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Driving therapeutic innovation forward Corporate Presentation November 2025
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Forward-Looking Statements © 2025 BioLineRx Ltd. All Rights Reserved. 2 This presentation contains “forward-looking statements,” including statements regarding expectations, beliefs, intentions or strategies for the future. These include statements regarding management's expectations, beliefs and intentions regarding, among other things, the potential success of our license agreements and joint venture, the commercial potential of motixafortide and GLIX1, expectations with regard to clinical trials of motixafortide and GLIX1, our expected cash runway, and our business strategy. These forward-looking statements involve known and unknown risks, uncertainties and other factors that may cause our actual results, performance or achievements to be materially different from any future results, performance or achievements expressed or implied by the forward-looking statements. In some cases, you can identify forward-looking statements by terms including “anticipates,” “believes,” “could,” “estimates,” “expects,” “intends,” “may,” “plans,” “potential,” “predicts,” “projects,” “should,” “will,” “would,” and similar expressions intended to identify forward-looking statements. Forward-looking statements reflect our current views with respect to future events and are based on assumptions and are subject to risks and uncertainties. You should not put undue reliance on any forward-looking statements. Factors that could our cause actual results to differ materially from those expressed or implied in such forward-looking statements include, but are not limited to: the clinical development, commercialization and market acceptance of our therapeutic candidates, including the degree and pace of market uptake of APHEXDA for the mobilization of hematopoietic stem cells for autologous transplantation in multiple myeloma patients; the initiation, timing, progress and results of our preclinical studies, clinical trials, and other therapeutic candidate development efforts; our ability to advance our therapeutic candidates into clinical trials or to successfully complete our preclinical studies or clinical trials, whether the clinical trial results for APHEXDA will be predictive of real-world results; our receipt of regulatory approvals for our therapeutic candidates, and the timing of other regulatory filings and approvals; whether access to APHEXDA is achieved in a commercially viable manner and whether APHEXDA receives adequate reimbursement from third-party payors; our ability to establish, manage, and maintain corporate collaborations, as well as the ability of our collaborators to execute on their development and commercialization plans; our ability to integrate new therapeutic candidates and new personnel as well as new collaborations; the interpretation of the properties and characteristics of our therapeutic candidates and of the results obtained with our therapeutic candidates in preclinical studies or clinical trials; the implementation of our business model and strategic plans for our business and therapeutic candidates; the scope of protection we are able to establish and maintain for intellectual property rights covering our therapeutic candidates and our ability to operate our business without infringing the intellectual property rights of others; estimates of our expenses, future revenues, capital requirements and our needs for and ability to access sufficient additional financing; risks related to changes in healthcare laws, rules and regulations in the United States or elsewhere; competitive companies, technologies and our industry; our ability to maintain the listing of our ADSs on Nasdaq; and statements as to the impact of the political and security situation in Israel on our business, which may exacerbate the magnitude of the factors discussed above. These and other factors are more fully discussed in the "Risk Factors" section of our most recent annual report on Form 20-F filed with the Securities and Exchange Commission on March 31, 2025. In addition, any forward-looking statements represent our views only as of the date of this presentation and should not be relied upon as representing its views as of any subsequent date. We do not assume any obligation to update any forward-looking statements unless required by law.
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We develop life-changing therapies for cancer and rare diseases. We have fully validated capabilities in all aspects of drug development – pre-clinical, CMC, clinical, regulatory, QA, IP, etc. We successfully developed APHEXDA® (motixafortide), our out-licensed FDA-approved drug, for stem cell mobilization in multiple myeloma We maintain US and EU rights to solid tumor indications for motixafortide, currently in Phase 2b development under collaboration in PDAC Our new asset, GLIX1, is positioned to change the lives of patients in a broad range of cancers © 2025 BioLineRx Ltd. All Rights Reserved. 3 BioLineRx at a glance
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Ongoing license revenue to partially fund future growth and operations © 2025 BioLineRx Ltd. All Rights Reserved. 4 Announced October 2023 Exclusive license to develop and commercialize APHEXDA (motixafortide) across all indications except solid tumors, and all territories except Asia Exclusive license to develop motixafortide across all indications in Asia ▪ Up to $87 million in commercial milestones ▪ Royalties on sales from 18%-23% ▪ Up to $200 million in commercial milestones ▪ Tiered double-digit royalties on sales Announced November 2024 (Ayrmid Ltd.)
