Medivir Ab · OMXSTO:MVIR
Medivir Ab — Investor Presentation (2026)
77 slides from Medivir Ab's investor presentation, 2026
Slide 1: Medivir
MEDIVIR INNOVATION IN AREAS OF HIGH UNMET MEDICAL NEED
Slide 2: Important notice
Important notice You must read the following before continuing. The following applies to this document and the information provided in this presentation by Medivir AB (publ) (the “Company”) or any person on behalf of the Company and any other material distributed or statements made in connection wit
Slide 3: A pipeline of first-in-class programs targeting patient populations without approved treatment options
A pipeline of first-in-class programs targeting patient populations without approved treatment options DISEASE PRE- ON POTENTIAL NEXT PROJECT PARTNER PH 1 PH 2 PH 3 FINANCIALS AREA CLINICAL MARKET EVENT(S) IN-HOUSE PROGRAMS Fostroxacitabine In-house HCC (mono) 100% Medivir Phase 2 start bralpamide
Slide 4: Main Projects & Potential New indication
Main Projects & Potential New indication • Fostrox in primary liver cancer: Blockbuster potential • MIV-711 in Osteogenesis Imperfecta: Blockbuster potential • MIV-701 in periodontitis in dogs: around SEK700m (Peak royalty) • MIV-711 in Perthes disease (Perthes sjukdom) • Orphan Drug Designation & R
Slide 5: Transformational progress
Transformational progress Two directed share issues of SEK 140 million & SEK 45 million to Carl Bennet AB and other institutional investors, enabling MIV-711 phase 2 studies in two rare, bone-related disorders, Osteogenesis Imperfecta & Perthes Disease and providing funding into 2030 Phase 1b/2a dat
Slide 6: Strong track-record in out-licensing
Medivir; Strongagenda Placeholder track-record in out-licensing Partnerships to effectively building shareholder value 2 approved drugs (Xerclear & Olysio) developed & out-licensed 3 first-in-class R&D programs out-licensed 3 in-house programs funded through phase 2, data read-outs in 27/28, for add
Slide 7: Leadership & board with extensive early & late stage drug development experience
Leadership & board with extensive early & late stage drug development experience CE0 – Jens Lindberg Chairman of the Board – Anders Hallberg > 25 years in pharma with focus in Oncology, late-stage Master's degree in economics from Lund University development & commercialization >25 years o
Slide 8: In-house programs
IN-HOUSE». * ~ ; PROGRAMS» * * ‘ MEDIVIR Slide 8
Slide 9: Improving life for advanced liver cancer (HCC) patients
Placeholder agenda Improving life Improving forfor life advanced liver liver advanced cancer (HCC) patients cancer (HCC) patients Fostrox – Displacing The first oral, chemotherapy liver-targeted with the treatment first oral, liver-activated forofadvanced inhibitor HCC DNA replication
Slide 10: First-to-market opportunity in 2nd line HCC market valued >$2.5bn
First-to-market opportunity in 2nd line HCC market valued >$2.5bn Slide 10
Slide 11: Primary Liver Cancer (HCC)
Primary Liver Cancer (HCC) • 3rd leading cause of cancer death globally • 70,000 new patients per year in Europe and USA • High unmet medical need for effective second-line treatment Slide 11
Slide 12: 45% of US adults are obese; fatty liver disease increases liver cancer risk
45% of US adults are obese Fatty Liver Disease increases More than 25% have Fatty Liver Disease risk of Liver Cancer 17-fold 12
Slide 13: Growth in Fatty Liver Disease expected to drive an alarming increase in liver cancer cases
