Purple Biotech Ltd. · TASE:PPBT

Purple Biotech — Investor Presentation (June 2026)

45 slides from Purple Biotech's investor presentation, Jun 23, 2026

  1. Slide 1: Corporate Presentation June 2026

    CORPORATE PRESENTATION June 2026 Advancing the Next Generation of Immuno - oncology NASDAQ/TASE : PPBT

  2. 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

  3. Slide 3: Snapshot: Company Highlights

    | 3 2 Lead program expected to enter the clinic in 2027 IM1240 (cappedCD3x 5T4 xNKG2A), a first - in - class CAPTN - 3 tri - specific antibody Second program, IM1305 (cappedCD3x TROP2 xNKG2A) 1 CAPTN - 3: differentiated tri - specific platform activating both innate and adaptive immune systems The o

  4. Slide 4: The Problem: T Cell Therapy Challenges in Solid Tumors

    | 4 Multi - specific T cell engagers show promise in blood cancers but face major hurdles in solid tumors Imprecise Targeting Many T cell engagers are 'always on' — activating systemically instead of selectively at tumor sites Severe Toxicity Cytokine release syndrome (CRS) limits dosing and tolerab

  5. Slide 5: CAPTN-3: A Tri-specific Platform Designed for Safer, Broader Tumor Killing

    5 Solid tumors meet tri - specific antibodies: CAPTN - ϯ activates immune cells selectively at tumors combining safety with potent anti - tumor activity STEP 1: SAFE - INACTIVE IN BLOOD → STEP 2 : ACTIVATED AT TUMOR Tumor enzymes remove cap, activating drug precisely where needed → STEP 3: DUAL IMMU

  6. Slide 6: CAPTN-3: Built to Stand Out – Enhanced Efficacy with Improved Safety

    | 6 CAPTN - 3 : Built to Stand Out – Enhanced Efficacy with Improved Safety * B ased on publicly available information • Masked TCE • Preclinical • $ 2.1 b deal size 2026 • nondisclosed masked TCE • Preclinical • $ 850 M deal size • PSMA masked TCE • Phase 1 • $1.7b deal size

  7. Slide 7: Plug & Play Tri-specific Scaffold: Differentiated by Capped TCE with NK Cell Activating Arm

    | 7 anti - TAA Plug & Play Tri - specific Scaffold: Differentiated by Capped TCE with an NK Cell Activating Arm 7 » Integrates multiple TAAs or NK - activating arms » Robust pipeline of novel candidates » Multiple development and partnership opportunities NKG 2 A NKG 2 D Other NK cell engagers NK en

  8. Slide 8: Plug & Play Platform Capabilities In-Vivo Validation

    | 8 Plug & Play Platform Capabilities In - Vivo Validation 8 CD 3 x 5 T 4 x NKG 2 D Pipeline and Platform Candidates Demonstrations Sustained tumor regression across multiple tri - specifics targeting TAAs and NK receptors CD 3 x 5 T 4 xNKG 2 A CD 3 x TROP 2 xNKG 2 A

  9. Slide 9: Activating Both Innate and Adaptive Immune Responses

    | 9 Activating Both Innate and Adaptive Immune Responses Multi MOA: Activation of T cells through CD3 engagement, NKG2A inhibition and NK cell activation. Dual role for NKG2A inhibition in unleashing both T - cell and NK - cell activity Stimulates both helper (CD 4 +) and killer (CD 8 +) effector T

  10. Slide 10: A CAPTN-3 Pipeline Dedicated to Advancing Oncology Therapies

    10 PROGRAM INDICATION PRECLINCAL PHASE 1 PHASE 2 COLLABORATOR KEY 2026 - 27 MILESTONES IM 1240 Capped - CD3x 5T4 xNKG2A Solid Tumors TOX, IND, Ph 1 Initiation IM 1305 Capped - CD 3 x TROP 2 xNKG 2 A Solid Tumors Major Inflection Point Expected After Proof - of - Concept Study within Two Years : Comp

  11. Slide 11: IM1240 Non-Human Primate Data: Masking extends half-life, reduces cytokine release

    11 IM 1240 Non - Human Primate Data: Masking extends half - life, increases exposure and reduces cytokine release at ~ 300 - fold higher dose vs non capped Non - GLP dose range finding (DRF) study in NHP • Safety : Improved safety at doses up to 300 - fold higher than a non - capped comparator (IM 1

  12. Slide 12: IM1240 NHP Toxicology Data: Dose-proportional pharmacokinetics and broad therapeutic window

    12 IM1240 Non - Human Primate Toxicology Data: Dose - proportional pharmacokinetics and a broad therapeutic window • IM 1240 demonstrated linear, dose - proportional pharmacokinetics in NHPs, with systemic exposure and Cmax scaling predictably with dose • Exposure levels associated with tumor regres