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Joint Venture with Hemispherian AS to develop GLIX1 © 2025 BioLineRx Ltd. All Rights Reserved. 5 Announced September 2025 Joint Venture to Develop GLIX1 for Glioblastoma and Other Indications ▪ BioLineRx and Hemispherian have established JV to develop GLIX1 in glioblastoma and other cancers ▪ Hemispherian will contribute to JV global rights to GLIX1, with BioLineRx responsible for managing, performing and funding all JV development activities; no initial upfront payment – all funding goes to development ▪ Initial economic stakes: Hemispherian 60%; BioLineRx 40%, with BioLineRx stake increasing incrementally to potential maximum of 70% in parallel with its continued investment in the program ▪ JV has first look at other Hemispherian pipeline assets – all of which are focused on DNA repair pathways ▪ Hemispherian is a Norwegian biotech company developing early-stage next- generation therapeutics for aggressive cancers ▪ The company’s lead compound, GLIX1, has a unique mechanism of action that selectively targets DNA repair pathways in tumor cells while sparing healthy tissue ▪ GLIX1 has FDA-approved IND and is set to begin Phase 1 development in Q1 2026
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PRE-CLINICAL PHASE I PHASE 2 PHASE 3 APPROVED Pancreatic Cancer Asia development and commercial rights * Asia development and commercial rights Bridging Study Approved in USMotixafortide Multiple Myeloma Approved in US Global development and commercial rights except Asia** Motixafortide Solid Tumors Stem Cell Mobilization Sickle Cell Disease * * Global development and commercial rights except Asia** *Investigator Initiated Study **Rights exclude solid-tumors Studies in Planning © 2025 BioLineRx Ltd. All Rights Reserved. 6 PARTNERED GLIX1 Solid Tumors Glioblastoma Pipeline assets Other Cancers
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GLIX1 – a TET2 enhancer for the treatment of glioblastoma and other cancers
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Key attributes of GLIX1 © 2025 BioLineRx Ltd. All Rights Reserved. 8 ▪ First-in-class, oral medication with a novel mechanism of action in cancer therapy landscape ▪ Mechanism of action (restoring TET2 activity) applicable to most cancers ▪ Excellent pre-clinical safety profile, allowing long-term treatment and potential combination treatment with other cancer agents ▪ Excellent blood-brain-barrier penetration ▪ Glioblastoma, the first target indication, expected to provide data to support development in CNS and additional cancers
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Role of Ten-Eleven Translocation 2 (TET2) in essential DNA processes © 2025 BioLineRx Ltd. All Rights Reserved. 9 ▪ DNA methylation/demethylation is essential for normal cell function ▪ TET2 is responsible for initiating the DNA demethylation cycle, resulting in single stranded DNA breaks1 ▪ In cancers, alterations in DNA methylation are common, and TET2 activity is inhibited2 by oncometabolites, giving rise to increased DNA methylation in close genomic proximity3 ▪ Restoration of TET2 activity generates large amounts of single stranded DNA breaks in close proximity, resulting in double stranded DNA breaks, which overwhelm the repair capacity of the cell, killing the cancer cell4 1. Jinrong Zhu at al, Cancer Bio Med, 2023, 21(2):111–116 2. Wenxin Da et al, Clinical and Translational Oncology, 2024, 26:2156–2165 3. Johnson KC et al, Nature Communications, 2016, 7, 13177 4. Luisa Cimmino et al, Cell, 2017, 170(6):1079-1095
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Restoration of TET2 activity by GLIX1 causes cancer cell death – by targeting the DNA damage response © 2025 BioLineRx Ltd. All Rights Reserved. 10 Reduced TET2 activity is a common feature of all cancers As a result, large quantities of 5mC accumulates in close proximity in cancer. GLIX 1 enhances TET2 activity resulting in increased TET2 product (5hmC) 0.010 p<0.001 Control GLIX1 0.008 0.006 0.004 0.002 0.000 5hmC (%) Resected tumor tissue confirms increased 5hmC levels after GLIX treatment. 5hmC is processed to DNA breaks, overwhelming the repair capacity of the cancer cell 𝛾-H2AX 53BP1 Control Tet2 Restoring the 5hmC levels in cancer cells leads to double stranded DNA breaks, which cause cell death. GLIX1 1 2 3 5-methylcytosine (5mC) 5-hydroxymethylcytosine (5hmC) TET2