Growth in Fatty Liver Disease expected to drive an alarming increase in liver cancer cases1 Fatty Liver Disease (MASLD/MASH) expected to rise dramatically over the next 30 years The number of newly diagnosed liver cancer patients each year is expected to double HCC market growth further spurred by m
Slide 14: Fostrox + Lenvima is at the forefront of development in population where no treatments are approved today
Fostrox + Lenvima is at the forefront of development in population where no treatments are approved today Advanced HCC – Treatment Algorithm 1L 90% 10% • Majority treated with IO combo • Tecentriq + Avastin preferred with recent data strengthening its position IO combination Lenvatinib (or Sorafenib
Slide 15: 2nd line HCC – a ~$3bn commercial opportunity
2nd line HCC – a ~$3bn commercial opportunity3 $4.0 bn Growth driven by: HCC to increase +122% in the US and +82% in China2 by 2030, caused by fatty liver disease +115% $2.8 bn With improved 1L treatment, more patients will be fit enough for 2L, 50% 70% RoW – 28% $1.3 bn China – 30% 2030 Upsid
Slide 16: Fostrox – tailored for the specific needs of HCC
Fostrox – tailored for the specific needs of HCC Slide 16
Slide 17: Fostrox – designed to selectively kill tumor cells in the liver
Fostrox – designed to selectively kill tumor cells in the liver Prodrug transports inactive payload to the liver, where it is rapidly activated by liver enzymes1 Kills tumor cells2,3,4 Spares healthy cells2,3,4 Liver-guided Tumor-selective delivery – payload – prodrug troxacitabine 1Bethell, R. et a
Slide 18: Fostrox MoA – tailored for HCC to achieve targeted DNA damage in liver tumor cells
Fostrox MoA – tailored for HCC to achieve targeted DNA damage in liver tumor cells with minimal impact on healthy liver cells Inactive Prodrug cytotoxic Fostrox taken as oral tablet Prodrug transports inactive payload via first-pass metabolism to the liver1 Rapidly activated by liver enzymes Trapped
Slide 19: 100-fold higher liver targeting vs IV administration & selective DNA damage in tumor cells
100-fold higher liver targeting vs IV administration & selective DNA damage in tumor cells enabling highly targeted mechanism >100-fold higher liver targeting with Liver tumor cells divide significantly Fostrox induces DNA damage in tumor fostrox than iv troxacitabine in rats more often than non-tum
Slide 20: Fostrox + Lenvima shows promise of improved outcomes in 2L HCC
Fostrox + Lenvima shows promise of improved outcomes in 2L HCC Slide 20
Slide 21: Fostrox Clinical Development Program
Fostrox Clinical Development Program; monotherapy PoC established, focus on combination approach in 2L HCC FLEX-HCC – Phase 1a Mono Phase 1b Mono Phase 1b Combo Phase 2a Combo Phase 2 Combo Single patient Fostrox + lenvatinib Fostrox + lenvatinib 3+3 dose Fostrox + lenvatinib Intrapatient dose dose
Slide 22: Fostrox + Lenvima phase 1b/2a study design
Fostrox + Lenvima phase 1b/2a study design Fostrox + LEN Treatment until PD Fostrox + LEN • Adv/inop HCC 30 mg RP2D – 30 mg (n=15) Primary Endpoint: • 2L/3L (n=3) Safety • ≥ 18 y • ECOG ≤ 1 Fostrox + LEN* Key Secondary • Child-Pugh A 20 mg Endpoints: ORR, DCR, (n=3) TTP/PFS Patients were enrolled at
Slide 23: Global phase 1b/2a study with fostrox + Lenvima positive, data published in Clinical Cancer Research
Global phase 1b/2a study with fostrox + Lenvima (TKI) positive, data published in Clinical Cancer Research1 UK 3 centres Korea 6 centres Spain 6 centres Slide 23 1Chon et al., Clinical Cancer Research 2026.
