Biolinerx Ltd. · TASE:BLRX

Biolinerx — Q1 2026 Earnings Presentation

28 slides from Biolinerx's earnings presentation, May 27, 2026

  1. Slide 1: Driving cancer innovation forward

    Driving cancer innovation forward Corporate Presentation April 2026 1

  2. Slide 2: Forward-Looking Statements

    Forward-Looking Statements Various statements in this presentation concerning BioLineRx's future expectations constitute "forward-looking statements" within the meaning of the Private Securities Litigation Reform Act of 1995. These statements include words such as "anticipates," "believes," "could,"

  3. Slide 3: BioLineRx investor highlights

    BioLineRx investor highlights Leveraging successful track record of clinical and regulatory development to advance targeted therapies for cancers with high unmet needs GLIX1, our new lead asset, targets a broad range of cancers with reduced TET2 activity • Novel MOA focused on DNA damage repair • Po

  4. Slide 4: Pipeline assets

    *Investigator-initiated study Pipeline assets **Rights exclude solid-tumors Studies in Planning PRE-CLINICAL PHASE I PHASE 2 PHASE 3 APPROVED PARTNERED GLIX1 (lead development asset) Glioblastoma Other Cancers Other Cancers w/PARPi Motixafortide Solid Tumors * Pancreatic Cancer Asia development and

  5. Slide 5: GLIX1: A first-in-class, oral, small molecule with a novel mechanism of action

    GLIX1: A first-in-class, oral, small molecule with a novel mechanism of action applicable across a broad range of cancer indications

  6. Slide 6: GLIX1 is positioned to address unmet needs for novel and more effective cancer treatments

    GLIX1 is positioned to address unmet needs for novel and more effective cancer treatments First-in-class, novel mechanism of action, applicable to a broad range of cancers – targeting DNA Oral route of administration damage repair Excellent pre-clinical safety profile, allowing long-term Proven bloo

  7. Slide 7: GLIX1 activates Ten-Eleven Translocation (TET2) that is commonly inhibited in cancer

    GLIX 1 activates Ten-Eleven Translocation 2 (TET2) that is commonly inhibited in cancer • TET2 initiates the DNA demethylation Normal cytosine metabolism cycle by oxidizing 5-methylcytosine (5mc) to 5-hydroxymethylcytosine (5hmc), resulting in single-stranded DNA breaks1. These single- TDG/BER DNMT1

  8. Slide 8: Illustration of TET2 activity in healthy versus cancer cells

    Illustration of TET2 activity in healthy versus cancer cells Healthy Cancerous Cancerous with GLIX1 treatment 5mC 5mC 5mC 5mC 5mC TET2 TET2 TET2 5hmC 5hmC 5hmC 5hmC 5fC or 5caC 5fC or 5caC 5fC or 5caC Base Excision Repair Base Excision Repair BaseExcision Base Excision Repair Repair Double stranded

  9. Slide 9: Pre-clinical studies confirm increase in 5hmC levels after GLIX1 treatment

    Pre-clinical studies confirm increase in 5hmC levels after GLIX1 treatment – leading to double-stranded DNA breaks and cancer cell death GLIX 1 enhances TET2 activity 5hmC is processed to DNA Double stranded DNA breaks resulting in increased TET2 product breaks, overwhelming the repair cause cell de

  10. Slide 10: GLIX1 shows efficacy in numerous different cancer cell lines

    GLIX1 shows efficacy in numerous different cancer cell lines High potency of GLIX1 (reflected by low IC50) demonstrated in a number of different cancer cell lines © 2026 BioLineRx Ltd. All Rights Reserved. 10

  11. Slide 11: Glioblastoma (GBM) chosen as initial indication supported by strong rationale

    Glioblastoma (GBM) chosen as initial indication supported by strong rationale GBM has significantly more 5mC in close proximity 5hmC levels are significantly reduced in GBM in the genome vs normal cell lines Healthy human brain tissue Higher grade gliomas, have lower has high levels of 5hmC.1 5hmC l

  12. Slide 12: GBM is one of most challenging cancers with no effective treatment options

    GBM is one of most challenging cancers with no effective treatment options • GBM is the most common and most aggressive primary brain tumor • Poor prognosis with median survival of 12–18 months1,2 • SoC for newly diagnosed GBM is surgery + radiotherapy + Temozolomide (TMZ)3 established in 2005 − Dem

  13. Slide 13: GLIX1 demonstrated significant efficacy in multiple GBM models

    GLIX1 demonstrated significant efficacy in multiple GBM models Potent anti tumor activity in Orthotopic GBM xenograft model Day 12 Day 40 Control GLIX1 Treatment 12 23 33 45 55 66 Nude mice inoculated with SNB-19-Luc cells; treatment started at day 12 for 2 weeks; n=7 per group © 2026 BioLineRx Ltd.

