Purple Biotech Ltd. · TASE:PPBT
Purple Biotech — Investor Presentation (July 2025)
55 slides from Purple Biotech's investor presentation, July 2025
Slide 1: Corporate Presentation
CORPORATE PRESENTATION NASDAQ/TASE: PPBT July 2025
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: Purple Biotech develops first-in-class drug candidates to treat cancers
Purple Biotech develops promising first-in-class drug candidates to treat cancers with high unmet medical need Two Phase 2 clinical stage first-in-class drugs with demonstrated activity • CM24, CEACAM1 antibody: Unlocking personalized immunotherapy through biomarker-guided patient targeting • NT219
Slide 4: A pipeline dedicated to advancing oncology therapies
A pipeline dedicated to advancing oncology therapies Project Target Indications Pre-Clinical Phase I Phase II Phase III Value Drivers Collaborator CEACAM1 Pancreatic Cancer Initiation of Phase CM24 mAb (+nivolumab+SoC) 2b 2H25 Capped- CD3x5T4xNKG2A FIH 2026 IM1240 CAPTN-3 Solid Tumors Tri-specific A
Slide 5: Multiple Pillars of Growth
Multiple Pillars of Growth CM24 CAPTN-3 NT219 CEACAM1 Conditionally activated TCE + IRS1/2 degrader and Antibody NK cell engager + TAA STAT3 blocker Tri-specific Platform • Targeting cancer patients • Modular plug & play platform • Potential in EGFRi, MAPKi based on clinically identified enabling r
Slide 6: 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 7: 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 8: 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 9: 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 10: 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 • CEACAM1 expression correlates • ~60K new cases/year in the with poor prognosis in US1; 140K new cases in EU in pancreatic cancer5 2023 • Clinical and preclinical data • 5-yea
Slide 11: 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 12: 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 13: Post-hoc Phase 2 Biomarkers Analysis
Post-hoc Phase 2 Biomarkers Analysis Patients with either Patients with either Patients with both Serum CEACAM1 or serum CEACAM1 or tumor CEACAM1 and tumor CEACAM1+ MPO (NET marker) PD-L1 CPS • Represents a subgroup • Represents a subgroup • Support the rationale of of 52% of patients of 80% of pati
Slide 14: Post-hoc analysis in serum or tumor CEACAM1 enriched patients
Post-hoc analysis in serum or tumor CEACAM1 enriched patients Significantly improved OS, PFS Statistically significant results in patients CEACAM1+Tumor cell H score 115-275 or Serum CEACAM1 6K-15K pg/mL with pre-treatment serum CEACAM1 levels (6K-15K pg/mL) or tumor CEACAM1 HR = 0.22 HR = 0.05 Prog
Slide 15: Results in serum CEACAM1 or MPO enriched patients
Results in serum CEACAM1 or MPO enriched patients Significantly improved OS, PFS Statistically significant results in patients with baseline serum CEACAM1 or serum Overall Survival Progression Free Survival 6K < sCCAM1 < 15K pg/mL or 200 < MPO < 600 ng/mL 6K < sCCAM1 < 15K pg/mL or 200 < MPO < 600 n
Slide 16: Combination of CEACAM1 and PDL1 as predictive biomarkers
Combination of CEACAM1 and PDL1 as predictive biomarkers Opportunity to treat patients currently not eligible for PD1 inhibitors Statistically significant results for patients with High CEACAM1 (H-score>100) and Low Overall Survival Progression Free Survival PDL1 (CPS ≤ 1 ) expression in tumors: ➢ 9
Slide 17: 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 18: CAPTN-3: Conditionally-Activated Tri-Specific Antibody Platform
CAPTN-3: Conditionally- Activated Tri-Specific Antibody Platform
Slide 19: CAPTN-3: Tri-specific antibody activates innate and adaptive immune responses
CAPTN-3: Tri-specific antibody activates innate and adaptive immune responses while increasing the therapeutic index • Multi-specific biologics are revolutionizing immuno-oncology, initial success in hematologic cancers • Solid tumors present the next frontier, with novel formats enabling precise, p
Slide 20: Plug & Play Tri-specific scaffold
CAPTN-3 Platform Plug & Play Tri-specific scaffold • Modular format for targeting various TAAs or NK engager arms • Data presented for several tri-specifics, targeting different receptors and TAA: Cap- HSA o CD3x5T4xNKG2A o CD3xEGFRxNKG2A o CD3x5T4XNKG2D CD3 TAA NK engager • Tri-specific antibodies
Slide 21: 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 21
Slide 22: Significant contribution of the NK and CD3 arms anti-tumor activity in vivo
