Medivir : Presentation

MEDIVIR Q4 2025 REPORT

FEBRUARY 18, 2026

Q4 Highlights

SEK 45 million directed issue to Carl Bennet AB, enabling MIV-711 clinical development in Osteogenesis Imperfecta, with market opportunity comparable to fostrox in HCC, while strengthening company financial position

FLEX-HCC study preparations with Korean Cancer Study Group continues to progress, all sites selected, including the three largest hospitals

VBX-1000 (MIV-701) initiation of randomized, placebo-controlled study to confirm disease-modifying benefit & unlock blockbuster potential, results expected Q4 2026

Slide

2

A pipeline of first-in-class programs targeting patient populations without approved treatment options

PROJECT PARTNER DISEASE AREA

PRE-CLINICAL

PH 1 PH 2 PH 3 ON

MARKET

FINANCIALS POTENTIAL NEXT EVENT(S)

• Phase 2 PoC study

100% Medivir

• Phase 2 start

100% Medivir

HCC (mono)

HCC (combo)

Osteogenesis Imperfecta

bralpamide development

MIV-711 In-house development

Fostroxacitabine In-house

IN-HOUSE PROGRAMS

PARTNERED PROGRAMS - NO FURTHER INVESTMENT REQUIRED BY MEDIVIR

Xerclear GSK, SYB Herpes Royalties ▪ Registration in China

Remetinostat Biossil

CTCL, BCC, SCC

Royalties & up to $60m ▪ Phase 2/3 study start in milestones

MIV-701

Vetbiolix

Periodontal

disesase in dogs

Royalties & revenue

share agreement on Vetbiolix partnering

• Phase 2 study results

MET-X Infex

Therapeutics

Critical MBL Infections

Slide

Revenue Share Agreement

• Phase 1 study start

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Slide 4

Today's presenters

CEO

Jens Lindberg

CMO

Pia Baumann

CFO

Magnus Christensen

CSO

Fredrik Öberg

Slide 5

MIV-711

SEK 45 million directed issue enabling MIV-711 clinical development in Osteogenesis Imperfecta, with market opportunity comparable to fostrox in HCC

Slide 6

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 and impact on life length

• Characterized by defective bone and cartilage causing fragile bone structure (brittle bone) leading to frequent fractures that can lead to deformities, pain and impacted mobility

• There are no approved medical treatments in OI

• Bisphosphonates are used of label, particularly in pediatric care to reduce vertebral deformities, pain and to improve adult length

Significant unmet medical need

1. One-year-old infant diagnosed with severe type III OI. Note the severe bowing of the legs and the lack of bone modeling in both femurs and tibiae.

2. A nine-month-old infant with moderate type IV OI.

   
   
   

   Slide 7

   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

   Type III

   15%

   • Severe with short stature and deformities/scoliosis.

   Up to 100 fractures during life span

   ▪

   Type IV

   15%

   Moderate with moderately short stature and variable scoliosis.

   Up to 50 fractures during life span

   Subtypes suitable for treatment

   10%

   10%

   Type II

   • Type 2 is lethal with multiple fractures at birth with marked deformities. Dies at birth, or shortly after

     Other

   • There are many other rarer types of OI, present in ~10%

Slide 8

1Sillence DO, Rimoin DL, Danks DM. Clinical variability in osteogenesis imperfecta-variable expressivity or genetic heterogeneity. Birth Defects Orig Artic Ser 1979; 15: 113-29.

2https://www.orpha.net/

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 matrix and initiating mineralization.

