Purple Biotech Ltd. · TASE:PPBT
Purple Biotech — Investor Presentation (January 2026)
59 slides from Purple Biotech's investor presentation, January 2026
Slide 1: Advancing the next Generation of Immuno-oncology
Advancing the next Generation of Immuno-oncology CORPORATE PRESENTATION NASDAQ/TASE: PPBT January 2026
Slide 2: Forward-looking Statements and Safe Harbor
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 forward-look
Slide 3: Snapshot: Company Highlights
Snapshot: Company Highlights FINANCIALS 1 Lead Program Entering the Clinic IM1240, our first tri-specific antibody from the CAPTN-3 platform, is on track for Phase 1 Cash initiation in H2 2026 $10.5M As of September 30, 2025 2 CAPTN-3: Differentiated multi-specific platform with Efficacy & Safety ad
Slide 4: The Problem: T Cell Therapies Need a New Approach
The Problem: T Cell Therapies Need 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. 51-90% CRS rates with current TCEs * Syn
Slide 5: Our Lead Program: CAPTN-3 Platform
Our Lead Program: CAPTN-3 Platform 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: STEP 2: STEP 3: SAFE-INACTIVE IN BLOOD ACTIVATED AT TUMOR DU
Slide 6: A pipeline dedicated to advancing oncology therapies
A pipeline dedicated to advancing oncology therapies PROGRAM INDICATION PRECLINCAL PHASE 1 PHASE 2 COLLABORATOR KEY NEXT MILESTONES CAPTN-3 PLATFORM — Lead Program IM1240 TOX, IND, Solid Tumors Ph 1 Initiation Capped-CD3x5T4xNKG2A in 2026 IM1305 Solid Tumors Capped-CD3xTROP2xNKG2A CLINICAL ASSETS —
Slide 7: 2026: Multiple Upcoming Value-Creating Catalysts
2026: Multiple Upcoming Value-Creating Catalysts Mid 2026 Q3 2026 Q4 2026 Ongoing IM1240 GLP Tox Complete IM1240 IND Submission IM1240 Phase 1 Start NT219 Interim Data Final safety studies to support FDA application to begin human trials First patient dosed Phase 2 head and neck readout IND filing I
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
CAPTN-3: Built to Stand Out — Enhanced Efficacy with Improved Safety 9 *Based on publicly available information
Slide 10: Plug & Play Tri-specific Scaffold
Plug & Play Tri-specific Scaffold Differentiated by Capped TCE with an NK Cell Activating Arm Cap- HSA CD3 TAA NK engager ▪ α 5T4 ▪ NKG2A New TAA ▪ α TROP2 ▪ NKG2D NK cell ▪ α EGFR ▪ Other engagers anti-TAA ▪ Other Modular TCE architecture allows integration of Differentiated TCE platform – multi
Slide 11: Plug & Play Platform Capabilities Demonstrated In-Vivo
Plug & Play Platform Capabilities Demonstrated In-Vivo Sustained tumor regression was presented for several tri-specifics, targeting various TAAs and NK receptors: Pipeline candidates Platform demonstrations CD3x5T4xNKG2A CD3xTROP2xNKG2A CD3x5T4xNKG2D CD3xEGFRxNKG2A 11 11
Slide 12: 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 Activates NK cells by blocking the inhibitory Stimulates both helper (CD4+) and Dual mechanism: turns on killer T cells and NKG2A–HLA-E interaction killer (CD8+) effector T c
Slide 13: Significant contribution of the NK and CD3 arms to anti-tumor activity in vivo
Significant contribution of the NK and CD3 arms to the anti- tumor activity in vivo (EACR 2025) Substantial contribution of the NKG2A arm was TNBC tumor growth inhibition in IL15 KI mice* demonstrated: Significant effects of the NK and CD3 arms • in-vivo: IL15 KI mouse model Tumor volume (mm3) CAPTN
Slide 14: The power of NK arm inclusion in CAPTN-3 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 expre
Slide 15: Sought-after targets in oncology expressed on solid tumors
5T4 & TROP2 Sought-after targets in oncology expressed on solid tumors 5T4 is a Tumor Associated Antigen Trop-2 expression distribution across prevalent in several large indications multiple solid tumors Kemper et al. LSA 2022;5:e202201481 Kuo, Peiwen, et al. PloS one 20.4 (2025): e0321555 15 CESC,
Slide 16: IM1240: capped-CD3x5T4xNKG2A
IM1240: capped-CD3x5T4xNKG2A In vivo efficacy and synergistic effect of the CD3 and NKG2A arms In vivo anti-tumor efficacy of IM1240 & IM1222* Patient-derived explants (PDE) of 5T4+NSCLC ** Effective cleavage (p<0.0001 ) Synergistic effect of the CD3 and NKG2A arms 100 94 cResponse Score 80 60 40 49
