Biolinerx Ltd. · TASE:BLRX
Biolinerx — Investor Presentation (July 2026)
39 slides from Biolinerx's investor presentation, July 2026
Slide 1: Driving cancer innovation forward
Driving cancer innovation forward Investor Presentation July 2026 1
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,"
Slide 3: BioLineRx investor highlights
BioLineRx GLIX1, our new lead asset, targets a broad range of cancers with reduced TET2 activity investor • Novel MOA focused on DNA damage repair • Potential for strong synergy demonstrated in combination with PARP inhibitors highlights • Initial development in glioblastoma (GBM), followed by other
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
Slide 5: GLIX1: first-in-class, oral, small molecule with 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
Slide 6: GLIX1 is positioned to address unmet needs for novel 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
Slide 7: GLIX1 mechanism of action
GLIX1 mechanism of action
Slide 8: GLIX1 activates TET2 that is commonly inhibited in cancer (1/3)
GLIX 1 activates Ten-Eleven Translocation 2 (TET2) that is commonly inhibited in cancer (1/3) • 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
Slide 9: GLIX1 activates TET2 that is commonly inhibited in cancer (2/3)
GLIX 1 activates Ten-Eleven Translocation 2 (TET2) that is commonly inhibited in cancer (2/3) TET2 in cancer cells • TET2 initiates the DNA demethylation cycle by oxidizing 5-methylcytosine (5mc) to 5-hydroxymethylcytosine (5hmc), resulting in single-stranded DNA breaks1. These single- TDG/BER DNMT1
Slide 10: GLIX1 activates TET2 that is commonly inhibited in cancer (3/3)
GLIX 1 activates Ten-Eleven Translocation 2 (TET2) that is commonly inhibited in cancer (3/3) GLIX1 restores TET2 activity in cancer cells • TET2 initiates the DNA demethylation cycle by oxidizing 5-methylcytosine (5mc) to 5-hydroxymethylcytosine (5hmc), resulting in single-stranded DNA breaks1. The
Slide 11: GLIX1-driven TET2 activity overwhelms DNA repair in cancer cells
GLIX1-driven TET2 activity overwhelms DNA repair in cancer cells Healthy cells Cancer cells Cancer cells with GLIX1 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 str
Slide 12: TET2 as a tumor suppressor
TET2 as a tumor suppressor • TET2 knockdown results in tumor growth1 • Low TET2 expression and Low 5-hmC levels are correlated with shorter overall survival in several cancers.2,3,4,5,7,9 • TET2 knockdown significantly promotes, while TET2 overexpression inhibits, the proliferation, migration and •
Slide 13: GLIX1 is active only in the presence of TET2
GLIX1 is active only in the presence of TET2 TET2 deficient cell lines (TALL-1) are resistant to GLIX1 treatment TET2 deficient cell line TET2 expression TET2 expressing cell line TET2 expression 8 U87MG 96h TET2 expression (tpm) TALL1- 96h 6 100 100 Cell Viability (%) Cell Viability (%) 80 80 4 60
Slide 14: Pre-clinical studies confirm MOA
Pre-clinical studies confirm MOA Studies confirm increase in 5hmC levels after GLIX1 treatment, leading to DNA damage and cancer cell death GLIX1 enhances TET2 activity 5hmC is processed to DNA damage, DNA damage cause resulting in increased TET2 product overwhelming the repair capacity of cancer ce
Slide 15: GLIX1 safety
GLIX1 safety
Slide 16: GLP tox studies in rats and dogs demonstrate safety at high doses
GLP tox studies in rats and dogs demonstrate safety at high doses In-life Phase Parameters Safety Pharmacology No mortalities and no test-item clinical signs No effect on CNS, cardiovascular or respiratory No ocular abnormalities system Rats No neurobehavioral changes No changes in body weight and f
Slide 17: GLIX1 has no toxicity in normal cells
GLIX1 has no toxicity in normal cells Lack of cytotoxicity demonstrated in human peripheral blood mononuclear cells (PBMCs) PBMC A PBMC_C PBMC_M PBMC_C PBMC_M PBMC A 150 150 Cell viability (%) Cell viability (%) 150 Cell viability (%) 100 100 100 50 50 50 0 0 10 20 30 40 50 60 70 80 90 100 110 0 0 0
Slide 18: GLIX1 efficacy
GLIX1 efficacy
Slide 19: 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. 19
Slide 20: Glioblastoma 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 has high levels of 5hmC.1 lower 5hmC l
Slide 21: 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
Slide 22: GLIX1 demonstrated anti-tumor activity and prolonged survival in orthotopic GBM model