Slide 24: Patient characteristics reflecting generous inclusion criteria
Patient characteristics reflecting generous inclusion criteria Patient characteristics1 N = 21 Mean age (range) 62 yrs (42 - 82) Gender, Female / Male (%) 24 / 76 ECOG Performance status 0/1 (%) 71 / 29 Child-Pugh A (%) 100 Viral/Non-viral (%) 76* / 24 Extra hepatic lesion(s) Y/N (%) 67 / 33 AFP ≥40
Slide 25: More than 75% of patients experiencing tumor shrinkage
More than 75% of patients experiencing tumor shrinkage1 Best percentage change in target lesion size related to treatment response in first line 30% 20% Disease control on prior therapy Best % change in target lesion 16% Primary refractory on prior therapy 10% 11% Median duration of response 7.0 2
Slide 26: Median TTP 10.9 months, indicating substantially improved efficacy compared with Lenvima alone
Median TTP 10.9 months, indicating substantially improved efficacy compared with Lenvima alone1 Median time to progression (TTP) with fostrox + LEN – investigator review, RECISTv1.1 Fostrox + LEN (n =21)1 Median TTP, mo 10.9 95% CI (4.1 – 18.1) ORR 24% • Median time to progression 10.9 months DCR 81
Slide 27: Median TTP 10.9 months, remarkably longer than Lenvima monotherapy and other 2L HCC treatments
Median time to progression (TTP) 10.9 months, remarkably longer than Lenvima monotherapy and other 2L HCC treatments Median TTP (Kaplan-Meier) with fostrox + Lenvima Median TTP/PFS vs previous studies in 2L HCC ~3.5-4 months Lenvima after IO combo: Fostrox + LEN (n =21)1 Kobayashi et al. 2023 (n=12)
Slide 28: Korean Cancer Study Group prospective study data with Lenvima post Tecentriq + Avastin
Korean Cancer Study Group prospective study data with Lenvima post Tecentriq + Avastin, aligns with other 2nd line outcome data Slide 1Kim et al., Journal of Hepatology, Sept 04 2025
Slide 29: Similar patient characteristics across the Lenvima monotherapy study and the fostrox + Lenvima study
Similar patient characteristics across the Lenvima monotherapy study and the Phase 1b/2a fostrox + Lenvima study N = 50 N = 21 Patient characteristics Lenvima monotherapy Fostrox + Lenvima 13 sites in Korea1 15 sites in Korea, UK & Spain2 Mean age (range) 66 (32-86) 62 yrs (42 - 82) Gender, Female /
Slide 30: Fostrox + Lenvima phase 1b/2a data showed substantially better outcome than Lenvima monotherapy
Fostrox + Lenvima phase 1b/2a data showed substantially better outcome data compared to the Lenvima montherapy study Median TTP – Fostrox + Lenvima1 Median PFS – Lenvima monotherapy2 Fostrox + Lenvima (n=21)1 Lenvima (n=50)2 Median TTP, mo 10.9 Median PFS, mo 5.4 95% CI (4.1 – 18.1) 95% CI (4.2 – 7.
Slide 31: Fostrox + Lenvima shows encouraging tolerability
Fostrox + Lenvima shows encouraging tolerability enabling patients to remain on treatment long-term Slide 31
Slide 32: Absolute neutrophil and platelet counts were stable over the course of treatment
Absolute neutrophile and platelet counts were stable over the course of treatment, enabling long-term use1 Longitudinal neutrophil & platelet counts, at all time points measured over first 10 months of treatment 8 000 Neutrophils Platelets 350 000 7 000 300 000 6 000 neutrophils per microliter 250 0
Slide 33: Stable liver function during treatment with fostrox + Lenvima
Stable liver function during treatment with fostrox + Lenvima – no deterioration in liver enzymes or change in ALBI score ALT change over duration of AST change over duration of ALBI score change over duration of treatment treatment treatment 200 -1,50 80 ALBI Score -2,00 150 60 -2,50 100 -3,00 40 -
Slide 34: FLEX-HCC: Phase 2 study enables rapid generation of randomized, comparative data
FLEX-HCC: Phase 2 study enables rapid generation of randomized, comparative data to confirm benefit of fostrox combination with Lenvima in 2nd line HCC Slide 34
Slide 35: FLEX-HCC Fostrox + Lenvatinib Combination for Advanced HCC
FLEX-HCC Fostrox + Lenvatinib Combination for Advanced HCC Yonsei University College of Seoul National University Medicine Severance Hospital Medical Center Primary Investigator Asan Medical Center Samsung Medical Center CHA Bundang Hospital Gachon University Gil Medical Center Seoul National Univer
Slide 36: FLEX-HCC: Randomized, comparative phase 2 study design
FLEX-HCC: Randomized, comparative phase 2 study to confirm benefit for fostrox + Lenvima combination in 2nd line HCC 2026 2027 Study design: • 80 pts randomized to fostrox + Lenvima or Inclusion criteria Primary endpoint: Lenvima alone Fostrox 30 mg + Lenvima SD* • ORR (BICR) • 8 sites in Korean Can
