Purple Biotech Ltd. · TASE:PPBT
Purple Biotech — Investor Presentation (March 2026)
59 slides from Purple Biotech's investor presentation, Mar 19, 2026
Slide 1: Corporate Presentation March 2026
CORPORATE PRESENTATION March 2026 Advancing the next Generation of Immuno - oncology NASDAQ/TASE : PPBT
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: Snapshot: Company Highlights
| 3 1 Lead Program Entering the Clinic IM1240, our first tri - specific antibody from the CAPTN - 3 platform 2 CAPTN - 3: Differentiated multi - specific platform with Efficacy & Safety advantages The only platform designed to engage both T cells AND NK cells for enhanced anti - tumor potency, while
Slide 4: The Problem: T Cell Therapies Need a New Approach
| 4 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 Many T - cell engagers are "always on" — activating throughout
Slide 5: Solid tumors are the next frontier for T-cell engagers: CAPTN-3
| 5 Solid tumors are the next frontier for T - cell engagers: With CAPTN - ϯ , 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 whi
Slide 6: A pipeline dedicated to advancing oncology therapies
6 PROGRAM INDICATION PRECLINCAL PHASE 1 PHASE 2 COLLABORATOR KEY NEXT MILESTONES CAPTN - 3 PLATFORM — Lead Program IM1240 Capped - CD3x5T4xNKG2A Solid Tumors TOX, IND, in 2026 , Ph 1 Initiation in 2027 IM1305 Capped - CD3xTROP2xNKG2A Solid Tumors CLINICAL ASSETS — Partnership Opportunities CM24 CEAC
Slide 7: 2026: Multiple Upcoming Value-Creating Catalysts
| 7 Q 3 2026 Q 4 2026 Q1 2027 Ongoing IM 1240 GLP Tox Complete Final safety studies to support IND filing IM1240 IND Submission FDA application to begin human trials IM 1240 Phase 1 Start First patient dosed NT219 Interim Data Phase 2 head and neck readout IM 1305 Advancement TROP 2 program preclini
Slide 8: CAPTN-3: Conditionally-Activated Tri-Specific Antibody Platform
CAPTN - 3 : Conditionally - Activated Tri - Specific Antibody Platform YL1
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 * B ased on publicly available information
Slide 10: Plug & Play Tri-specific Scaffold Differentiated by Capped TCE
10 anti - TAA Plug & Play Tri - specific Scaffold Differentiated by Capped TCE with an NK Cell Activating Arm 10 » Allows integration of multiple TAAs or NK - activating arms, enabling a robust pipeline of novel drug candidates. » Multiple opportunities for development and partnering NKG 2 A NKG
Slide 11: Plug & Play Platform Capabilities Demonstrated In-Vivo
11 Plug & Play Platform Capabilities Demonstrated In - Vivo 11 CD3x 5T4 xNKG2A CD3x EGFR xNKG2A CD 3 x 5 T 4 x NKG 2 D Platform demonstrations Pipeline candidates Sustained tumor regression was presented for several tri - specifics, targeting various TAAs and NK receptors: CD 3 x TROP 2 xNKG 2 A
Slide 12: Unleashing both innate and adaptive immune response
12 Unleashing both innate and adaptive immune response Dual activation of cytotoxic T - cells by CD3 engagement & NKG2A 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 unle
Slide 13: Substantial contribution of the NKG2A arm was demonstrated
13 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
Slide 14: The power of NK arm inclusion in CAPTN-3 structure
14 The power of NK arm inclusion in CAPTN - 3 structure NKG2A is consistently accompanied by tumor expression of 5T4 or TROP2 (ESMO - IO 2025) » NKG 2 A and HLA - E expression in tumors demonstrates an invariant relationship . » NKG 2 A expression was strongly correlated to 5 T 4 and TROP 2 expressi
Slide 15: 5T4 & TROP2: Sought-after targets in oncology
15 5 T 4 & TROP 2 Sought - after targets in oncology expressed on solid tumors 5 T 4 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): e03215
Slide 16: Synergistic effect of the CD3 and NKG2A arms
| 16 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) 5T4xCD3 (cleavable cap; mutated NKG2A) Patient - derived explants (PDE) of 5 T 4 + NSCLC ** Synergistic effect of the CD 3 and NKG 2 A arms
Slide 17: IM1305: capped-CD3xTROP2xNKG2A In vivo PoC
| 17 IM 1305 : capped - CD 3 xTROP 2 xNKG 2 A In vivo PoC: Dose Depended, Effective and Sustainable In - vivo Tumor Regression by IM 1305 & IM 1302 * • Sustained tumor regression by IM1305. No tumor recurrence observed. • Similar results were obtained with equimolar doses of the non - capped variant
Slide 18: Next Steps: IM1240 and Other CAPTN-3 Antibodies
18 Next Steps: IM1240 and Other CAPTN - 3 Antibodies GLP tox • Q3 26 IND submission • Q4 26 Initiation of FIH clinical trials • Q 1 27 Non GLP Dose range finding toxicology study in non - human primates for IM 1240 completed successfully: • Demonstrated improved safety at doses up to 300 - fold high
Slide 19: 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
Slide 20: CM24: Targeting CEACAM1 expressing tumors
20 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 • CM 24 increases T cell an
Slide 21: CM24: Immune modulation of CEACAM1 expressing TMEs
21 CM 24 : Immune modulation of CEACAM 1 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 :e 911 - 22 , 2020 . ; Gerstel, D.