Significant contribution of the NK and CD3 arms anti-tumor activity in vivo (EACR 2025) A: Contribution of the NK arm B: Contribution of the CD3 arm Cap-CD3x5T4XNKG2A (IM1240), 0.75 mg/kg Cap-CD3x5T4XNKG2A (IM1240), 1.5mg/kg Cap-CD3x5T4XmutatedNKG2A (IM1340), 0.75 mg/kg non-cleavable capCD3x5T4xNKG2
Slide 23: CD3 Cap inhibits T cell binding and cleavage restores activity
CD3 Cap inhibits T cell binding and cleavage restores activity 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 CAPTN-3(no (noproteases) proteases) 100 ProTribody CAPTN-3 (no
Slide 24: 5T4: a Novel Target in Oncology
5T4: a Novel Target in Oncology 5T4 is highly expressed on certain tumors 5T4 is a Tumor Associated Antigen and correlates with 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. LSA 2022;5:e202201481 Opportun
Slide 25: IM1240: In vivo efficacy and synergistic effect of the CD3 and NKG2A arms
IM1240: In vivo efficacy and synergistic effect of the CD3 and NKG2A arms In vivo anti-tumor efficacy of IM1240 & IM1222* Synergistic effect of the aCD3 and aNKG2A arms** Effective cleavage (p<0.0001 ) 100 94 cResponse Score 80 60 40 49 38 20 Treatment 5 0 Days following treatment initiation Contr
Slide 26: Cytokine release is 5T4-dependent and suppressed by the cap
Cytokine release is 5T4-dependent and suppressed by the cap for improved safety • 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-capped variant showed a decreased IFN releas
Slide 27: Next steps CAPTN3 program - IM1240 and other Abs
Next steps CAPTN3 program - IM1240 and other Abs Non GLP tox IND submission • Q4 25 • H1 26 GLP tox FIH – IM1240 • H1 26 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, SCCHN
Slide 28: 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 29: 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 degradation and Innovative blocks STAT3 MOA • Affects both the tumor and the TME • Suppresses cancer stem cells Robust preclinical • Outstanding efficacy in vari
Slide 30: Dose escalation in combination with cetuximab: well tolerated
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 31: 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 32: Activated IGF1R and STAT3 as potential predictive biomarkers
Activated IGF1R and STAT3 as potential predictive biomarkers Biomarker analysis at the 50&100mg/kg doses of NT219 350 with cetuximab: 300 pSTAT3 • Significant differences in the 250 H Score (IHC) pIGF1R MC activated pIGF1R and pSTAT3 200 150 were revealed in the 100 responders (PR) compared to 50 th
Slide 33: NT219 + pembro or cetuximab in patients with R/M HNSCC
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 n=10 +19
Slide 34: Purple Biotech develops promising first-in-class drug candidates
Purple Biotech develops promising first-in-class drug candidates to treat cancers with high unmet medical need Two Phase 2 clinical-stage first-in-class drugs with demonstrated activity • CM24, CEACAM1 antibody: Unlocking personalized immunotherapy through biomarker-guided patient targeting • NT219
Slide 35: 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 36: Thank You
THANK YOU Contact Us: ir@purple-biotech.com 36
Slide 37: Appendix A | CM24
ce foe ~©Appendix A | CM24
Slide 38: 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 39: 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 40: 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 41: 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 42: 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 43: 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 44: 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 45: Appendix B | NT219
Appendix B | NT219
Slide 46: 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 47: 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 48: 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 49: 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 50: 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 51: NT219 combination with αPD1 achieves profound reprograming of the TME
NT219 combination with αPD1 achieves a profound 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 CD45
Slide 52: 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+ • Presented at the AACR 2023 PD1+ ** Sanchez-Lopez et al. Oncogene (2016) NT219* 35:2634; Rampias et al. Oncogene (2016) NT219* 35:2562; Flashner, Reuveni, Levitzki et al. On
Slide 53: Selected Publications
Selected Publications Michael Alexander Karin Levitzki Menashe Michael Bar-Eli Cox 53
Slide 54: 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 55: 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