Purple Biotech Ltd. · TASE:PPBT

Purple Biotech — Investor Presentation (November 2025)

57 slides from Purple Biotech's investor presentation, Nov 19, 2025

  1. Slide 1: Corporate Presentation November 2025

    NASDAQ/TASE: PPBT November 2025 CORPORATE PRESENTATION

  2. Slide 2: Forward-looking Statements and Safe Harbor

    2 Forward - looking Statements and Safe Harbor Certain statements in this presentation that are forward - looking and not statements of historical fact are forward - looking statements within the meaning of the safe harbor provisions of the Private Securities Litigation Reform Act of 1995 . Such for

  3. Slide 3: Purple Biotech develops first-in-class drug candidates to treat cancers

    3 Purple Biotech develops promising first - in - class drug candidates to treat cancers with high unmet medical need Next generation tri - specific antibody platform • CAPTN - 3: Conditionally activated T - cell engager (TCE) enhanced by NK cell engager arm and a Tumor Associated Antigen engager Par

  4. Slide 4: A pipeline dedicated to advancing oncology therapies

    4 Collaborator Value Drivers Phase III Phase II Phase I Pre - Clinical Indications Target Project FIH 2026 Solid Tumors Capped - CD3x5T4xNKG2A CAPTN - 3 Tri - specific Ab IM1240 Solid Tumors Capped - CD3xTROP2xNKG2A CAPTN - 3 Tri - specific Ab IM1305 Phase 2b Pancreatic Cancer (+ nivolumab+SoC ) CEA

  5. Slide 5: CAPTN-3: Conditionally-Activated Tri-Specific Antibody Platform

    CAPTN - 3: Conditionally - Activated Tri - Specific Antibody Platform

  6. Slide 6: Uniquely positioned: first-in-class dual conditionally-activated T and NK cell engagers

    6 Uniquely positioned: First - in - class dual conditionally - activated T and NK Cell Engagers on the same antibody * B ased on publicly available information

  7. Slide 7: CAPTN-3: Tri-specific antibody activates innate and adaptive immune responses

    7 CAPTN - 3: Tri - specific antibody activates innate and adaptive immune responses while increasing the therapeutic index Engagement Masked TCE activated in TME TCE + NK cell engager Cancer binder α TAA Abs a - NK binder Abs T - cell - binder a - CD3 Abs  CD3 masking moiety Tumor cell NK cell Canc

  8. Slide 8: Plug & Play Tri-specific Scaffold Differentiated by Capped TCE

    8 Plug & Play Tri - specific Scaffold Differentiated by Capped TCE with an NK Cell Activating Arm 8 Multiple opportunities for development and partnering Modular TCE architecture allows integration of multiple TAAs or NK - activating arms, enabling a robust pipeline of novel drug candidates. ▪  NKG

  9. Slide 9: Plug & Play Platform Capabilities Demonstrated In-Vivo

    9 Plug & Play Platform Capabilities Demonstrated In - Vivo 9 CD3x 5T4 xNKG2A CD3x EGFR xNKG2A CD3x5T4x NKG2D CD 3 x TROP 2 xNKG 2 A Platform demonstrations Pipeline candidates Sustained tumor regression was presented for several tri - specifics, targeting various TAAs and NK receptors: Can we make t

  10. Slide 10: Unleashing both innate and adaptive immune response

    10 Unleashing both innate and adaptive immune response Dual activation of cytotoxic T - cells by CD 3 engagement & NKG 2 A inhibition Stimulates both helper (CD 4 +) and killer (CD 8 +) effector T cells via CD 3 targeting Dual mechanism: turns on killer T cells and blocks an immune “ off switch ” to

  11. Slide 11: CD3 cap inhibits T cell binding and cleavage restores activity

    11 • Binding to CD3 and cytotoxic effect is retained following protease cleavage of the CD3 cap • CAPTN - 3 uses multiple TME - specific proteases – increasing likelihood for cleavage by broad - tumor types CD 3 Cap inhibits T cell binding and cleavage restores activity: CAP advantages: improved saf

  12. Slide 12: Substantial contribution of the NKG2A arm demonstrated

    12 Substantial contribution of the NKG 2 A arm was demonstrated: • in - vivo : IL 15 KI mouse model • in patient - derived explants (PDE) • in cell - based assays: • reinvigoration of exhausted T cells • NKG 2 A + gd 2 cell activation and anti - cancer activity • Blocking of NK arm function through