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© 2025 BioLineRx Ltd. All Rights Reserved. 11 TET2 5mC Cancerous 5mC 5mC Healthy 5hmC 5fC or 5caC 5mC Double stranded DNA breaks cause cell death Cancerous with GLIX1 treatment 5mC 5hmC 5hmC 5fC or 5caC 5hmC 5fC or 5caC TET2 TET2 Base Excision Repair Base Excision Repair Base Excision Repair GLIX1 MOA results in double-stranded DNA breaks in cancer cells only
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GLIX1 shows efficacy in numerous different cancer cell lines © 2025 BioLineRx Ltd. All Rights Reserved. 12 GLIX1 shows efficacy in a number of different cancer cell lines Starting clinical development in Glioblastoma but also exploring additional cancer indications in preclinical models
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Glioblastoma (GBM) chosen as initial indication supported by strong rationale © 2025 BioLineRx Ltd. All Rights Reserved. 13 5hmC levels are significantly reduced in GBM Higher grade gliomas, have lower 5hmC levels.2 Healthy brain tissue has high levels of 5hmC.1 GBM has significantly more 5mC in close proximity in the genome 5hmC Level 5mC Level Healthy tissue Cancer 1- Journal of Nucleic Acids, 2011 Jun 9; 870726. 2- Nature, 2016 Feb 11;6:20882
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GBM represents high unmet need © 2025 BioLineRx Ltd. All Rights Reserved. 14 ▪ 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 ▪ Demonstrated marginal increase in OS:14.6 months with TMZ vs. 12.1 months without TMZ ▪ Mainly improves outcome for patients with methylated MGMT promoter (only ~30% of GBM patients) ▪ No established SoC for recurrent GBM 1. Biomedicines, 2021 Mar 22;9(3):324 2. SEER 2017 3. N Engl J Med 2005;352:987-996
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GLIX1 demonstrated significant efficacy in Orthotopic xenograft model © 2025 BioLineRx Ltd. All Rights Reserved. 15 Day 12 Day 40 ControlGLIX1 Nude mice inoculated with SNB-19-Luc cells; treatment started at day 12 for 2 weeks; n=7 per group
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GLIX1 addresses key challenges for GBM drug development © 2025 BioLineRx Ltd. All Rights Reserved. 16 Efficacy in TMZ resistant cell lines Brain Plasma Time (hrs) Concentration (nM) 10³ 10⁴ 10⁵ 10⁶ 100 20 30 More than half of all GBM patients are TMZ-resistant, due to unmethylated MGMT promoter status. For these patients, there are no other treatment options. GLIX1 showed efficacy in such TMZ-resistant cell lines. Group AUC (nM*Hours) Cmax (nM) Tmax (Hours) T1/2 (Hours) Plasma 1600000 132000 2 5 Brain 692000 90200 2 5 Good BBB penetration in healthy mice following 1000 mg/kg PO
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GLIX1 clinical trial design - Phase 1/2a © 2025 BioLineRx Ltd. All Rights Reserved. 17 Phase 1: • Recurrent and progressive GBM • Open label, dose escalation (BOIN) • MTD and recommended dose based on safety, PK/PD and preliminary efficacy • N: up to 30 • Timeline: ~1.5 years Phase 2a: − Potential population cohorts: • Recurrent and progressive GBM • Newly diagnosed GBM – likely a “window of opportunity” trial • Additional cancers and/or combination therapy with PARPi − Open label, dose expansion − Efficacy based on PFS and OS − PD markers − Dose optimization − N: up to 20 per cohort − Timeline: ~2.5 years Ditte Primdahl, MD Assistant Professor of Neuro-Oncology Roger Stupp, MD Chief of Neuro-Oncology Michael Lim, MD Professor and Chair of Neurosurgery Isabelle Germano, MD, PhD, MBA Professor of Neurosurgery Clinical Advisors:
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GBM incidence and market opportunity © 2025 BioLineRx Ltd. All Rights Reserved. 18 Estimated diagnosed annual incidence in 2030: 18.5K in US, 70K in major markets Estimated total addressable market in 2030 for US + 4EU major markets + UK: >$3.7B $1B/year peak sales while on patent 50-75% of patients do not respond 2.5 months improvement in overall survival Data on Temozolomide (current standard of care) Incidence and market data herein specifically presented for GBM as first indication; potential significant upside in additional cancers
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GLIX1 and PARPi – potential for strong synergy in HR-proficient cancers © 2025 BioLineRx Ltd. All Rights Reserved. 19 PARP inhibitors alone are only efficacious in HR-deficient cancers HR-deficient cancers (treatable with PARPi) HR-proficient cancers (potentially treatable with PARPi +GLIX1 ) 94% 6% GLIX1 substantially expands the range of cancers that can be treated with PARP inhibitors by facilitating the formation of single stranded DNA breaks