  14. Slide 14: GLIX1 addresses key challenges for GBM drug development

    GLIX1 addresses key challenges for GBM drug development Good blood-brain-barrier penetration in healthy mice Efficacy in TMZ resistant cell lines following 1000 mg/kg PO 10⁶ • More than half of all GBM patients are TMZ-resistant, due to unmethylated MGMT promoter status • For these patients, there a

  15. Slide 15: GLIX1 clinical trial design – Phase 1/2

    GLIX1 clinical trial design – Phase 1/2 Phase 1: Phase 2: Recurrent and progressive GBM Potential population cohorts: Open label, dose escalation (BOIN) ▪ GBM – newly diagnosed and/or recurrent ▪ Additional cancers – with/without PARPi combination Maximum tolerated dose (MTD) and recommended dose ba

  16. Slide 16: GLIX1 represents a multi-billion-dollar market opportunity in GBM

    GLIX1 represents a multi-billion-dollar market opportunity in GBM Data on Temozolomide (current standard of care) 70K 2.5 months 18.5K improvement in overall survival Estimated diagnosed annual incidence in 2030: in US in major markets 50-75% of patients do not respond >$3.7B $1B/year Estimated tota

  17. Slide 17: GLIX1 and PARP inhibitors – potential for strong synergy

    GLIX1 and PARP inhibitors (PARPi) – potential for strong synergy GLIX1 substantially expands the range of cancers and patient populations that can be treated with PARP inhibitors by facilitating the formation of single-stranded DNA breaks Homologous recombination (HR) Deficiency in Cancers HR-defici

  18. Slide 18: GLIX1 shows strong synergy with PARPi in HR-proficient cancers

    GLIX1 shows strong synergy with PARPi in HR-proficient cancers Synergy demonstrated in various HR proficient-ovarian cancer cell lines Dose-response matrix (inhibition) Dose-response matrix (inhibition) Dose-response matrix (inhibition) NCI/ADR-RES SKOV-3 OVCAR-8 Synergy also demonstrated in differe

  19. Slide 19: GLIX1 has potential upside in broadening market for PARPi

    GLIX1 has potential upside in broadening market for PARPi Approved Indication Approved Assets Market Size* Ovarian Cancer Olaparib, Rucaparib, Niraparib ~$4B Breast Cancer Olaparib, Talazoparib ~$33B Total market ~$50B Prostate Cancer Olaparib, Rucaparib, Talazoparib ~$11B Pancreatic Cancer Olaparib

  20. Slide 20: Motixafortide in cancer immunotherapy for pancreatic ductal adenocarcinoma (PDAC) and other solid tumors

    Motixafortide in cancer immunotherapy for pancreatic ductal adenocarcinoma (PDAC) and other solid tumors

  21. Slide 21: Motixafortide facilitates T cell trafficking and infiltration

    Motixafortide facilitates T cell trafficking and infiltration into tumor and modulates TME immune cell composition in PDAC patients Motixafortide is a high affinity CXCR4 inhibitor Biopsies from PDAC patients before and after treatment with combination of motixafortide + pembrolizumab that blocks th

  22. Slide 22: Rationale for motixafortide in combination with PD-1 inhibitors and chemotherapy

    Rationale for motixafortide in combination with PD-1 inhibitors and chemotherapy Solid tumors with low immune system visibility require a multi-pronged approach 4 Trafficking of T cells to tumors (CTLs) Priming and 3 activation (APCs & T cells) 5 Motixafortide Infiltration of T • Motixafortide facil

  23. Slide 23: Chemo4MetPanc Phase 2 clinical trial in first-line PDAC: pilot phase

    Chemo4MetPanc Phase 2 clinical trial in first-line PDAC: pilot phase IIS under collaboration with Columbia University, equally funded by Regeneron and BioLineRx PILOT TRIAL DESIGN BASELINE CHARACTERISTICS Characteristic N = 11 Biopsy 3 Age 60 y (46–69) Biopsy 1 Biopsy 2 Upon progression Sex (optiona

  24. Slide 24: Encouraging response and survival data from pilot phase

    Encouraging response and survival data from pilot phase Radiological Radiological Response1 Response N = 11 (%) Duration2 Disease Progression 1 (9%) Stable Disease (SD) 3 (27%) Partial Response (PR) 7 (64%) Confirmed PR 6 (55%) Disease Control Rate (DCR) (91%) Compares favorably to historical PR (23

  25. Slide 25: Motixafortide combination treatment resulted in 64% ORR and 9.6-month median PFS

    Motixafortide combination treatment resulted in 64% ORR and 9.6-month median PFS with a favorable tolerability profile in pilot phase Efficacy data: 2 patients underwent definitive treatment: Gemcitabine, nab-paclitaxel, • One had complete resolution of all liver lesions and underwent definitive rad

  26. Slide 26: Chemo4MetPanc Phase 2b clinical trial in first-line PDAC - randomized phase

    Chemo4MetPanc Phase 2b clinical trial in first-line PDAC - randomized phase IIS under collaboration with Columbia University, equally funded by Regeneron and BioLineRx – currently enrolling Randomized Trial Recruiting Study Design N=108 Primary Endpoint Gemcitabine and median PFS N=36 nab-paclitaxel

  27. Slide 27: Upcoming milestones

    Upcoming milestones

  28. Slide 28: Expected milestones in next 18-24 months

    Expected milestones in next 18-24 months Q1 2026 H1 2027 Initiation of Phase 1/2 trial Data from Phase 1 part of of GLIX1 in glioblastoma GLIX1 trial* 2026 Interim futility analysis H2 2027 from Phase 2b PDAC trial Initiation of Phase 2 part with motixafortide of the GLIX1 trial * In addition, as th

BioLineRx — Q1 2026 Earnings Presentation on 6ix