  13. Slide 13: 5T4: a Novel Target in Oncology Expressed on Solid Tumors

    13 5 T 4 : a Novel Target in Oncology Expressed on Solid Tumors 5 T 4 is highly expressed on common cancer types and relates to a poor prognosis Am J Cancer Res 2018 ; 8 ( 4 ): 610 - 623 www.ajcr.us /ISSN: 2156 - 6976 /ajcr 0074519 5 T 4 is a Tumor Associated Antigen prevalent in several large indic

  14. Slide 14: Synergistic effect of CD3 and NKG2A arms

    | 14 5 38 49 94 0 20 40 60 80 100 Control IM1242 IM1340 IM1240 cResponse Score CD3x5T4 x NKG2A (cleavable cap) IM1240 5T4xNKG2A (non - cleavable) capped  CD3) 5 T 4 xCD 3 (cleavable cap; mutated NKG 2 A) Patient - derived explants (PDE) of 5 T 4 + NSCLC ** Synergistic effect of the CD 3 and NKG 2 A

  15. Slide 15: Next Steps: IM1240 and Other CAPTN Antibodies

    15 Next Steps: IM 1240 and Other CAPTN - 3 Antibodies Non GLP tox • Q 4 25 GLP tox • H1 26 IND submission • mid 26 FIH – IM1240 clinical trial • H2 26 Planned IM1240 Phase 1 Study • Basket trial in certain advanced/metastatic solid tumors likely to express 5T4 potentially including: TNBC, esophageal

  16. Slide 16: CM24: an α-CEACAM1 mAb

    CM 24 : an α - CEACAM 1 * mAb Significant opportunity in multiple large indications with unmet medical need Clinical POC achieved in PDAC *Carcinoembryonic Antigen Cell Adhesion Molecule

  17. Slide 17: CM24: Targeting CEACAM1 expressing tumors

    17 CM24: Targeting CEACAM1 expressing tumors • CEACAM1 is overexpressed in >90% of colon, pancreatic and bladder cancers and in >70% in lung, gastric and biliary tract cancers • CEACAM1 is a part of the Neutrophil Extracellular Traps (NETs) structure Attractive new target • CM24 increases T cell and

  18. Slide 18: CM24: Immune modulation of CEACAM1 expressing TMEs

    18 CM24: Immune modulation of CEACAM1 expressing TMEs Markel et al, J Immunol 2002, 2006; Immunology, 2008; Cancer Immunol Immunother 2010; Ortenberg et al, Mol Cancer Ther 2012; Zhou, 2009; Li, 2013; Huang, 2015; Acharya N, et al. J Immunotherapy Canc 8:e911 - 22, 2020. ; Gerstel, D. et al. CEACAM1

  19. Slide 19: CM24 blocks NET-related activities by CEACAM1 inhibition

    19 CCAM 1 CM 24 CM 24 CCAM1 CM24 CM24 b locks NET - related activities by CEACAM1 inhibition (adapted from ‘Chen, Q et al. Cancers 2021, 13, 2832’); Rayes RF, et al. Neutrophil Extracellular Trap - Associated CEACAM1 as a Putative Therapeutic Target to Prevent Metastatic Progres sion of Colon Carcin

  20. Slide 20: Large market opportunity based on CEACAM1 expression in PDAC

    20 Large market opportunity based on CEACAM1 expression in PDAC 1.https://seer.cancer.gov/ statfacts /html/pancreas.html , 2. De Jesus VHF, Camandaroba MPG, Calsavara VF, Riechelmann RP. 3. Systematic review and meta - analysis of gemcitabine - based chemotherapy after FOLFIRINOX in advanced pancrea

  21. Slide 21: Randomized Phase 2 study of CM24 plus nivolumab and chemotherapy in PDAC

    21 A randomized Bayesian study of CM 24 in combination with nivolumab plus SoC chemotherapy in 2 nd line PDAC patients* Primary endpoint : OS Secondary endpoints: PFS, ORR, DCR OS rate @ 6 & 12 months, PFS rate @ 3 & 6 months Completed Randomized Phase 2 Combination Study (NCT 04731467 ) – Experimen

  22. Slide 22: Phase 2 efficacy proof of concept demonstrated

    22 Phase 2 Efficacy Proof of Concept demonstrated: Consistent efficacy across all endpoints » Higher objective response rate ( ORR) (25% vs 6.7% ) » Higher disease control rate ( DCR) (62.5% vs 46.7%) » Consistent and continuous decrease of CA19 - 9 Median CA 19 - 9 levels % change in tumor size » 1