Cathepsin K

Enzyme secreted by osteoclasts that degrades type I collagen driving bone resorption

Slide 9

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 mutations leads to reduced and/or defect Type I collagen resulting in increased bone resorption by osteoclasts and reduced formation of qualitative bone

3. Studies in children with OI show high levels of Cathepsin K

Slide 10

Rauch et al 2000, Baron et al 1983, Braga et al 2004; Garnero et al 2009; Rousseau et al 2010)

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 bone remodeling is maintained as the osteoclast-osteoblast coupling is preserved

3. As a result, MIV-711 helps restore the balance between bone resorption and bone formation in the continues bone remodeling

Slide 11

Rauch et al 2000, Baron et al 1983, Braga et al 2004; Garnero et al 2009; Rousseau et al 2010)

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 - osteoblast coupling → induces formation of new bone

Anti-sclerostin mAb

Bisphosphonates

Prevents bone resorption by killing osteoclasts

+ Effectively prevents bone resorption

• Lost coupling between osteoblast and osteoclast

• Negative impact on formation of new bone

• Not approved in OI

  Induces bone formation via

  osteoblast…

  + Effectively induces new bone formation

  + Indirect reduction of bone resorption

• Benefit diminishes after 6-12 months due to induction of escape pathway activation

• Failed phase 3 study in Q4 2025

Slide 12

Cathepsin K inhibition showing significant benefit across multiple bone-related disorders

Cathepsin K inhibition - Significant bone & cartilage benefit in Osteoarthritis1

Cathepsin K inhibition -

prevents fractures in Osteoporosis2

Cathepsin K inhibition - promising signals in Osteogenesis Imperfecta

• Significant and dose dependent improvement in bone volume & quality vs placebo in OI mouse model

1Conaghan et al, Annals of Internal Medicine 2019

2McClung et al., The Lancet Diabetes & Endocrinology, P899-911, Dec 2019

Slide 13

Draft design of phase 2 randomized POC study with MIV-711 in OI to inform next pivotal development phase

• Patients with

  Osteogenesis Imperfecta

• Fractures within the previous 2 yr

• N ~20

MIV-711

High dose

Endpoints:

N~10

1:1

MIV-711

Low dose

• Change in Biomarkers including

  BMD

• PK

• Safety

• Number of fractures

N~10

Phase 2 POC study in Osteogenesis Imperfecta

• ~20 patients randomized 1:1 to two dose arms with MIV-711 oral treatment once daily for 12 months

• Enrollment in Europe

• Patients eligible for this study are already known at sites positively impacting enrollment

Slide 14

~2/3 of OI subtype patients candidates for drug treatment providing significant market opportunity1,2

Estimated prevalent OI population OI subtypes candidates for 711-treatment Sizeable market opportunity - MIV-711

45,000

40,000

35,000

30,000

25,000

20,000

15,000

10,000

5,000

0

USA EU Japan/Korea

Type 1 -

not diagnosed 12,5%

Type 1 -

diagnosed 37,5%

Other

10%

Type 2

10%

Type 3

15%

Type 4

15%

• Up to 25% of Type 1 patients are not diagnosed until late in life

• Significant unmet medical need with no approved treatment options

• Anti-sclerostin antibody (setrusumab) with phase 3 failure in Q4 2025

• Market opportunity across USA, EU and Japan/Korea >$3.5bn annually

• Potential for rare Pediatric Disease Designation & Priority Voucher

  
  
  

  Slide 15

  1 Sillence DO, Rimoin DL, Danks DM. Clinical variability in osteogenesis imperfecta-variable expressivity or genetic heterogeneity. Birth Defects Orig Artic Ser 1979; 15: 113-29.

  2https://www.orpha.net/

  MIV-711 - Highly selective cathepsin K inhibitor in development for patients with Osteogenesis Imperfecta (OI)

  3rd generation, highly selective cathepsin K inhibitor

  • ~250 subjects in phase 1/2 Osteoarthritis study, confirming ability to prevent cartilage degradation

  • PoC established in Osteogenesis Imperfecta animal model,

    Proven ability to prevent cartilage & bone degradation & improve bone quality

    OA - prevention of cartilage loss1

    
    
    

    OI - Improved bone volume & quality2

    Bone mineral density (g/cm3) 1.0 0.9 0.8 0.7 0.6

    ***

    Inhibits cathepsin K, the main protease of

    bone-degrading osteoclasts, to restore bone matrix quality

    increasing bone volume & quality

  • MOA enabling long-term bone formation & anti-resorption

    0.5 0.4 WT Vehicle 5 20 μmol/kg

    +/G610C mice

    Phase 2 proof-of-concept study underway with ODD granted and potential for RPDD

Total market opportunity in Osteogenesis Imperfecta

>$3.5bn across key markets

~80.000 potential patients estimated across the US, EU

and Japan and Korea

• 2/3 of patients suitable for drug treatment

• No approved treatment options available

▪

• Significant clinical exposure and proven benefit across multiple bone-related diseases

• Orphan drug designation (ODD) approved in the US with potential for rare pediatric disease designation (RPDD).