Slide 37: Fostrox: The first oral, liver-targeted treatment tailored for HCC
Fostrox (fostroxacitabine bralpamide) The first oral, liver-targeted treatment tailored for HCC Oral, liver-activated small molecule Promising efficacy in 2nd line HCC in First-to-market opportunity in patient selectively targeting tumor cells3 combination with lenvatinib1,2 population worth >$2.5bn
Slide 38: US Notice of Allowance extends fostrox + lenvatinib patent protection to April 2041
US Notice of Allowance extends fostrox + lenvatinib patent protection to April 2041 Medivir receives Notice of Allowance Covers the combination of fostrox + Lenvima for the treatment of HCC and for the fostrox plus lenvatinib metastases to the liver combination patent from the US Patent and Trademar
Slide 39: MIV-711 – Highly selective oral cathepsin-K inhibitor for Osteogenesis Imperfecta
MIV-711 – Highly Improving selective life for oral, cathepsin-K advanced liver cancerinhibitor (HCC)forpatients Potentialchemotherapy Displacing treatment with of Osteogenesis Imperfecta the first oral, liver-activated inhibitor of DNA replication
Slide 40: MIV-711 – Clear, scientific rationale for treatment of Osteogenesis Imperfecta
MIV-711 – Clear, scientific rationale for treatment of Osteogenesis Imperfecta Slide 40
Slide 41: Osteogenesis Imperfecta (brittle bone disease)
Osteogenesis Imperfecta (brittle bone disease) • Rare, life-threatening disease: 1 in 15,000 births • Genetic mutations – born with the disease • Defective or insufficient collagen production • Fragile bones that fracture easily • Children suffer up to five fractures per year • Bone deformities and
Slide 42: Osteogenesis Imperfecta (OI) – a rare disease with significant unmet medical need
Osteogenesis Imperfecta (OI) – a rare disease from pediatric to adulthood with significant unmet medical need Clinical rationale & unmet medical need • Heterogenous rare disorder with 85% having dominant inherited mutations in genes for collagen 1 (COL1A1/COL1A2), causing varying degrees of severity
Slide 43: OI are divided into subtypes according to clinical severity
OI are divided into subtypes according to clinical severity 1,2 Type I 50% Mild with usually normal height or short stature. Up to 30 fractures during life span Potential Severe with short stature and deformities/scoliosis. candidates for Type III 15% Up to 100 fractures during life span pharmac
Slide 44: Bone remodelling is a continuous process requiring interplay between osteoclasts & osteoblasts
Bone remodelling is a continuous process requiring interplay between osteoclasts & osteoblasts Osteoclasts Cells responsible for resorbing old bone Osteoblasts Cells responsible for synthesizing new bone. Cathepsin K Enzyme secreted by osteoclasts driving bone resorption Elevated in OI Slide 44
Slide 45: Cathepsin K activity is increased in Osteogenesis Imperfecta
Cathepsin K activity is increased in Osteogenesis Imperfecta and drives increased bone resorption 1. Type I collagen is the major component in bone, making up ~90% of bone matrix. It is the skeleton of the bone and provides flexible strength and regulates the mineralization process 2. The OI mutatio
Slide 46: MIV-711 restores balance between bone resorption and bone formation
MIV-711, a selective cathepsin K inhibitor, restores balance between bone resorption and bone formation 1. MIV-711 is a highly selective inhibitor of Cathepsin K, preventing degradation of type I collagen 2. While MIV-711 inhibits the in OI increased bone degrading osteoclast activity, continuous bo
Slide 47: Inhibiting cathepsin K prevents bone resorption and restores bone remodelling
Inhibiting cathepsin K prevents bone resorption and restores bone remodelling and formation of new bone Cathepsin K inhibition Prevents bone resorption by selective inhibition of cathepsin K + Effectively prevents bone resorption while saving osteoclast functionality + Preserves osteoclast – osteobl
Slide 48: Cathepsin K inhibition showing significant benefit across multiple bone-related disorders
Cathepsin K inhibition showing significant benefit across multiple bone-related disorders Cathepsin K inhibition – Significant bone Cathepsin K inhibition – Cathepsin K inhibition – promising & cartilage benefit in Osteoarthritis1 prevents fractures in Osteoporosis2 signals in Osteogenesis Imperfect
Slide 49: Highly experienced scientific expert council to support design of clinical development program