Slide 17: IM1305: capped-CD3xTROP2xNKG2A In vivo PoC
IM1305: capped-CD3xTROP2xNKG2A In vivo PoC: Dose Depended, Effective and Sustainable In-vivo Tumor Regression by IM1305 & IM1302* ✱✱✱✱ Vehicle 0.3 IM1305-0.4mpk Q2D Tumor Weight (g) IM1305-0.8mpk Q2D Mean ± SEM 0.2 IM1305-1.6mpk Q2D IM1302-1mpk Q2D 0.1 0.0 2D 2D 2D 2D e cl Q Q Q Q hi Ve pk k pk pk p
Slide 18: Next Steps: IM1240 and Other CAPTN-3 Antibodies
Next Steps: IM1240 and Other CAPTN-3 Antibodies GLP tox Initiation of FIH clinical trial •H1 26 •H2 26 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 than a non-
Slide 19: 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 20: CM24: Targeting CEACAM1 expressing tumors
CM24: Targeting CEACAM1 expressing tumors • CEACAM1 is overexpressed in >90% of colon, pancreatic and bladder cancers and in Attractive >70% in lung, gastric and biliary tract cancers new target • CEACAM1 is a part of the Neutrophil Extracellular Traps (NETs) structure Demonstrated • CM24 increases
Slide 21: CM24: Immune modulation of CEACAM1 expressing TMEs
CM24: Immune modulation of CEACAM1 expressing TMEs Activating the immune response CEACAM1 expression on tumor and tumor-infiltrating immune cells in PDAC Normal PDAC tumor cells Immune cells Tumor CEACAM1 CEACAM5 CM24 CEACAM1+ CD8+ CD 80µm 80µm CEACAM1 CEACAM1 CEACAM1+NK cells CD 80µm 80µm CD8+T & N
Slide 22: CM24 blocks NET-related activities by CEACAM1 inhibition
CM24 blocks NET-related activities by CEACAM1 inhibition CEACAM1 is a part of the Neutrophil extracellular traps (NET) structure CM24 binds to CEACAM1 on NETs CM24 CCAM1 CCAM1 CM24 CM24 MPO (green) DAPI (blue), CM24 (red) NETs are web-like structures involved in: CM24 (red) • Tumor immune evasion •
Slide 23: Large market opportunity based on CEACAM1 expression in PDAC
Large market opportunity based on CEACAM1 expression in PDAC Key PDAC Statistics Limited Treatment Options CM24 Opportunity Advanced PDAC • CEACAM1 expression correlates • ~60K new cases/year in the with poor prognosis in US1; 140K new cases in EU in PS 0-1 Bilirubin PS 2 PS 2 & KPS <70 pancreatic c
Slide 24: Completed Randomized Phase 2 Combination Study
Completed Randomized Phase 2 Combination Study (NCT04731467) A randomized Bayesian study of CM24 in combination with nivolumab plus SoC chemotherapy in 2nd line PDAC patients* PDAC patients Experimental arm Primary endpoint : OS Exploratory biomarkers: progressing on or after CM24 + nivolumab & Nal-
Slide 25: Phase 2 Efficacy Proof of Concept demonstrated
Phase 2 Efficacy Proof of Concept demonstrated: Consistent efficacy across all endpoints ➢ 19% reduction in risk of death (HR=0.81) and 25% ➢ Higher objective response rate (ORR) (25% vs 6.7%) reduction in the risk of progression or death (HR=0.75) ➢ Higher disease control rate (DCR) (62.5% vs 46.7%
Slide 26: Phase 2 Biomarkers analysis in serum or tumor
Phase 2 Biomarkers analysis in serum or tumor Significantly improved OS, PFS and ORR Serum/tumor CEACAM1 enriched patients serum CEACAM1 or MPO enriched patients CEACAM1+Tumor cell H score 115-275 or Serum CEACAM1 6K-15K pg/mL 6K < sCCAM1 < 15K pg/mL or 200 < MPO < 600 ng/mL HR = 0.39 HR = 0.28 HR =
Slide 27: 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 28: NT219: Novel IRS1/2 and STAT3 dual inhibitor for multiple indications
NT219: Novel IRS1/2 and STAT3 dual inhibitor for multiple indications • Covalently binds to Insulin Receptor Substrate IRS1/2 and leads to their degradation Innovative • Dual inhibitor of STAT3 & IRS1/2, both required to overcome drug resistance MOA • Affects both the tumor and the TME • Suppresses
Slide 29: Dose escalation in combination with cetuximab
Dose escalation in combination with cetuximab: Well tolerated, target exposure reached, responses observed Dose-proportional increase in AUC and Cmax values Target engagement demonstrated in patients’ biopsies SCCHN patient NT219+cetuximab Membranal IRS2 H-Score IRS2 in the biopsy tumor cells pre-tr