  23. Slide 23: Post-hoc Phase 2 Biomarkers Analysis

    23 Post - hoc Phase 2 Biomarkers Analysis Patients with either Serum CEACAM 1 or tumor CEACAM 1 + • Represents a subgroup of 52 % of patients • Suggests multifaceted MoA and the crosstalk of the tumor with the TME and the whole body Patients with either serum CEACAM 1 or MPO (NET marker) • R epresen

  24. Slide 24: Post-hoc analysis in serum or tumor CEACAM enriched patients

    24 Post - hoc analysis in serum or tumor CEACAM 1 enriched patients – Significantly improved OS, PFS Statistically significant results in patients with pre - treatment serum CEACAM 1 levels ( 6 K - 15 K pg /mL) or tumor CEACAM 1 expression (H - score 115 - 275 ) » 78 % reduction in risk of death ( H

  25. Slide 25: Results in serum CEACAM or MPO enriched patients

    25 Results in serum CEACAM 1 or MPO enriched patients Significantly improved OS, PFS 6 K < sCCAM 1 < 15 K pg /mL or 200 < MPO < 600 ng/mL PFS (%) EXP CONT Progression Free Survival 6K < sCCAM1 < 15K pg /mL or 200 < MPO < 600 ng/mL Overall Survival (%) EXP CONT Overall Survival Statistically signific

  26. Slide 26: Combination of CEACAM1 and PDL1 as predictive biomarkers

    26 Combination of CEACAM 1 and PDL 1 as predictive biomarkers Opportunity to treat patients currently not eligible for PD 1 inhibitors PFS (%) EXP CONT Overall Survival (%) EXP CONT Progression Free Survival Overall Survival Statistically significant results for patients with High CEACAM 1 (H - scor

  27. Slide 27: Planned Phase 2b PDAC study design

    27 Planned 2 nd & 3 rd line PDAC Phase 2 b study design To demonstrate enhanced efficacy in enriched population and contribution of parts – Advanced metastatic PDAC pts progressing on or after SoC chemotherapy or targeted therapy Serum CEACAM 1 /MPO within cutoffs of previous study Arm A SoC chemoth

  28. Slide 28: NT219: Small Molecule Degrader of IRS1/2 and Blocker of STAT3

    NT 219 : Small Molecule Degrader of IRS 1 / 2 and Blocker of STAT 3 Recurrent/Metastatic Head & Neck Cancer (R/M SCCHN)

  29. Slide 29: NT219: Novel IRS1/2 and STAT3 dual inhibitor for multiple indications

    29 NT 219 : Novel IRS 1 / 2 and STAT 3 dual inhibitor for multiple indications • Covalently binds to Insulin Receptor Substrate IRS 1 / 2 and leads to their degradation • Dual inhibitor of STAT 3 & IRS 1 / 2 , both required to overcome drug resistance • Affects both the tumor and the TME • Suppresse

  30. Slide 30: Dose escalation in combination with cetuximab

    30 Dose escalation in combination with cetuximab: Well tolerated, target exposure reached, responses observed • NT 219 was well tolerated as monotherapy and in combination with cetuximab ; No DLTs reported • Human Equivalent Dose exposure was reached at 50 mg/kg • RP 2 D determined at 100 mg/kg IRS

  31. Slide 31: NT219 activity in mono and combo dose escalation

    31 Monotherapy efficacy: • 20 evaluable patients (all doses): 2 PR (confirmed - GEJ, unconfirmed - PDAC), 5 SD Efficacy overview of combination arm in SCCHN patients: • 16 evaluable patients (all doses 6 , 12 , 24 , 50 , 100 mg/kg ) • Median follow - up of 9.4 months ( 95 % CI: 3.4 - 10.0 ) • Out of

  32. Slide 32: Activated pIGF1R and STAT3 as potential predictive biomarkers

    32 Activated pIGF1R and STAT3, NT219 targets, as potential predictive biomarkers Biomarker analysis at the effective doses of NT 219 ( 50 & 100 mg/kg) with cetuximab: • Significant differences in the pretreatment levels of activated pIGF 1 R and pSTAT 3 were revealed in the responders (PR) compared

  33. Slide 33: Phase 2: NT219 + pembro or cetuximab in R/M HNSCC

    33 Phase 2 : NT 219 + pembro or cetuximab in patients with R/M HNSCC – Phase 2 study initiated June 2025 Lead PI: Antonio Jimeno MD, PhD; U. Colorado Recurrent metastatic HNSCC ECOG PS 0 - 2 RECIST measurable disease n= 58 N 219 100 mg/kg Q 1 W+ pembro 200 mg Q 3 W n= 10 + 19 Simon 2 stage N 219 100

  34. Slide 34: Purple Biotech develops first-in-class drug candidates to treat cancers

    34 Purple Biotech develops promising first - in - class drug candidates to treat cancers with high unmet medical need Next generation tri - specific antibody platform • CAPTN - 3: Conditionally activated T - cell engager (TCE) enhanced by NK cell engager arm and a Tumor Associated Antigen engager Pa

  35. Slide 35: Leadership Team

    35 Leadership Team Michael Schickler, PhD Head of Clinical and Regulatory Affairs Formerly at Hoffmann - La Roche, CEO at CureTech Hadas Reuveni, PhD VP Research & Development Formerly at Keryx (NASDAQ:KERX) Gil Efron Chief Executive Officer Former Deputy CEO & CFO at Kamada (NASDAQ:KMDA) Eric K. Ro

  36. Slide 36: Contact Us / Thank You

    36 Contact Us: ir@purple - biotech.com THANK YOU

  37. Slide 37: Appendix A | CAPTN-3

    Appendix A | CAPTN - 3

  38. Slide 38: Cytokine release is T-dependent and suppressed by the cap

    38 Cytokine release is 5 T 4 - dependent and suppressed by the cap for improved safety Two safety factors through the design of the tri - specific Ab: the TCE capping and the advantage of its TAA arm: • Safety factor # 1 : The capped variant vs the non capped, showed a decreased IFN  release > 150

  39. Slide 39: Appendix B | CM24

    Appendix B | CM 24

  40. Slide 40: CEACAM1 Plays a Key Role in Cancer Biology

    40 Confidential CEACAM 1 Plays a Key Role in Cancer Biology 01 | ADHESION Horst, 2011 “ CEACAM 1 creates a pro - angiogenic tumor microenvironment that supports tumor vessel maturation ” “ Neutrophil extracellular trap - associated CEACAM 1 as a putative therapeutic target to prevent metastatic prog

  41. Slide 41: CM24 binds to CEACAM1 on NETs

    41 CM 24 binds to CEACAM 1 on NETs CM 24 Inhibits NET - Induced migration of CEACAM 1 expressing cancer cells CM 24 - Nivo treatment significantly reduced the enhanced NET levels in patient ’ s serum CM 24 binding/efficacy can be predicted by MPO levels MPO ( green ) DAPI ( blue ), CM 24 ( red ) CM

  42. Slide 42: CM24 Reduces Tumor Burden & Synergistic with α-PD-1

    42 Confidential CM 24 Reduces Tumor Burden & Synergetic with α - PD - 1 Xenograft, lung lesion melanoma model (Mel 526 , IV), 7 mice/group (NOD/SCID), 4 TIL injections IV, every 10 days, Ab Dose: 10 mg/kg, Ab Regimen: twice a week, study duration 70 days (last treatment day – 44 ), tumor burden was

  43. Slide 43: Phase 1 Dose Escalation Interim Results: CM24 Safe and Well Tolerated

    43 Phase 1 Dose Escalation Interim Results CM24 is Safe and Well Tolerated in Combi na tion with Nivolumab Grade Total AE Term 4/5 3 2 1 1 4 5 Diarrhea 3 1 4 Abdominal pain 2 2 4 Fever 1 3 4 Headache 4 4 Fatigue 2 1 3 Nausea 1 2 3 Creatinine increased 2 2 Hypokalemia 1 1 2 Dyspnea 2 2 Constipation 2

  44. Slide 44: CM24 Phase 1 Combination Study Demographics

    44 Confidential CM24 Phase 1 Combination Study (NCT04731467) Demographics In the Phase 1 part, patients with indicated refractory cancers were administered CM24 at 10, 15, and 20mg/kg q2w and nivolumab 480mg q4w. • The primary objective of this part was to evaluate safety, tolerability, pharmacokine

  45. Slide 45: Confirmed Partial Response in a 3L PDAC Patient

    45 Confidential Confirmed Partial Response in a 3L PDAC Patient Patient Profile • 65 y/o female, pancreatic cancer • 2 prior lines of treatments: FOLFIRINOX and gemcitabine/nab - paclitaxel • Post Whipple Procedure • Patient had a germline NF1 VUS, with MSI - S and PDL - 1 IHC 2+ and 5% staining • C

  46. Slide 46: CM24 Phase 1 Dose Escalation Results

    46 Confidential CM24 Phase 1 Dose Escalation Results E ncouraging data in 2L/3L Pancreatic Ductal Adenocarcinoma (PDAC) patients Study Results 14 patients were evaluable for efficacy: • Best overall response included 1 Partial Response (PR) (PDAC) and 4 Stable Disease (SD) (3 PDAC and 1 papillary th

  47. Slide 47: Appendix C | NT219

    Appendix C | NT219

  48. Slide 48: NT219 targets critical signalling pathways simultaneously

    | 48 NT219 targets 2 critical signalling pathways simultaneously leading IRS1/2 to degradation and blocking STAT3 IRS1/2 • Promotes a tumor - protective microenvironment • O verexpressed in multiple tumor types • Activated as a feedback response to anti - cancer therapies • Regulates major survival

  49. Slide 49: Novel MOA: IRS Degradation By NT219

    49 Novel MOA: IRS Degradation By NT219 Blocking IGF1R - AKT Pathway 1 Binding to IRS 1 1 Reuveni et al. Cancer Res 2013 ; Ibuki et al. Mol Cancer Ther 2014 Ser - phosphorylation 2 Degradation 3 Covalent binding to IRS1/2 leads to the dissociation of IRS1/2 from IGF1R Serine phosphorylation prevents

  50. Slide 50: Novel MOA: STAT3 Inhibition

    50 Novel MOA Signal Transducer and Activator of Transcription 3 ( STAT 3 ) Inhibition • Point of convergence for numerous oncogenic signaling pathways • Central in regulating the anti - tumor immune response • Broadly hyperactivated both in cancer and non - cancerous cells within the tumor ecosystem

  51. Slide 51: Simultaneous Blockade of STAT3 and AKT Pathways Overcomes EGFRi Resistance

    51 Simultaneous Blockade of STAT 3 and AKT Pathways are Required to Overcome Resistance to EGFRi Overcoming drug resistance NT 219 NT 219 STAT 3 IRS EGFR EGFRi MEK / ERK TUMOR REGRESSION Proof of Concept: PDX model of Head and Neck Cancer Erlotinib+Ruxolitinib (n= 6 ) Erlotinib+Buparlisib (n= 6 ) Co

  52. Slide 52: NT219 re-sensitizes PD1-refractory models and restores sensitivity to EGFRi

    52 NT 219 re - sensitizes  PD 1 - refractory models and restores sensitivity to EGFRi NT 219 +Pembrolizumab reverse  PD 1 - resistant GEJ tumors in a PDX model Days following tumor challenge (n= 10 ) (n= 10 ) (n= 10 ) (n= 10 ) * Collaboration with Prof. Bareli and Prof. Curran, M.D. Anderson cance

  53. Slide 53: NT219 combination with αPD1 reprograms the TME

    53 NT 219 combination with α PD 1 achieves significant reprograming of the TME NT 219 and  PD 1 combination converted immuno - suppressive TME to immuno - reactive • Immune profiling of the ICB - resistant melanoma tumors following treatment of the mice with the NT 219 + αPD 1 revealed significant

  54. Slide 54: NT219 + αPD1 Converted Immuno-suppressive to Immuno-reactive TME

    54 NT 219 +  PD 1 Converted Immuno - suppressive to Immuno - reactive TME Zou et al. Molecular Cancer ( 2020 ) 19:145 ; Rampias et al. Oncogene ( 2016 ) 35:2562 ; Flashner, Reuveni, Levitzki et al. Oncogene ( 2016 ) 35:2675 ; Sanchez - Lopez et al. Oncogene ( 2016 ) 35:2634  PD 1 + NT 219  PD 1 +

  55. Slide 55: Selected Publications

    55 Selected Publications Michael Karin Alexander Levitzki Menashe Bar - Eli Michael Cox

  56. Slide 56: NT219 inhibits the IRS to β-catenin pathway

    56 AACR Annual Meeting, April 2021 , AACR Virtual Special Conference on Epigenetics and Metabolism, Oct 2020 , Ido Wolf, MD, Head of Oncology Division, Tel Aviv Sourasky Medical Center Colon cancer LS - 513 cells overexpressing IRS 2 demonstrate enhanced  - catenin activity. Targeted inhibition of

  57. Slide 57: Market Opportunity: Recurrent or Metastatic SCCHN

    57 Market size forecasted to >$ 5 b in 2030 Market Opportunity Recurrent or Metastatic Squamous Cell Carcinoma of Head and Neck (R/M SCCHN) Global Data Epidemiology and Market Size for 8 MM, accessed March 2025 . Rationale for combining cetuximab or pembrolizumab + NT 219 • STAT 3 and IRS - to - AKT

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