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GLIX1 shows strong synergy with PARPi in HR-proficient cancers © 2025 BioLineRx Ltd. All Rights Reserved. 20 GLIX1 sensitizes HR-proficient cancers to PARP inhibitors
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GLIX1 for use in treating cancer of the central nervous system, such as Glioblastoma GLIX1 for use in treating any cancer in which CDA is not over-expressed** GLIX1, combined with a PARP inhibitor, for use in treating HR-proficient cancers** Global portfolio of patents, both issued and pending, that secure GLIX1’s value GLIX1 IP overview © 2025 BioLineRx Ltd. All Rights Reserved. 21 Granted in the US, Europe, and 13 other countries; valid until at least 2040* Granted in the US and pending in Europe and other countries; valid until at least 2040* Pending int’l patent application; national-phase patents, if granted, will be valid until at least 2044* * Not including possible patent term extension of up to the 5 years ** Majority of cancers
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Highlights of GLIX1 © 2025 BioLineRx Ltd. All Rights Reserved. 22 Phase 1/2a expected to initiate in Q1 2026 Small molecule PO administration Excellent blood brain barrier penetration Highly effective in preclinical models Not reliant on immune system Targets cancer cells only GLP tox studies in rats and dogs demonstrated safety at high doses Granted Orphan Drug Designation by both FDA and EMA Received FDA IND clearance Applicable to broad spectrum of cancers Potential for strong synergy with PARPi ✓ ✓ ✓ ✓ ✓ ✓ ✓ ✓ ✓ ✓ ✓
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Motixafortide in cancer immunotherapy – pancreatic ductal adenocarcinoma (PDAC) and other solid tumors
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Significant unmet need and opportunity in PDAC PDAC is associated with poor patient outcomes because efficacious therapies do not yet exist For all stages, the five- year survival rate in the US is only PDAC incidence is growing, and it is estimated that there will be 815,000 cases by 20403 Newer treatments like immunotherapy do not address all unmet needs, demonstrating a clear need to co-target alternative pathways 1 12% – the highest mortality rate among solid tumor malignancies – and globally, nearly a half million people were diagnosed in 2020 alone2 3% © 2025 BioLineRx Ltd. All Rights Reserved. 24 For metastatic PDAC (>50% of diagnosed cases), the five-year survival rate in the US is only 2 1. Pancreatic Cancer Action Network; 2. Cancer Net – Pancreatic Cancer Statistics; 3. The Global Cancer Observatory
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Role of motixafortide, a high-affinity CXCR4 inhibitor, in solid tumors + proof of mechanism from COMBAT Phase 2 PDAC study © 2025 BioLineRx Ltd. All Rights Reserved. 25 *Representative MultiOmyxTM data taken from SD patient with long treatment duration (11 combo cycles ~34 weeks). Data shown before treatment vs. after ~7w of treatment (end of cycle 2)1 • Increased activated cytotoxic T cells • Decreased suppressor cells in tumor microenvironment • Reduction in tumor cell numbers 1. Bruno, Nature Medicine, 26, 878–885 (2020)
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1. O’Reilly, EM JAMA Oncol. 1431-1438 (2019); Wainberg ZA Clin. Cancer Res. 4814–22 (2020) ; Renauf DJ Nat Commun. 13:5020 (2022) 2. Renauf DJ Nat Commun. 2022; 13: 5020 Solid tumors with low immune system visibility require a multi-pronged approach Rationale for motixafortide triple combination therapy Checkpoint Inhibitor Chemotherapy • Chemotherapy induces tumor death, reducing tumor burden • Chemotherapy induces immunogenic cell death, leading to activation & expansion of new tumor- reactive T-cell clones Motixafortide • Motixafortide facilitates T cell trafficking and infiltration into tumor core; TME modulation Priming and activation (APCs & T cells) Cancer antigen presentation (dendritic cells / APCs) Infiltration of T Cells into tumors (CTLs, endothelial cells) 3 4 2 1 7 5 6 Release of cancer cell antigens (cancer cells death) Recognition of cancer cells by T cells (CTLs, cancer cells) Killing of cancer cells (Immune and cancer cells) Trafficking of T cells to tumors (CTLs) Adapted from Chen, D. et al. Immunity Review 2013 • PD-1 maintains and restores activity of T cells within tumor • Effectiveness of ICIs in mPDAC remains limited1,2 © 2025 BioLineRx Ltd. All Rights Reserved. 26