Slide 30: NT219: Activity in mono and combo dose escalation
NT219: Activity in mono and combo dose escalation Monotherapy efficacy: NT219+cetuximab • 20 evaluable patients (all doses): 2 PR (confirmed-GEJ, 100 Waterfall for tumor size change unconfirmed-PDAC), 5 SD 90 80 Efficacy overview of combination arm in SCCHN patients: 70 Best % change from baseline 6
Slide 31: Activated pIGF1R and STAT3 as potential predictive biomarkers
Activated pIGF1R and STAT3, NT219 targets, as potential predictive biomarkers Responders (PR) Non-responders (PD) 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
Slide 32: Phase 2: NT219 + pembro or cetuximab in patients with R/M HNSCC
Phase 2: NT219 + pembro or cetuximab in patients with R/M HNSCC Cohort 1 1st Line ICI Naive N219 100mg/kg Q1W+ pembro 200mg Q3W n=10 +19 Simon 2 stage Recurrent metastatic HNSCC ECOG PS 0-2 2nd Line RECIST measurable R disease n=58 Cohort 2 3rd Line N219 100mg/kg Q1W+ cetuximab 400mg/m2 -> 250mg/m2
Slide 33: Snapshot: Company Highlights
Snapshot: Company Highlights FINANCIALS 1 Lead Program Entering the Clinic IM1240, our first tri-specific antibody from the CAPTN-3 platform, is on track for Phase 1 Cash initiation in H2 2026 $10.5M As of September 30, 2025 2 CAPTN-3: Differentiated multi-specific platform with Efficacy & Safety ad
Slide 34: Leadership Team
Leadership Team Eric K. Rowinsky, MD Gil Efron Shai Lankry Chairman of the Board Chief Executive Officer Chief Financial Officer Former Deputy CEO & CFO at Former CFO at Gamida Cell Ltd. Former CMO at ImClone, Stemline, Kamada (NASDAQ:KMDA) (NASDAQ:GMDA) Board member at Biogen Inc. Michael Schickler
Slide 35: Thank You
THANK YOU Contact Us: ir@purple-biotech.com 35
Slide 36: Appendix A | CAPTN-3
Appendix A | CAPTN-3
Slide 37: 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 5T4 is a Tumor Associated Antigen types and relates to a poor prognosis prevalent in several large indications Am J Cancer Res 2018;8(4):610-623 www.ajcr.us /ISSN:2156-6976/ajcr0074519 Kemper et al. LS
Slide 38: CD3 Cap inhibits T cell binding and cleavage restores activity
CD3 Cap inhibits T cell binding and cleavage restores activity: CAP advantages: improved safety, PK, and therapeutic window ELISA CD3 binding assay PBMCs mediated cytotoxicity assay Binding of CAPTN-3 to CD3 is dependent on protease cleavage Cytotoxic effect is restored following protease cleavage C
Slide 39: 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 • Safet
Slide 40: Appendix B | CM24
ce foe i ~©=AppendixB | CM24
Slide 41: CEACAM1 Plays a Key Role in Cancer Biology
CEACAM1 Plays a Key Role in Cancer Biology 01 | ADHESION 02 | IMMUNE CELLS/ 03 | IMMUNO-ONCOLOGY IMMUNE EXCLUSION Horst, 2011 Tsuzuki, 2020 Blumberg, 2015 “CEACAM1 creates a pro-angiogenic “Immune‐checkpoint molecules on “CEACAM1 regulates tumor microenvironment that regulatory T‐cells as a potentia
Slide 42: CM24 binding/efficacy can be predicted by MPO levels
CM24 binding/efficacy can be predicted by MPO levels CM24 Inhibits NET-Induced migration of CM24-Nivo treatment significantly reduced CM24 binds to CEACAM1 on NETs CEACAM1 expressing cancer cells the enhanced NET levels in patient’s serum Level of MPO in patient serum (% of Pre-treatment) MPO (green
Slide 43: CM24 Reduces Tumor Burden & Synergetic with α-PD-1
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 days post
Slide 44: Phase 1 Dose Escalation Interim Results
Phase 1 Dose Escalation Interim Results CM24 is Safe and Well Tolerated in Combination with Nivolumab Study Design Safety • As of March 8th, 2022, a total of 13 patients were enrolled and 11 • No DLTs were observed across all dose levels; no Grade 4 patients were evaluable for DLT determination (8 P
Slide 45: CM24 Phase 1 Combination Study (NCT04731467)
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. Demographics of patients treated with CM24 (10, 15, 20mg/kg) • The primary objective of this part was t