Highly experienced scientific expert council to support design of clinical development program Dr. Andreas Kindmark • Associate Professor and Senior Consultant in Endocrinology at Uppsala University Hospital, specializing in the investigation of skeletal metabolic disorders Dr. Bente Lomholt Langdah
Slide 50: Clinical, regulatory and patient organization input on MIV-711 in OI
Clinical, regulatory and patient organization input on MIV-711 in Osteogenesis Imperfecta External engagements and interactions Take aways to shape PoC study design • Scientific Expert Council: study design in the context of • Strong engagement from external experts with current/ future management o
Slide 51: Preparation for the randomized phase 2 PoC study with MIV-711 in OI
Preparation for the upstart of the randomized phase 2 PoC study with MIV-711 in OI well underway • Patients with MIV-711 Endpoints: Osteogenesis Imperfecta High dose • Change in Biomarkers including • Fractures within the N~10 BMD previous 5 yr 1:1 • PK • N ~20 • Safety MIV-711 • Number of fractures
Slide 52: Osteogenesis Imperfecta - Economics
Osteogenesis Imperfecta - Economics • Rare but life-threatening disease: 1 in 15,000 births • Primary market: 58,000 patients in Europe and USA • Orphan Drug Disease – Premium pricing • Rare Pediatric Disease Voucher at market approval* – value ~USD200m • Market worth at least USD2.5bn - Blockbuster
Slide 53: MIV-711 in Perthes Disease
MIV-711 in Perthes Disease — Addressing a significant unmet medical need in children Slide 53
Slide 54: Legg-Calvé-Perthes disease – a rare, life-altering disease in children
Legg-Calvé-Perthes disease – a rare, life-altering disease in children with no approved drug treatment • Rare, life-altering disease in children: 1 in 1,500 • Most commonly affects boys aged 4–8 years • Sudden disruption of blood supply to the femoral head • Bone necrosis, collapse and deformity of
Slide 55: MIV-711 would target 60-80% of the patient population at diagnosis
MIV-711 would target 60-80% of the patient population at diagnosis Necrosis Fragmentation Re-ossification Remodelling Initial period of Re-absorption of New bone re- Femoral head ischemia/loss of bone with grows to reshapes itself blood supply to femoral head reshape the femoral head collapse femora
Slide 56: MIV-711 in Perthes disease – a second rare bone indication
MIV-711 in Perthes disease – a second rare bone indication built on the same established profile Rationale for MIV-711 in Perthes disease Development plan and status • MIV-711 counteracts deformity of the femoral head in a • Funding secured for phase 2 PoC study, financed by disease-specific animal
Slide 57: Perthes disease – significant commercial opportunity with orphan drug premium pricing
Perthes disease – significant commercial opportunity with orphan drug premium pricing • Primary market: 8,800 children annually in Europe and USA • Patients accessible for treatment: ~80% • Orphan Drug Disease – Premium pricing • Rare Pediatric Disease Voucher potential** – ~USD200m • Estimated annu
Slide 58: MIV-711 – highly selective cathepsin K inhibitor now in two rare bone indications
MIV-711 – highly selective cathepsin K inhibitor now in two rare bone indications 3rd generation, highly selective Proven ability to prevent bone Two first-to-market opportunities in cathepsin K inhibitor degradation & improve bone quality1,2 rare bone disease LCPD No approved treatment options in
Slide 59: Partnered Programs
a — 7 * Z PARTN ERED . ; 2 PROGRAMS * Py MEDIVIR Slide 59
Slide 60: VBX-1000 (MIV-701) – potential disease-modifying treatment of periodontal disease in dogs
VBX-1000 (MIV-701) – The first, potential disease- modifying treatment of periodontal disease in dogs Slide 60
Slide 61: Exclusive licensing agreement with Vetbiolix for MIV-701 (VBX-1000)
Exclusive licensing agreement with French biotech Vetbiolix for the development of MIV-701 (VBX-1000) in animal health Positive POC established in periodontitis in dogs with topline results from randomized, placebo-controlled study expected during Q4 2026 Global, exclusive, licensing agreement to de
Slide 62: Periodontal disease in dogs (PD)
Periodontal disease in dogs (PD) • 160 million dogs in Europe and USA; >80% of dogs by age 3 has PD • Periodontal disease is the number one disease in dogs • UK study (n=22 300): PD 12.5%, ear infections 7.3%, obesity 7.1% • Standard of care: Dental cleaning/surgery/tooth extraction • No drug treatm
Slide 63: Landmark POC Study in periodontal disease in dogs
