Purple Biotech Ltd. · TASE:PPBT
Purple Biotech — Investor Presentation (July 2025)
55 slides from Purple Biotech's investor presentation, Jul 10, 2025
Slide 1: Corporate Presentation July 2025
NASDAQ/TASE: PPBT July 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 Two Phase 2 clinical stage first - in - class drugs with demonstrated activity CM24, CEACAM1 antibody: Unlocking personalized immunotherapy through biomarker - guided patient targetin
Slide 4: A pipeline dedicated to advancing oncology therapies
4 Collaborator Value Drivers Phase III Phase II Phase I Pre - Clinical Indications Target Project Initiation of Phase 2b 2H25 Pancreatic Cancer (+ nivolumab+SoC ) CEACAM1 mAb CM24 FIH 2026 Solid Tumors Capped - CD3x5T4xNKG2A CAPTN - 3 Tri - specific Ab IM1240 Interim data 2026 Head and Neck Cancer (
Slide 5: Multiple Pillars of Growth
5 Multiple Pillars of Growth Targeting cancer patients based on clinically identified biomarkers Completed Phase 2 in PDAC Opportunity to leverage the MoA in multiple indications (Lung, GI, Pancreatic etc.) Potential in EGFRi , MAPKi and ICI resistant cancers Completed P1 in SCCHN Significant market
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
7 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 NK cel
Slide 8: CM24: Immune modulation of CEACAM1 expressing TMEs
8 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 9: CM24 blocks NET-related activities by CEACAM1 inhibition
9 CCAM1 CM24 CM24 CCAM1 CM24 CM24 b locks 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 Progres sion of Colon Carcinoma.
Slide 10: Large market opportunity based on CEACAM1 expression in PDAC
10 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 pancrea
Slide 11: Randomized Bayesian study of CM24 with nivolumab plus SoC in 2L PDAC
11 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 12: Phase 2 Efficacy Proof of Concept demonstrated
12 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 13: Post-hoc Phase 2 Biomarkers Analysis
13 Post - hoc Phase 2 Biomarkers Analysis Patients with either Serum CEACAM1 or tumor CEACAM1 + 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 CEACAM1 or MPO (NET marker) R epresents a subgr
Slide 14: Post-hoc analysis in serum or tumor CEACAM1 enriched patients
14 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
Slide 15: Results in serum CEACAM1 or MPO enriched patients
15 Results in serum CEACAM1 or MPO enriched patients Significantly improved OS, PFS 6K < sCCAM1 < 15K pg /mL or 200 < MPO < 600 ng/mL PFS (%) EXP CONT Progression Free Survival 6K < sCCAM1 < 15K pg /mL or 200 < MPO < 600 ng/mL Overall Survival (%) EXP CONT Overall Survival Statistically significant
Slide 16: Combination of CEACAM1 and PDL1 as predictive biomarkers
16 Combination of CEACAM 1 and PDL 1 as predictive biomarkers Opportunity to treat patients currently not eligible for PD 1 inhibitors PFS (%) EXP CONT Overall Survival (%) EXP CONT Progression Free Survival Overall Survival Statistically significant results for patients with High CEACAM 1 (H - scor
Slide 17: Planned 2nd & 3rd line PDAC Phase 2b study design
17 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 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
19 CAPTN - 3: Tri - specific antibody activates innate and adaptive immune responses while increasing the therapeutic index Engagement Masked TCE activated in TME TCE + NK cell engager Cancer binder a - TAA Abs a - NK binder Abs T - cell - binder a - CD 3 Abs aCD3 masking moiety Tumor cell NK cell C
Slide 20: CAPTN-3 Platform – Plug & Play Tri-specific scaffold
20 CAPTN - 3 Platform – Plug & Play Tri - specific scaffold 20 ▪ NKG 2 A ▪ NKG 2 D ▪ Other NK cell engagers Tumor - associated antigen (TAA) Ab NK engager Cap - HSA CD 3 TAA ▪ α 5 T 4 ▪ α EGFR ▪ α TAA 1 ▪ α TAA 2 Multiple opportunities for development and partnering Modular format for targeting vari
Slide 21: Unleashing both innate and adaptive immune response
21 Unleashing both innate and adaptive immune response Dual activation of cytotoxic T - cells by CD3 engagement & NKG2A inhibition
Slide 22: Significant contribution of the NK and CD3 arms to anti-tumor activity in vivo
22 Significant contribution of the NK and CD 3 arms anti - tumor activity in vivo (EACR 2025 ) B : Contribution of the CD 3 arm A : Contribution of the NK arm Cap - CD 3 x 5 T 4 XmutatedNKG 2 A (IM 1340 ), 0.75 mg/kg non - cleavable capCD 3 x 5 T 4 xNKG 2 A (IM 1242 ), 1.5 mg/kg *xenograft model ino
Slide 23: Binding to CD3 and cytotoxic effect retained following protease cleavage
23 Binding to CD 3 and cytotoxic effect is retained following protease cleavage Multiple TME - specific proteases - increase likelihood for cleavage by broad - tumor types CD3 Cap inhibits T cell binding and cleavage restores activity PBMCs mediated cytotoxicity assay Cytotoxic effect is restored fo
Slide 24: 5T4: a Novel Target in Oncology
24 5 T 4 : a Novel Target in Oncology 5 T 4 is highly expressed on certain tumors and correlates with poor prognosis Am J Cancer Res 2018 ; 8 ( 4 ): 610 - 623 www.ajcr.us /ISSN: 2156 - 6976 /ajcr 0074519 5 T 4 is a Tumor Associated Antigen prevalent in several large indications Opportunity of patien