Slide 46: Confirmed Partial Response in a 3L PDAC Patient
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 Partial Respo
Slide 47: CM24 Phase 1 Dose Escalation Results
CM24 Phase 1 Dose Escalation Results Encouraging data in 2L/3L Pancreatic Ductal Adenocarcinoma (PDAC) patients Study Results 14 patients were evaluable for efficacy: SD PR • Best overall response included 1 Partial SD Response (PR) (PDAC) and 4 Stable Disease (SD) (3 PDAC and 1 papillary thyroid ca
Slide 48: Planned 2nd & 3rd line PDAC Phase 2b study design
Planned 2nd & 3rd line PDAC Phase 2b study design To demonstrate enhanced efficacy in enriched population and contribution of parts Simon 2-Stage Stage 1 (n=20/arm) Stage 2 (n=35/arm) Advanced metastatic Arm A Arm A PDAC pts progressing SoC chemotherapy 1 SoC chemotherapy 1 on or after SoC chemother
Slide 49: Appendix C | NT219
Appendix C | NT219
Slide 50: NT219 targets critical signalling pathways simultaneously
NT219 targets 2 critical signalling pathways simultaneously leading IRS1/2 to degradation and blocking STAT3 IRS1/2 STAT3 • Promotes a tumor-protective • Well-established transcription factor microenvironment associated with the tumorigenic phenotype • Overexpressed in multiple tumor types • Hyperac
Slide 51: Novel MOA: IRS Degradation By NT219
Novel MOA: IRS Degradation By NT219 Blocking IGF1R-AKT Pathway1 1 Binding to IRS 2 Ser-phosphorylation 3 Degradation IGF1 IGF1R IGF1 IGF1 IGF1 IGF1R IGF1R IGF1R IRS NT pS PI3K IRS IRS pS AKT AKT AKT AKT CANCER CELL SURVIVAL CANCER CELL APOPTOSIS Covalent binding to IRS1/2 leads to the Serine phospho
Slide 52: Novel MOA: STAT3 Inhibition
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 and plays
Slide 53: Simultaneous Blockade of STAT3 and AKT
Simultaneous Blockade of STAT3 and AKT Pathways are Required to Overcome Resistance to EGFRi Overcoming drug resistance Proof of Concept: PDX model of Head and Neck Cancer Erlotinib Control (n=6) Erlotinib (n=8) EGFRi Erlotinib+NT219 (n=6) EGFR Erlotinib+Ruxolitinib (n=6) EGFR Erlotinib+Buparlisib (
Slide 54: NT219 re-sensitizes PD1-refractory models and restores sensitivity to EGFRi
NT219 re-sensitizes PD1-refractory models and restores sensitivity to EGFRi NT219+Pembrolizumab reverse PD1-resistant GEJ tumors in a PDX SCCHN PDX model model Tumor Volume (mm3) Head & Neck Cancer Recurrent/metastatic squamous cell carcinoma of the head and neck (R/M SCCHN) metastasis, patient pr
Slide 55: NT219 combination with αPD1 achieves significant reprograming of the TME
NT219 combination with αPD1 achieves significant reprograming of the TME NT219+PD1 leads to a significant increase in NT219+PD1 leads to a significant reduction in cytotoxic effector cells (T & NK cells) myeloid derived suppressor cells (MDSC) cells (% CD8+GZMB +) Activated cytotoxic T (out of CD4
Slide 56: NT219+PD1 Converted Immuno-suppressive to Immuno-reactive TME
PD1+ NT219+PD1 NT219 Converted PD1+ Immuno- NT219 suppressive to Immuno- PD1+ reactive TME NT219 PD1+ NT219 PD1+ Zou et al. Molecular Cancer (2020) 19:145; PD1+ Rampias et al. Oncogene (2016) 35:2562; NT219 Flashner, Reuveni, Levitzki et al. Oncogene NT219 (2016) 35:2675; Sanchez-Lopez et al.
Slide 57: Selected Publications
Selected Publications Michael Alexander Karin Levitzki Menashe Michael Bar-Eli Cox 57
Slide 58: NT219 inhibits the IRS to β-Catenin pathway and synergizes with 5FU
NT219 inhibits the IRS to β-Catenin pathway and synergizes with 5FU to suppress CRC tumor growth in mouse brain In Vitro In Vivo A. Silencing IRS2 inhibits C. DAPI IRS2 β-catenin Merge D. B. NT219 downregulates IRS2 and suppresses the -catenin activity LS513sh-IRS2 LS513sh-NS -catenin activity 1 1
Slide 59: Market Opportunity
Market Opportunity Recurrent or Metastatic Squamous Cell Carcinoma of Head and Neck (R/M SCCHN) Targeting the unmet medical need • SCCHN is the 6th most • 1L standard of care has shifted from chemotherapy towards immuno- common cancer type oncology + chemotherapy • 175k new cases/year are • EGFR and
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