Purple Biotech Ltd. · TASE:PPBT
Purple Biotech — Investor Presentation (January 2026)
62 slides from Purple Biotech's investor presentation, Jan 13, 2026
Slide 1: Corporate Presentation January 2026
CORPORATE PRESENTATION January 2026 Advancing the next Generation of Immuno - oncology NASDAQ/TASE : PPBT
Slide 2: Forward-looking statements
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 forward - looking statements include, but are not
Slide 3: Snapshot | Company Highlights
1 Lead Program Entering the Clinic IM1240, our first tri - specific antibody from the CAPTN - 3 platform, is on track for Phase 1 initiation in H2 2026 2 CAPTN - 3: Differentiated multi - specific platform with Efficacy & Safety advantages The only platform designed to engage both T cells AND NK cel
Slide 4: The Problem: T Cell Engagers Immunotherapy Needs a New Approach
While multi - specific biologics have demonstrated initial success in hematologic cancers, current T - cell engagers face substantial challenges that have constrained their broader clinical impact in solid tumors. Imprecise Targeting Current T - cell engagers are "always on" — activating throughout
Slide 5: Our Lead Program: CAPTN-3 tri-specific antibodies
Solid tumors are the next frontier for T - cell engagers: With CAPTN - 3, tri - specific antibodies that enhance immune activation only at tumors site - combining safety with powerful anti - tumor activity STEP 1: SAFE - INACTIVE IN BLOOD TCE is "capped" — not triggering immune activation while targ
Slide 6: A pipeline dedicated to advancing oncology therapies
6 PHASE 1 PHASE 2 COLLABORATOR KEY NEXT MILESTONES PROGRAM INDICATION PRECLINCAL CAPTN - 3 PLATFORM — Lead Program IM1240 Capped - CD3x5T4xNKG2A Solid Tumors TOX, IND, Ph 1 Initiation in 2026 IM1305 Capped - CD3xTROP2xNKG2A Solid Tumors CLINICAL ASSETS — Partnership Opportunities CM24 CEACAM1 mAb Pa
Slide 7: 2026 Catalysts: Multiple Upcoming Value-Creating Milestones
| 7 Mid 2026 Q3 2026 Q4 2026 Ongoing IM1240 GLP Tox Complete Final safety studies to support IND filing IM1240 IND Submission FDA application to begin human trials IM1240 Phase 1 Start First patient dosed NT219 Interim Data Phase 2 head and neck readout մ IM1240 advancement into Phase 1 initiation r
Slide 8: CAPTN-3: Conditionally-Activated Tri-Specific Antibody Platform
CAPTN - 3: Conditionally - Activated Tri - Specific Antibody Platform
Slide 9: CAPTN-3: Built to Stand Out — Enhanced Efficacy with Improved Safety
9 CAPTN - 3: Built to Stand Out — Enhanced Efficacy with Improved Safety *Based on publicly available information
Slide 10: CAPTN-3: Tri-specific antibody activates innate and adaptive immune responses
10 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 Cance
Slide 11: CAPTN-3 - A Pipeline of Next-Generation TCEs
11 Collaborator Value Drivers Phase II Phase I Pre - clinical Indications Target Project GLP Tox, IND, Initiate FIH clinical study2026 Solid Tumors Capped - CD3x 5T4 xNKG2A CAPTN - 3 Tri - specific Ab IM1240 Solid Tumors Capped - CD3x TROP2 xNKG2A CAPTN - 3 Tri - specific Ab IM1305 CAPTN - 3 - A Pip
Slide 12: Plug & Play Tri-specific Scaffold
12 Plug & Play Tri - specific Scaffold Differentiated by Capped TCE with an NK Cell Activating Arm 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. ▪ NKG2A
Slide 13: Plug & Play Platform Capabilities Demonstrated In-Vivo
Plug & Play Platform Capabilities Demonstrated In - Vivo CD3x 5T4 xNKG2A CD3x EGFR xNKG2A CD3x5T4x NKG2D Platform demonstrations Pipeline candidates Sustained tumor regression was presented for several tri - specifics, targeting various TAAs and NK receptors: CD3x TROP2 xNKG2A 13
Slide 14: Unleashing both innate and adaptive immune response
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 st
Slide 15: Substantial contribution of the NKG2A arm
15 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 16: The power of NK arm inclusion in CAPTN structure
The power of NK arm inclusion in CAPTN - 3 structure NKG2A is consistently accompanied by tumor expression of 5T4 or TROP2 (ESMO - IO 2025) Transcriptomic analysis of approximately ~11,000 primary cancers (TCGA) » NKG2A and HLA - E expression in tumors demonstrates an invariant relationship. » NKG2A
Slide 17: 5T4 & TROP2 sought-after targets in oncology
17 5T4 & TROP2 Sought - after targets in oncology expressed on solid tumors 5T4 is a Tumor Associated Antigen prevalent in several large indications Kemper et al. LSA 2022;5:e202201481 Trop - 2 expression distribution across multiple solid tumors Kuo, Peiwen, et al. PloS one 20.4 (2025): e0321555 CE
Slide 18: IM1240 preclinical study notes
*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 19: IM1305: capped-CD3xTROP2xNKG2A In vivo PoC
| 19 IM1305: capped - CD3xTROP2xNKG2A In vivo PoC: Dose Depended, Effective and Sustainable In - vivo Tumor Regression by IM1305 & IM1302* Tumor Weight (g) Mean “ SEM ٓٓٓٓ 0.3 0.2 0.1 0.0 • Sustained tumor regression by IM1305. No tumor recurrence observed. • Similar results were obtained with equim
Slide 20: Next Steps: IM1240 and Other CAPTN Antibodies
Next Steps: IM1240 and Other CAPTN - 3 Antibodies GLP tox • H1 26 Initiation of FIH clinical trial • H2 26 20 IND submission • mid 26 Non GLP Dose range finding toxicology study in non - human primates for IM1240 completed successfully: • Demonstrated improved safety at doses up to 300 - fold higher