Slide 25: Synergistic effect of the aCD3 and aNKG2A arms
| 25 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) 5 T 4 xCD 3 (cleavable cap; mutated NKG 2 A) Synergistic effect of the aCD 3 and aNKG 2 A arms** *TNBC MDA - MB - 231 cells were s.c. inoculat
Slide 26: Cytokine release is T-dependent and suppressed by the cap
26 Cytokine release is 5 T 4 - 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 5 T 4 - expressing cancer cells the non - capped variant showed a decreas
Slide 27: Next steps CAPTN-3 program - IM1240 and other Abs
27 Next steps CAPTN 3 program - IM 1240 and other Abs Non GLP tox Q 4 25 GLP tox H 1 26 IND submission H 1 26 FIH – IM1240 clinical trial H2 26 Planned IM 1240 Phase 1 Study Basket trial in certain advanced/metastatic solid tumors likely to express 5 T 4 potentially including: TNBC, esophageal, SCCH
Slide 28: 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 29: NT219: Novel IRS1/2 and STAT3 dual inhibitor for multiple indications
29 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 degradation and blocks STAT 3 Affects both the tumor and the TME Suppresses cancer stem cells Innovative MOA Outstanding efficacy in various PDX models
Slide 30: Dose escalation in combination with cetuximab: well tolerated, responses observed
30 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 IRS 2 in t
Slide 31: NT219: Activity in mono and combo dose escalation
31 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 32: Activated IGF1R and STAT3 as potential predictive biomarkers
32 Activated IGF 1 R and STAT 3 as potential predictive biomarkers Biomarker analysis at the 50 & 100 mg/kg doses of NT 219 with cetuximab: Significant differences in the activated pIGF 1 R and pSTAT 3 were revealed in the responders (PR) compared to the 2 non - responders (PD,SD) 0 50 100 150 200 2
Slide 33: NT219 + pembro or cetuximab in patients with R/M HNSCC
33 NT 219 + pembro or cetuximab in patients with R/M HNSCC – 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 mg/kg Q 1 W+ cetuximab 400 mg/m 2 - > 250 m
Slide 34: Purple Biotech develops promising first-in-class drug candidates to treat cancers
34 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 targe
Slide 35: Leadership Team
35 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 36: Contact Us / Thank You
36 Contact Us: ir@purple - biotech.com THANK YOU
Slide 37: Appendix A | CM24
Appendix A | CM 24
Slide 38: CEACAM Plays a Key Role in Cancer Biology
38 CEACAM 1 Plays a Key Role in Cancer Biology 01 | ADHESION Horst, 2011 “ CEACAM 1 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 col
Slide 39: CM24 binds to CEACAM1 on NETs
39 CM 24 binds to CEACAM 1 on NETs CM24 Inhibits NET - Induced migration of CEACAM1 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 ) CM 24
Slide 40: CM24 Reduces Tumor Burden & Synergetic with α-PD-1
40 CM 24 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 da
Slide 41: Phase 1 Dose Escalation Interim Results: CM24 Safe and Well Tolerated
41 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 42: CM24 Phase 1 Combination Study Demographics
42 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 determ
Slide 43: Confirmed Partial Response in a 3L PDAC Patient
43 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 Respon
Slide 44: CM24 Phase 1 Dose Escalation Results
44 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 (P
Slide 45: Appendix B | NT219
_ Appendix B | NT219
Slide 46: NT219 targets critical signalling pathways simultaneously
| 46 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 pathways
Slide 47: Novel MOA: IRS Degradation By NT219
47 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 48: Novel MOA: STAT3 Inhibition
48 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 and p
Slide 49: Simultaneous Blockade of STAT3 and AKT Pathways Overcomes Resistance to EGFRi
49 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 50: NT219 re-sensitizes PD-1 refractory models and restores sensitivity to EGFRi
50 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 cancer ce
Slide 51: NT219 combination with αPD-1 reprograms the TME
51 NT 219 combination with α PD 1 achieves a profound reprograming of the TME NT 219 and PD 1 combination converted immuno - suppressive TME to immuno - reactive * Collaboration with Prof. Bareli and Prof. Curran, M.D. Anderson cancer center, presented at AACR 2023 Activated cytotoxic T cells (% CD
Slide 52: NT219 + PD-1 Converted Immuno-suppressive to Immuno-reactive TME
52 NT 219 + PD 1 Converted Immuno - suppressive to Immuno - reactive TME Presented at the AACR 2023 ** Sanchez - Lopez et al. Oncogene ( 2016 ) 35:2634 ; Rampias et al. Oncogene ( 2016 ) 35:2562 ; Flashner, Reuveni, Levitzki et al. Oncogene ( 2016 ) 35:2675 ; PD 1 + NT 219 * PD 1 + NT 219 * PD 1 + N
Slide 53: Selected Publications
53 Selected Publications Michael Karin Alexander Levitzki Menashe Bar - Eli Michael Cox
Slide 54: NT219 inhibits the IRS to β-Catenin pathway in colon cancer
54 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 IR
Slide 55: Market Opportunity: Recurrent or Metastatic SCCHN
55 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/