Slide 22: CM24 blocks NET-related activities by CEACAM1 inhibition
22 CCAM1 CM 24 CM24 CCAM1 CM24 CM 24 b locks NET - related activities by CEACAM 1 inhibition (adapted from ‘ Chen, Q et al. Cancers 2021 , 13 , 2832 ’ ); Rayes RF, et al. Neutrophil Extracellular Trap - Associated CEACAM 1 as a Putative Therapeutic Target to Prevent Metastatic Progression of Colon C
Slide 23: Large market opportunity based on CEACAM1 expression in PDAC
23 Large market opportunity based on CEACAM 1 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 pan
Slide 24: Randomized Phase 2 study of CM24 with nivolumab plus chemotherapy
24 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
Slide 25: Phase 2 Efficacy Proof of Concept demonstrated
25 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 CA 19 - 9 Median CA 19 - 9 levels % change in tumor s
Slide 26: Phase 2 Biomarkers analysis in serum or tumor
26 Phase 2 Biomarkers analysis in serum or tumor Significantly improved OS, PFS and ORR 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. 22 , p 0
Slide 27: 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) YL1
Slide 28: NT219: Novel IRS1/2 and STAT3 dual inhibitor
28 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
Slide 29: Dose escalation in combination with cetuximab
29 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 IRS2
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
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 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
Slide 32: Phase 2: NT219 + pembro or cetuximab in R/M HNSCC
32 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
Slide 33: Snapshot: Company Highlights
33 1 Lead Program Entering the Clinic IM1240, our first tri - specific antibody from the CAPTN - 3 platform 2 CAPTN - 3 : Differentiated multi - specific platform with Efficacy & Safety advantages The only platform designed to engage both T cells AND NK cells for enhanced anti - tumor potency, while
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: 5T4: a Novel Target in Oncology Expressed on Solid Tumors
37 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 5T4 is a Tumor Associated Antigen prevalent in several large indicat
Slide 38: CD3 cap inhibits T cell binding and cleavage restores activity
38 • Binding to CD 3 and cytotoxic effect is retained following protease cleavage of the CD 3 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 s
Slide 39: Cytokine release is T-dependent and suppressed by the cap
39 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
Slide 40: Appendix B | CM24
Appendix B | CM 24
Slide 41: CEACAM1 Plays a Key Role in Cancer Biology
41 CEACAM 1 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 CEACAM 1 as a putative therapeutic target to prevent metastatic progression of col
Slide 42: CM24 binds to CEACAM1 on NETs
42 CM24 binds to CEACAM1 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 ) CM24
Slide 43: CM24 Reduces Tumor Burden & Synergistic with α-PD-1
43 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 monitored 26 d
Slide 44: Phase 1 Dose Escalation Interim Results: CM24 Safe and Well Tolerated
44 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
Slide 45: CM24 Phase 1 Combination Study Demographics
45 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 46: Confirmed Partial Response in a 3L PDAC Patient
46 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 47: CM24 Phase 1 Dose Escalation Results
47 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 thyroid cancer
Slide 48: Planned 2nd & 3rd line PDAC Phase 2b study design
48 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 chemothera
Slide 49: Appendix C | NT219
Appendix C | NT219
Slide 50: NT219 targets critical signalling pathways simultaneously
| 50 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
Slide 51: Novel MOA: IRS Degradation By NT219
51 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
Slide 52: Novel MOA: STAT3 Inhibition
52 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
Slide 53: Simultaneous Blockade of STAT3 and AKT Pathways Overcomes Resistance
53 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
Slide 54: NT219 re-sensitizes PD-1 refractory models and restores sensitivity to EGFRi
54 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
Slide 55: NT219 combination with αPD1 achieves reprograming of the TME
55 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
Slide 56: NT219 + αPD1 Converted Immuno-suppressive to Immuno-reactive TME
56 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 +
Slide 57: Selected Publications
57 Selected Publications Michael Karin Alexander Levitzki Menashe Bar - Eli Michael Cox
Slide 58: NT219 inhibits the IRS to β-catenin pathway in colon cancer
58 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
Slide 59: Market Opportunity: Recurrent or Metastatic SCCHN
59 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