Slide 21: A clinical pipeline dedicated to advancing oncology therapies
Collaborator Value Drivers Phase III Phase II Phase I Pre - Clinical Indications Target Project Phase 2b Pancreatic Cancer (+nivolumab+SoC) CEACAM1 mAb CM24 Interim data 2026 Head and Neck Cancer (+cetuximab/ pembrolizumab) IRS1/2 degrader & STAT3 blocker NT219 A clinical pipeline dedicated to advan
Slide 22: 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 23: CM24: Targeting CEACAM1 expressing tumors
23 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 24: CM24: Immune modulation of CEACAM1 expressing TMEs
24 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 25: CM24 blocks NET-related activities by CEACAM1 inhibition
25 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 26: Large market opportunity based on CEACAM1 expression in PDAC
26 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 27: Randomized Bayesian study of CM24 with nivolumab plus SoC in 2L PDAC
27 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 28: Efficacy Proof of Concept demonstrated
28 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 29: Biomarkers analysis in serum or tumor
29 Phase 2 Biomarkers analysis in serum or tumor Significantly improved OS, PFS and ORR Statistically significant results in patients with pre - treatment serum CEACAM1 levels (6K - 15K pg/mL) or tumor CEACAM1 expression (H - score 115 - 275) » 78% reduction in risk of death ( HR 0.22 , p 0.006) and
Slide 30: NT219: Small Molecule Degrader of IRS 1/2 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 31: NT219: Novel IRS1/2 and STAT3 dual inhibitor
31 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 32: Dose escalation in combination with cetuximab
32 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 33: NT219: Activity in mono and combo dose escalation
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 treated
Slide 34: Activated pIGF1R and STAT3 as potential predictive biomarkers
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 non
Slide 35: Phase 2: NT219 + pembro or cetuximab in R/M HNSCC
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+ cetuxim
Slide 36: Snapshot | Company Highlights
36 1 Lead Program Entering the Clinic IM1240, our first tri - specific antibody from the CAPTN - 3 platform, is on track for Phase 1 initiation in H2 2026 2 CAPTN - 3: Differentiated multi - specific platform with Efficacy & Safety advantages The only platform designed to engage both T cells AND NK
Slide 37: Leadership Team
37 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 38: Contact Us / Thank You
38 Contact Us: ir@purple - biotech.com THANK YOU
Slide 39: Appendix A | CAPTN-3
Appendix A | CAPTN - 3
Slide 40: 5T4: a Novel Target in Oncology Expressed on Solid Tumors
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 Multiple 5T4
Slide 41: CD3 cap inhibits T cell binding and cleavage restores activity
• 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 safety,
Slide 42: Cytokine release is 5T4-dependent and suppressed by the cap
Cytokine release is 5T4 - 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 - fold •
Slide 43: Appendix B | CM24
Appendix B | CM24
Slide 44: CEACAM1 Plays a Key Role in Cancer Biology
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 progression of colon ca
Slide 45: CM24 binds to CEACAM1 on NETs
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 ) Le
Slide 46: CM24 Reduces Tumor Burden & Synergetic with α-PD-1
46 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 47: Dose Escalation Interim Results: CM24 safe with nivolumab
47 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 48: CM24 Phase 1/2 Combination Study Demographics
48 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, pharmacokinetics and dete
Slide 49: Confirmed Partial Response in a 3L PDAC Patient
49 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 • Confirmed Part
Slide 50: Dose Escalation Results in 2L/3L PDAC patients
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 thyroid cancer (PTC
Slide 51: Planned 2nd & 3rd line PDAC Phase 2b study design
51 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 52: Appendix C | NT219
Appendix C | NT219
Slide 53: NT219 targets critical signalling pathways simultaneously
| 53 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 54: Novel MOA: IRS Degradation By NT219
54 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 55: Novel MOA: STAT3 Inhibition
55 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 56: Simultaneous Blockade of STAT3 and AKT Pathways
56 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 57: NT219 re-sensitizes PD1-refractory models and restores sensitivity to EGFRi
57 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 58: NT219 combination with αPD1 reprograms the TME
58 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 59: NT219+PD1 Converted Immuno-suppressive to Immuno-reactive TME
59 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 60: Selected Publications
60 Selected Publications Michael Karin Alexander Levitzki Menashe Bar - Eli Michael Cox
Slide 61: NT219 inhibits the IRS to β-Catenin pathway in colon cancer
61 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 62: Market size forecasted to >$5b in 2030
62 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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