GLIX1 demonstrated anti-tumor activity and prolonged survival in initial orthotopic GBM model Potent anti-tumor activity in orthotopic GBM xenograft model Day 12 Day 40 Treatment Treatment Control GLIX1 Control N=14 TMZ 1.5mg/kg QD N=7 GLIX1 1000mg/kg BID N=7 Nude mice inoculated with SNB-19-Luc cel
Slide 23: GLIX1 demonstrated robust dose-dependent efficacy in additional orthotopic GBM models
GLIX1 demonstrated robust efficacy in dose-dependent manner in additional orthotopic GBM models Strong anti tumor activity even at the lowest dose tested in orthotopic GBM xenograft model Mean Total Flux ± SEM Mean Total Flux ± SEM 3.0E+10 2.5E+10 Vehicle,QD*21days Vehicle,QD*21days GLIX1 500mg/kg,Q
Slide 24: GLIX1 also demonstrated potent anti-tumor activity in TMZ-resistant PDX model
GLIX1 also demonstrated potent anti-tumor activity in TMZ-resistant patient-derived xenograft (PDX) model Efficacy in TMZ-resistant model supports GLIX1’s potential to treat a broad range of GBM patients, including patients with unmethylated MGMT promoter status (more than half of all GBM patients)
Slide 25: GLIX1 addresses key challenges in GBM drug development
GLIX1 addresses key challenges in GBM drug development
Slide 26: GLIX1 demonstrates BBB penetration
GLIX1 demonstrates BBB penetration BBB penetration is the first feature to impair efficacy and a major challenge to chemotherapies and immunotherapies Strong blood-brain-barrier penetration in healthy mice following GLIX1 enters the brain via nucleoside transporters 1000 mg/kg PO • GLIX1 is a substr
Slide 27: GLIX1 shows efficacy in patient-derived neurospheres (glioma stem cells)
GLIX1 shows efficacy in patient-derived neurospheres (glioma stem cells) GLIX1 has potential to target cancer stem cells that contribute to tumor development, heterogeneity, drug resistance and cancer recurrence Head-to-head comparison of GLIX1 and TMZ in patient-derived Potency of GLIX1 (reflected
Slide 28: GLIX1's potential to address common reasons for failure in GBM trials
GLIX1’s potential to address common reasons for failure in GBM trials Common reason for failure GLIX1 potential to overcome failure ✓ Demonstrated BBB penetration Lack of BBB penetration ✓ Crosses the BBB via nucleoside transporters Complex tumor biology: ✓ Cytotoxic to patient-derived neurospheres
Slide 29: GLIX1 clinical development plan
GLIX1 clinical development plan
Slide 30: GLIX1 Phase 1/2 clinical trial design
GLIX1 Phase 1/2 clinical trial design 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 based
Slide 31: Phase 1/2 dose escalation plan
Phase 1/2 dose escalation plan Expansion Set-Up Expansion MTD and/or RD Dose level 5* Survival Follow up Dose level 4* Survival Follow up Dose level 3* Survival Follow up Dose level 2* Survival Follow up Dose level 1* Survival Follow up * Safety, PK and PD assessments First patient In: April 2026 ~Q
Slide 32: 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) >33K 2.5 months 18.5K improvement in overall survival Estimated diagnosed annual incidence in 2030: in US in US and Europe 50-75% of patients do not respond >$3.7B $1B/year Estimated tot
Slide 33: 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
Slide 34: 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. Data support synthetic lethality between GLIX1 & PARPi indicating that GLIX1 removes the HRD requirement for PARPi activity Dose-response matrix (inhibition) Dose-r
Slide 35: Strong synergy between GLIX1 and PARPi in ovarian cancer PDX model
Strong synergistic effect demonstrated between GLIX1 and PARPi in patient-derived xenograft (PDX) model in ovarian cancer Results reinforce synthetic lethality between GLIX1 and PARPi, indicating that GLIX1 can broaden the use of PARPi in ovarian cancer 2000 Mean Tumor Volume ± SEM • Synergy demonst
Slide 36: 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
Slide 37: Overview of GLIX1 IP
Overview of GLIX1 IP Global portfolio of patents, both issued and pending, that secure GLIX1’s value GLIX1 for use in treating cancer of the central nervous system, such as glioblastoma Granted in the US, Europe, and 13 other countries; valid until at least 2040* Overview of GLIX1 for use in treatin
Slide 38: Upcoming milestones
Upcoming milestones
Slide 39: 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