble et al. Eur Respir J. 2016; (2) Richeldi et al. N Engl J Med. 2014 Change in FVC at week 36 vs baseline Subgroup (# patients); observed mean (∆mL) 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 Observed FVC change (mL) mean +SEM Week ml ml ml ml ml ml ml Change in FVC at week 36 vs baseline Observed 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
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IPF Patient External Control Data Filter IPF Patient Data using Air Trial Inclusion Criteria Efficacy Testing External Control Arm Generation • 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 +23.2 ml • Control – mean FVC change -114.8ml Note: Qureight analysis Development of a Synthetic Control Arm analysis to contextualize buloxibutid’s effect in the AIR trial 27
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IPF patients selected for the Synthetic Control Arm analysis are highly matched to the Phase 2a AIR patient baseline characteristics 28 Mean similarity p-value after matching - 0.23 (SD=0.05) Note: Qureight analysis Graphs show baseline characteristics of the filtered external IPF population (before the matching) versus AIR
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A Synthetic Control Arm analysis supports a clinically meaningful treatment effect 29 408 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 is associated with a significant increase in ppFVC, consistent with its observed impact on absolute FVC 30 Average ppFVC change from baseline at week 36 (1) Average ppFVC for patients who have completed the week 36 visit in Phase 2a AIR (n=28); (2) 36 week estimated ppFVC for nintedanib and placebo, INPULSIS trial (Richeldi et al. N Engl J Med. 2014) Analysis based on historical data and does not represent head-to-head study. Cross-trial comparisons are challenging due to differences in trial design, patient selection, and analysis method. Average increase of 7.5 percentage points in ppFVC at 36 weeks from baseline -6 -4 -2 0 2 4 6 8 Average ppFVC change from baseline Buloxibutid1 7.5% Patients treated with buloxibutid also demonstrated a median FVC change from baseline at week 36 of +2.2% Untreated2 Nintedanib2 -4.2% -2.0% Ph2a AIR Ph3 INPULSIS
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Buloxibutid showed favorable results compared to historical standard of care and untreated decline at 36 weeks 31 75% 82% Buloxibutid vs Untreated1 Buloxibutid vs SoC1 100% Patients treated with buloxibutid showed more favorable expected change in FVC compared with untreated patients and those treated with current standard of care at 36 weeks Percentage of patients showing more favorable 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%. Analysis based on historical data and does not represent head-to-head study. Cross-trial comparisons are challenging due to differences in trial design, patient selection, and analysis method. 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 were observed to have improved lung function at 36 weeks, showing more favorable results compared to historical SoC and untreated patients
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Plasma TGFβ1 Buloxibutid is associated with increase of collagenase MMP-13 and decrease of TGFβ1 in the Phase 2a AIR trial 32 Plasma MMP-13 Note: Phase 2a 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 33 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=378 Buloxibutid 50mg BID Buloxibutid 100mg BID Placebo BID 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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ASPIRE includes a pre-planned, independent futility analysis 34 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. Rationale Method Timing and Communication • Results available after iDMC processing and review • Expected timing: Q4’26 • Vicore will remain blinded; no effect size or trends will be disclosed to preserve trial integrity • Based on efficacy data from the first ~100 randomized patients • Uses a conditional power approach, to estimate probability of success at final readout • Stopping threshold set conservatively; stop for futility will be considered if the conditional power is lower than 20% Purpose of the futility analysis: 1. Protect patients participating in the trial 2. Reduce risk of a negative readout at time of final analysis 3. Preserve trial integrity through a well- established futility approach consistent with regulatory expectations
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Phase 2b ASPIRE trial: designed to position buloxibutid as a differentiated and highly competitive therapy for IPF in a multi-billion-dollar market 35 01 Efficacy Clinically meaningful impact on FVC versus placebo 02 Tolerability Safety and tolerability profile supportive of chronic use, adherence, and quality of life 03 Combinability Mechanistic synergy and tolerability profile suitable for combination use Defining Success in IPF Low High Transformational efficacy Limited clinical impact Clinically meaningful efficacy Change in FVC (mL) vs. Placebo 68.8mL 45.5mL 111.8mL Graphic is not meant to represent head-to-head study. Cross-trial comparisons are challenging due to differences in trial design, patient selection, and analysis method. Phase 2b ASPIRE: target efficacy profile buloxibutid Admilparant Ph2 26 Weeks Jascayd (nerandomilast) Ph3 FIBRONEER-IPF 52 Weeks Tyvaso (treprostinil) Ph3 TETON-1&2 52 Weeks Buloxibutid combines the potential for disease-modifying efficacy with a favorable tolerability profile, positioning it to potentially reshape the IPF treatment paradigm
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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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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. ELISABETH BJÖRK, MD, PhD Broad drug development experience, formerly 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. PETER GUENTER Nearly four decades of global pharmaceutical leadership experience (e.g., former CEO of Merck Healthcare, former CEO of Almirall). Strong leadership team with extensive industry experience 37 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. ROBERT SLACK, PhD, FRSB CHIEF SCIENTIFIC OFFICER Former VP of respiratory biology at GSK; Former CSO at Galecto. 25 years of experience in drug development. HELEN BARKER CHIEF TECHNOLOGY OFFICER Pharmaceutical scientist and business leader, with over 25 years of experience delivering the technical and strategic development of novel compounds, devices, and companies. JIMMIE HOFMAN CHIEF BUSINESS OFFICER Business Development executive with extensive deal- making experience. BERNT VAN DEN BLINK, MD, PhD CHIEF MEDICAL OFFICER Board-certified pulmonologist with 25+ years of experience in IPF and ILD drug development. Former senior clinical leader at Kinevant, Promedior, and Galapagos. HANS JEPPSSON, PhD CHIEF FINANCIAL OFFICER Cross-disciplinary background in finance and medicine. Former Danske Bank: Equity analyst.
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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: Cambridge One Broadway, 14th Floor Cambridge, MA 02142 United States AHMED MOUSA, CEO, ahmed.mousa@vicorepharma.com HANS JEPPSSON, CFO, hans.jeppsson@vicorepharma.com IR Contacts: