Purple Biotech Ltd. · TASE:PPBT
Purple Biotech — Investor Presentation (September 2025)
56 slides from Purple Biotech's investor presentation, Sep 16, 2025
Slide 1: Corporate Presentation September 2025
NASDAQ/TASE: PPBT September 2025 CORPORATE PRESENTATION
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
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
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) CEACA
Slide 5: CAPTN-3: Conditionally-Activated Tri-Specific Antibody Platform
CAPTN - 3: Conditionally - Activated Tri - Specific Antibody Platform
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 *Based on publicly available information
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 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 Masked TCE activated in TME Cancer
Slide 8: Plug & Play Tri-specific Scaffold
8 Plug & Play Tri - specific Scaffold differentiated by Capped TCE + with an NK Cell Activating Arm ▪ NKG2A ▪ NK2D ▪ Other NK cell engagers NK engager Cap - HSA CD3 TAA ▪ α 5T4 ▪ α TROP2 ▪ α EGFR ▪ Other Multiple opportunities for development and partnering • Modular architecture allows integration
Slide 9: Unleashing both innate and adaptive immune response
9 Unleashing both innate and adaptive immune response Dual activation of cytotoxic T - cells by CD3 engagement & NKG2A inhibition Stimulates both helper (CD4+) and killer (CD8+) effector T cells via CD3 targeting Dual mechanism: turns on killer T cells and blocks an immune “off switch” to unleash a
Slide 10: CD3 cap inhibits T cell binding and cleavage restores activity
10 • 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 CD3 Cap inhibits T cell binding and cleavage restores activity: CAP advantages: improved safe
Slide 11: Contribution of the NKG2A arm demonstrated
11 Substantial contribution of the NKG2A arm was demonstrated: • in - vivo : IL15 KI mouse model • in patient - derived explants (PDE) • in cell - based assays: • reinvigoration of exhausted T cells • NKG2A + gd2 cell activation and anti - cancer activity • Blocking of NK arm function through mutati
Slide 12: 5T4: a Novel Target in Oncology Expressed on Solid Tumors
12 5T4: a Novel Target in Oncology Expressed on Solid Tumors 5T4 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/ajcr0074519 5T4 is a Tumor Associated Antigen prevalent in several large indications Opportuni
Slide 13: IM1240 preclinical efficacy data
*TNBC MDA - MB - 231 cells were s.c. inoculated 1:1 with PBMCs on day 0. Treatments: IV QOD 1mg/kg (non - capped) or equimolar dose 1.7 mg/kg (capped, 1240) till day 24, 8 mice per group, Follow up 20 days following treatment completion **5T4 + NCSLC Patient - Derived Explant (PDE)* at 10nM concentr
Slide 14: Next steps IM1240 and Other CAPTN Antibodies
14 Next steps IM1240 and Other CAPTN - 3 Antibodies Non GLP tox • Q4 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, S
Slide 15: CM24: an α-CEACAM1 mAb
CM24: an α - CEACAM1* mAb Significant opportunity in multiple large indications with unmet medical need Clinical POC achieved in PDAC *Carcinoembryonic Antigen Cell Adhesion Molecule
Slide 16: CM24: Targeting CEACAM1 expressing tumors
16 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
Slide 17: CM24: Immune modulation of CEACAM1 expressing TMEs
17 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
Slide 18: CM24 blocks NET-related activities by CEACAM1 inhibition
18 CM24 CCAM1 CM24 CCAM1 CM24 CM24 blocks 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 Progression of Colon Carcinoma.
Slide 19: Large market opportunity based on CEACAM1 expression in PDAC
19 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 pancreati
Slide 20: Randomized Bayesian study of CM24 with nivolumab plus SoC chemotherapy
20 A randomized Bayesian study of CM24 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 (NCT04731467) Experimental a
Slide 21: Phase 2 efficacy proof of concept demonstrated
21 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
Slide 22: Post-hoc Phase 2 Biomarkers Analysis
22 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) • Represents
Slide 23: Post-hoc analysis in serum or tumor CEACAM1 enriched patients
23 Post - hoc analysis in serum or tumor CEACAM1 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 ( HR 0
Slide 24: Results in serum CEACAM1 or MPO enriched patients
24 Results in serum CEACAM1 or MPO enriched patients Significantly improved OS, PFS PFS (%) EXP CONT Progression Free Survival 6K < sCCAM1 < 15K pg/mL or 200 < MPO < 600 ng/mL Overall Survival (%) EXP CONT Overall Survival 6K < sCCAM1 < 15K pg/mL or 200 < MPO < 600 ng/mL Statistically significant re
Slide 25: Combination of CEACAM1 and PDL1 as predictive biomarkers
25 Combination of CEACAM1 and PDL1 as predictive biomarkers Opportunity to treat patients currently not eligible for PD1 inhibitors PFS (%) EXP CONT Overall Survival (%) EXP CONT Progression Free Survival Overall Survival Statistically significant patients with High results for CEACAM1 (H - score>10
Slide 26: Planned Phase 2b PDAC study design
26 Planned 2 nd & 3 rd line PDAC Phase 2b 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 CEACAM1/MPO within cutoffs of previous study Arm A SoC chemotherapy
Slide 27: NT219: Small Molecule Degrader of IRS1/2 and Blocker of STAT3
NT219: Small Molecule Degrader of IRS 1/2 and Blocker of STAT3 Recurrent/Metastatic Head & Neck Cancer (R/M SCCHN)
Slide 28: NT219: Novel IRS1/2 and STAT3 dual inhibitor for multiple indications
28 NT219: Novel IRS1/2 and STAT3 dual inhibitor for multiple indications • Covalently binds to Insulin Receptor Substrate IRS1/2 and leads to their degradation • Dual inhibitor of STAT3 & IRS1/2 , both required to overcome drug resistance • Affects both the tumor and the TME • Suppresses cancer stem
Slide 29: Dose escalation in combination with cetuximab
29 Dose escalation in combination with cetuximab: Well tolerated, target exposure reached, responses observed • NT219 was well tolerated as monotherapy and in combination with cetuximab; No DLTs reported • Human Equivalent Dose exposure was reached at 50 mg/kg • RP2D determined at 100 mg/kg IRS2 in
Slide 30: NT219: Activity in mono and combo dose escalation
30 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 8 treat
Slide 31: Activated pIGF1R and STAT3 as potential predictive biomarkers
31 Activated pIGF1R and STAT3, NT219 targets, as potential predictive biomarkers Biomarker analysis at the effective doses of NT219 (50&100mg/kg) with cetuximab: • Significant differences in the pretreatment levels of activated pIGF1R and pSTAT3 were revealed in the responders (PR) compared to the n
Slide 32: Phase 2: NT219 + pembro or cetuximab in R/M HNSCC
32 Phase 2: NT219 + 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 N219 100mg/kg Q1W+ pembro 200mg Q3W n=10 +19 Simon 2 stage N219 100mg/kg Q1W+ cetu
Slide 33: Purple Biotech develops first-in-class drug candidates to treat cancers
33 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
Slide 34: Leadership Team
34 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
Slide 35: Contact Us / Thank You
35 Contact Us: ir@purple - biotech.com THANK YOU
Slide 36: Appendix A | CAPTN-3
Appendix A | CAPTN - 3
Slide 37: Cytokine release is 5T4-dependent and suppressed by the cap
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 - fold • Safety factor #2 : In the absence of 5T4 - expressing cancer cells, the non - cap
Slide 38: Appendix B | CM24
Appendix B | CM24
Slide 39: CEACAM1 Plays a Key Role in Cancer Biology
39 Confidential CEACAM1 Plays a Key Role in Cancer Biology 01 | ADHESION Horst, 2011 “ CEACAM1 creates a pro - angiogenic tumor microenvironment that supports tumor vessel maturation ” “ Neutrophil extracellular trap - associated CEACAM1 as a putative therapeutic target to prevent metastatic progres
Slide 40: CM24 binds to CEACAM1 on NETs
40 CM24 binds to CEACAM1 on NETs CM24 Inhibits NET - Induced migration of CEACAM1 expressing cancer cells CM24 - Nivo treatment significantly reduced the enhanced NET levels in patient’s serum CM24 binding/efficacy can be predicted by MPO levels MPO ( green ) DAPI ( blue ), CM24 ( red ) CM24 ( red )
Slide 41: CM24 Reduces Tumor Burden & Synergetic with α-PD-1
41 Confidential CM24 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 mon
Slide 42: Phase 1 Dose Escalation Interim Results: Safety
42 Phase 1 Dose Escalation Interim Results CM24 is Safe and Well Tolerated in Combination with Nivolumab Total Grade 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 2
Slide 43: CM24 Phase 1 Combination Study Demographics
43 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
Slide 44: Confirmed Partial Response in a 3L PDAC Patient
44 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
Slide 45: CM24 Phase 1 Dose Escalation Results
45 Confidential CM24 Phase 1 Dose Escalation Results Encouraging 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 thy
Slide 46: Appendix C | NT219
Appendix C | NT219
Slide 47: NT219 targets critical signalling pathways simultaneously
| 47 NT219 targets 2 critical signalling pathways simultaneously leading IRS1/2 to degradation and blocking STAT3 IRS1/2 • Promotes a tumor - protective microenvironment • Overexpressed in multiple tumor types • Activated as a feedback response to anti - cancer therapies • Regulates major survival p
Slide 48: Novel MOA: IRS Degradation By NT219
48 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 2 Ser - phosphorylation Degradation 3 Covalent binding to IRS1/2 leads to the dissociation of IRS1/2 from IGF1R Serine phosphorylation prevents
Slide 49: Novel MOA: STAT3 Inhibition
49 Novel MOA Signal Transducer and Activator of Transcription 3 (STAT3) 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 an
Slide 50: Simultaneous blockade of STAT3 and AKT pathways overcomes EGFRi resistance
50 Simultaneous Blockade of STAT3 and AKT Pathways are Required to Overcome Resistance to EGFRi Overcoming drug resistance NT219 NT219 STAT3 IRS EGFR EGFRi MEK / ERK TUMOR REGRESSION Proof of Concept: PDX model of Head and Neck Cancer Control (n=6) Erlotinib (n=8) Erlotinib+NT219 (n=6) Erlotinib+Rux
Slide 51: NT219 re-sensitizes PD1-refractory models and restores sensitivity to EGFRi
51 NT219 re - sensitizes PD1 - refractory models and restores sensitivity to EGFRi 6 8 20 22 0 500 1000 1500 2000 Tumor volume (mm 3 ) 10 12 14 16 18 Days following tumor challenge Control (n=10) α - PD - 1 (n=10) NT219 (n=10) NT219+α - PD - 1 (n=10) * Collaboration with Prof. Bareli and Prof. Curra
Slide 52: NT219 combination with αPD1 reprograms the TME
52 NT219 combination with α PD1 achieves significant reprograming of the TME NT219 and PD1 combination converted immuno - suppressive TME to immuno - reactive • Immune profiling of the ICB - resistant melanoma tumors following treatment of the mice with the NT219 + αPD1 revealed significant reprogra
Slide 53: NT219+PD1 Converted Immuno-suppressive to Immuno-reactive TME
53 NT219+ PD1 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 PD1+ NT219 PD1+ NT219 PD1+ NT219 PD1+
Slide 54: Selected Publications
54 Selected Publications Michael Karin Alexander Levitzki Menashe Bar - Eli Michael Cox
Slide 55: NT219 inhibits the IRS to β-catenin pathway in colon cancer
55 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 IRS2 demonstrate enhanced - catenin activity. Targeted inhibition of IRS2
Slide 56: Market size forecasted to >$5b in 2030
56 Market size forecasted to >$5b in 2030 Market Opportunity Recurrent or Metastatic Squamous Cell Carcinoma of Head and Neck (R/M SCCHN) Global Data Epidemiology and Market Size for 8MM, accessed March 2025. Rationale for combining cetuximab or pembrolizumab + NT219 • STAT3 and IRS - to - AKT/ cate
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