Landmark POC Study in periodontal disease (PD) in dogs showing significant & clinically relevant improvements Inclusion criteria High dose Primary endpoint: Study outcomes: VBX-1000 (MIV-701) • Plasma CTX1 • Client-owned dogs • The first treatment to show disease-modifying with alveolar bone N=10 be
Slide 64: Randomized, double-blind, placebo-controlled pilot study in dogs
Randomized, double-blind, placebo-controlled pilot study in dogs to confirm the efficacy of VBX-1000 (MIV-701) Inclusion criteria High dose Endpoints: Estimated study timelines: VBX-1000 (MIV-701) • Client-owned dogs • 29 dogs dosed to date (June 30) • Plasma CTX1 with alveolar bone N=17 • Top-line
Slide 65: Periodontal disease in dogs - Economics
Periodontal disease in dogs - Economics • Vetbiolix as collaboration partner assumes all development costs • Income split/Royalty agreement • Drug pricing: Low due to private pay (not covered by insurance) • Peak royalty potential: around SEK700m • No approved disease-modifying drug available Slide
Slide 66: Remetinostat – Phase 3 ready topical HDAC-inhibitor for non-melanoma skin cancer
Remetinostat – Phase 3 ready topical HDAC- inhibitor for non-melanoma skin cancer Slide 66
Slide 67: Remetinostat – Efficacy and safety shown in 3 skin cancers
Remetinostat – Efficacy and safety shown in 3 skin cancers Three Phase II trials completed Unique topical HDAC-inhibitor Cutaneous T-Cell Lymphoma (MF-CTCL) Stability of remetinostat • Open label, multicenter Phase II study (60 patients) results showed 40% ORR, and reduced pruritus (itching) in 80%
Slide 68: Medivir enters exclusive licensing agreement with Biossil, Inc. for remetinostat
Medivir enters exclusive licensing agreement with Biossil, Inc. for remetinostat Positive phase 2 data in basal cell carcinoma (BCC) and cutaneous T-cell lymphoma (CTCL) Global, exclusive, licensing agreement to develop and commercialize remetinostat Total, potential milestone payments of approximat
Slide 69: Remetinostat is an effective topical treatment for reducing BCC disease burden
Remetinostat is an effective topical treatment for reducing BCC disease burden in a clinically significant manner >50% of lesions achieving complete Encouraging efficacy across all subtypes of BCC lesions pathological resolution across full cohort Nodular 0% -10% -20% 70% -30% Percentage change -40%
Slide 70: MET-X – AMR resistance bypass drug candidate
MET-X – AMR resistance bypass drug candidate Slide 70
Slide 71: MET-X (MBLI) – FDA QIDP Designation received & sub-licensing agreement signed
MET-X (MBLI) – FDA QIDP Designation received & sub- licensing agreement signed to enter clinical development Potential best-in-class Metallo-β-Lactamase Inhibitor MET-X restores activity of Meropenem* • MET-X is a potent broad-spectrum MBL inhibitor in combination with β-lactams to restore their act
Slide 72: Strengthened financial position
Strengthened financial position Oversubscribed SEK 140 million directed share issue funds all three phase 2 studies; Slide 72
Slide 73: Oversubscribed SEK 140 million directed share issue secures funding for all three phase 2 studies
Oversubscribed SEK 140 million directed share issue secures funding for all three phase 2 studies The directed share issue A strengthened financial position • Cash and cash equivalents of SEK 253.5 million at the • Approximately SEK 140 million gross (SEK 134 million end of the quarter, versus SEK 3
Slide 74: Three phase 2 studies – all fully funded after the directed share issue
Three phase 2 studies – all fully funded after the directed share issue FLEX-HCC – fostrox + Lenvima in 2nd MIV-711 in Osteogenesis Imperfecta MIV-711 in Perthes disease line liver cancer Randomized phase 2, 80 patients, 12 Randomized phase 2 PoC, ~20 adult Funding secured for phase 2 PoC hosp
Slide 75: Financial summary Q2, 2026
Financial summary Q2, 2026 Consolidated Income Statement, summary Q2 Q1 - Q2 Full year (SEK m) 2026 2025 2026 2025 2025 Net turnover 1,2 1,5 2,3 2,1 8,5 Other operating income 0,0 0,3 0,2 0,5 0,4 Total income 1,2 1,8 2,5 2,6 8,9 Other external expenses -17,9 -17,0 -22,4 -23,2 -41,4 Personnel costs -
Slide 76: Value drivers in 2026/2027 – three funded programs and a partnered readout
Value drivers in 2026/2027 – three funded programs and a partnered readout Value drivers in our own programs Upcoming milestones • FLEX-HCC: continued patient recruitment towards full • Q4 2026: topline results from the Vetbiolix phase 2 enrollment within 12 months study with VBX-1000 (MIV-701) – 29
Slide 77: Thank You!
Thank You! Slide 77