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© 2025 BioLineRx Ltd. All Rights Reserved. 27 Biopsy 1 Motixafortide Cemiplimab Gemcitabine 1000mg/m2 Nab-paclitaxel 125mg/m2 Biopsy 2 Biopsy 3 Upon progression (optional) 1.25mg/kg SC 350mg IV qD21 IV D1, 8, 15 q28D IV D1, 8, 15 q28D Chemo4MetPanc Phase 2 clinical trial in first-line PDAC - pilot phase Pilot Trial Design Primary Endpoint Response rate by week 16 Characteristic N = 11 Age 60 y (46–69) Sex Female 2 (18%) Male 9 (82%) Race Black or African American 3 (27%) White 8 (73%) Site of Pancreas Primary Head 2 (18%) Neck/Uncinate/Body 3 (27%) Tail 4 (36%) Metastatic Sites at Baseline 1 9 (82%) Site of Metastasis at Baseline Liver 10 (91%) Peritoneum 1 (9%) Lung 1 (9%) Osseous 1 (9%) Comparable patient population to Van Hoff and Napoli3 PDAC trials (trials that led to approvals of Gem/Abrax and Nalirifox, respectively)
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© 2025 BioLineRx Ltd. All Rights Reserved. 28 1. Manji, GA ASCO 2025 2. Manji, GA AACR Pancreatic Cancer 2023 (Censor Date – July 20, 2023) N = 11 (%) 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%) and DCR (48%) with gemcitabine and nab-paclitaxel alone Radiological Response Duration2Radiological Response1 Median follow-up 13.4 m Median PFS 9.6m (95%CI: 3.78-NA) Encouraging response and survival data from pilot phase Progression-Free Survival Overall Survival
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© 2025 BioLineRx Ltd. All Rights Reserved. 29 Gemcitabine, nab-paclitaxel, motixafortide and cemiplimab resulted in • Overall Response Rate 64% • Median PFS 9.6 months The combination demonstrated a tolerable safety profile. No unexpected Grade 4 or 5 treatment related adverse events Correlative analysis on paired tumor and PBMCs reveal that CD8+ T-cell tumor infiltration increased across all 11 patients The encouraging preliminary efficacy prompted a change in clinical trial design to a randomized Phase 2 trial (Chemo4MetPanc; NCT NCT04543071) Pilot phase conclusions 2 patients underwent definitive treatment: • One had complete resolution of all liver lesions and underwent definitive radiation to the primary pancreatic tumor • One had a sustained partial response and underwent pancreaticoduodenectomy with pathology demonstrating a complete response Manji, GA ASCO 2025 Manji, GA AACR Pancreatic Cancer 2023 (Censor Date – July 20, 2023)
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© 2025 BioLineRx Ltd. All Rights Reserved. 30 2:1 Randomization N=108 N=36 N=72 Gemcitabine and nab-paclitaxel Gemcitabine, nab-paclitaxel with motixafortide and cemiplimab Key Eligibility • Stage IV PDAC • No prior systemic therapy • KPS ≥ 70 • RECIST measurable Study Design Primary Endpoint median PFS Secondary Endpoints OS, RR Correlates mIF, snRNAseq, cytokine IIS currently enrolling, equally funded by Regeneron and BioLineRx Randomized Trial Recruiting Trial Sites • Columbia University (PI Dr. Manji) • Brown University • University of California - San Francisco • Medical College of Wisconsin • Northwell Health • Pilot phase (promising findings reported at AACR Pancreas 2023) • Prespecified interim futility analysis (when 40% of PFS events observed) planned in 2026 • Full enrollment planned in 2027 Key Milestones* *Independent Investigator Study (IIS) timelines, as well as other study related decisions, are ultimately controlled by the independent investigator-sponsor and are, therefore, subject to change. Chemo4MetPanc Phase 2b clinical trial in first-line PDAC - randomized phase
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Corporate and summary
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Corporate and financials ▪ Cash of ~$28.2 million as of June 30, 2025 ▪ Two out-licensing transactions with potential royalty and milestone payments ▪ Shares outstanding – 4.3 million ADSs ▪ ~25 FTEs ▪ Cash runway into first half of 2027 © 2025 BioLineRx Ltd. All Rights Reserved. 32
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Focused vision for growth • Initiate Phase 1/2a trial of GLIX1 in glioblastoma FPI Q1 2026 • Data from Phase 1 part of GLIX1 trial* H1 2027 • Initiation of Phase 2a part of the GLIX1 trial H2 2027 • Ongoing randomized Phase 2 PDAC trial with motixafortide IA 2026 © 2025 BioLineRx Ltd. All Rights Reserved. 33 Expected milestones in next 18-24 months * In addition, as this trial is open-label, the data should be available on an ongoing basis; intention is to provide updates at medical conferences or other forums where possible