• Funding completed for phase 2 proof-of-concept study .

67%

1Conaghan et al, Annals of Internal Medicine 2019

2Data on file

Slide 16

Fostrox

FLEX-HCC study preparations with Korean Cancer Study Group continues to progress, all sites selected, including the three largest hospitals

Slide 17

FLEX-HCC study generating strong interest in Korea with key hospitals included preparing for recruitment start

Seoul National University Medical Center

Samsung Medical Center

Asan Medical Center

Primary Investigator

CHA Bundang Hospital

Chungbuk National

University Hospital Seoul National University Bundang Hospital

Inje University Haenundae Paik Hospital

Dr. Hong Jae Chon

CHA Bundang Hospital, Seoul, Korea

Chonnam National University Hwasun Hospital

Slide 18

Randomized phase 2 study to strengthen the benefit evidence of fostrox + Lenvima over Lenvima alone, in 2nd line liver cancer (HCC)

Inclusion criteria

• 2L advanced HCC

• One prior IO regimen

• Child-Pugh A

• ECOG PS 0-1

Fostrox 30 mg +

Lenvima SD* N=40

1:1

Lenvima SD*

N=40

*standard weight based dose in HCC

Response assessments every 6 week with CT or MRI

Study design:

Primary endpoint:

• ORR (BICR)

  Secondary endpoints:

• DoR

• PFS

• OS

• Safety

2026

2027

• 80 pts randomized to fostrox + Lenvima or Lenvima alone

• 8 sites in Korean Cancer Study Group

• Efficacy evaluated by Blinded Independent Central Review (BICR)

  Estimated study timelines:

• Enrollment time: 12 mo

• Topline results H2 2027

  Key benefits:

• Generation of robust comparative efficacy and safety data in collaboration with an established research consortium

• Enables rapid data read out

Slide 19

Fostrox (fostroxacitabine bralpamide)

The first oral, liver-targeted treatment tailored for HCC

Oral, liver-activated small molecule inducing DNA damage in tumor cells, sparing healthy liver cells3

10.9 months time to progression, substantially better than SoC1,2

Fostrox + LEN (n =21)1

12

Unique, liver-targeted approach in HCC

No DNA damage in healthy liver tissue

DNA damage in 10

Median TTP, mo 10.9

Median TTP/PFS - Months

tumor tissue

8

6

4

Liver-guided delivery -prodrug

Tumor-selective payload -troxacitabine

*see slide 20 for details regarding individual study data

2

0

Other 2nd line studies*

Fostrox + Lenvima

Absence of effective treatment options in 2nd line enables first-to-market opportunity for fostrox + Lenvima

Market opportunity in 2nd line HCC >$2.5bn, with significant upside potential

• No 2nd line treatments approved in advanced HCC

• FLEX-HCC Phase 2 study initiated, in collaboration with Dr Hong Jae Chon and the Korean Cancer Study Group, to confirm superior benefit of fostrox + Lenvima vs Lenvima alone in 2nd line HCC

>$2.5bn

2nd line HCC market by 2030, fastest growing cause of cancer death in US4

Significant upside in liver metastasis from other solid tumors

1Chon et al., ESMO, 2024, Poster 986

2Based on data from previous 2L phase 3 HCC studies with Stivarga, Cyramza & Cabometyx anSdliidneve2s0tigator initiated prospective & retrospective 2L studies with Lenvatinib

3Evans et al ASCO GI, 2021

4Ma et al., Cancer, June 15, 2019; 2089-2098