  13. Slide 13: IM1240 Patient-derived explants: synergistic effect of CD3 and NKG2A arms

    13 5 38 49 94 0 20 40 60 80 100 Control IM1242 IM1340 IM1240 cResponse Score CD3x5T4 x NKG2A (cleavable cap) IM1240 5 T 4 xNKG 2 A (non - cleavable) capped CD 3 ) 5 T 4 xCD 3 (cleavable cap; mutated NKG 2 A ) Patient - derived explants (PDE) of 5 T 4 + NSCLC ** Synergistic effect of the CD 3 and NKG

  14. Slide 14: IM1240 Induces Mature TLS Formation and Drives Immune Activation

    14 IM1240 Induces Mature TLS Formation and Drives Immune Activation NKG2A blockade is required for the effect IM 1240 IM 1340 (non active NKG 2 A) Spatial plot IM1240 IM 1340 Interaction Analysis • Tissue reorganization - IM 1240 treatment, compared with NKG 2 A loss - of - function variant IM 1340

  15. Slide 15: IM1240 Induces Apoptosis in Patient-Derived Biopsies from PD-1 Resistant Tumors

    15 IM 1240 Induces Apoptosis in Patient - Derived Biopsies from PD - 1 Resistant Tumors Both the CD 3 and NKG 2 A arms are required for full activity • Activity in resistant tumors: IM 1240 induced apoptosis in patient - derived samples from PD 1 - resistlant metastatic HNSCC (n= 6 ) and bladder can

  16. Slide 16: Both CD3 and NKG2A Contribute to Anti-tumor Activity In Vivo

    16 Both CD 3 and NKG 2 A Contribute to Anti - tumor Activity In Vivo (EACR 2025 ) CD 3 arm — primary driver IM1240 vs. IM1242 (no CD3) · 1.5 mg/kg NKG 2 A arm — significant benefit IM 1240 vs. IM 1340 (no NKG 2 A) · 0.75 mg/kg CD 3 engagement drives tumor killing | NKG 2 A blockade adds meaningful b

  17. Slide 17: NKG2A Blockade Amplifies Activity

    | 17 A. NKG 2 A+ 2 T cell activation & contribution of NKG 2 A arm B. T cell - mediated anti - cancer activity & contribution of NKG2A arm • CD 3 arm engagement is essential as capped CD 3 (IM 1240 ) and CD 3 - mutated (IM 1353 ) variants show no cytotoxic activity in vitro • The bispecific CD 3 x 5

  18. Slide 18: NKG2A is Relevant in the Targeted Patient Population

    18 NKG 2 A is Relevant in the Targeted Patient Population Transcriptomic analysis of ~ 11,000 primary human tumors (TCGA) (ESMO - IO 2025 ) » The Axis is Active - NKG 2 A and its inhibitory partner HLA - E are co - expressed across human tumors » NKG 2 A expression strongly correlated to 5 T 4 – NKG

  19. Slide 19: 5T4: Sought-after Oncology Target Expressed on Solid Tumors

    19 5 T 4 : Sought - after Oncology Target 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/ajcr0074519 5 T 4 is a Tumor Associated Antigen prevalent in several large indication

  20. Slide 20: 5T4: A Novel TAA with Renewed Therapeutic Potential

    20 5 T 4 : A Novel TAA with Renewed Therapeutic Potential IM1240 fi rst in class tri - specific T and NK cell engager targeting 5T4 – advantages: • Masked TCE - > Tumor - selective activation, improved PK profile, reduces on - target/off - tumor toxicity and systemic T cell activation • NKG2A - > ov

  21. Slide 21: TROP2 is Broadly Expressed Across Solid Tumors

    21 TROP2 is B roadly E xpressed A cross S olid T umors Supports its appeal as an oncology target Kuo, Peiwen, et al. PloS one 20.4 (2025): e0321555 CESC, cervical squamous cell carcinoma and endocervical adenocarcinoma; BLCA, bladder urothelial carcinoma; PRAD, prostate ad eno carcinoma; LUAD and LU

  22. Slide 22: IM1305: Dose-Dependent, Sustainable Efficacy

    22 IM 1305 : Dose - Dependent, Sustainable Efficacy Capped CD 3 xTROP 2 xNKG 2 A In vivo Proof of Concept In - vivo Tumor Regression by IM1305 & IM1302* • Sustained tumor regression by IM 1305 . No tumor recurrence observed. • Similar results were obtained with equimolar doses of the non - capped va

  23. Slide 23: Next Steps: IM1240 and Other CAPTN-3 Antibodies and Beyond

    23 Next Steps: IM1240 and Other CAPTN - 3 Antibodies and Beyond GLP tox 2026 IND submission 2027 FIH clinical trials initiation H 1 2027 End of P1 DE H1 2028 P 1 Expansion cohorts H 2 2028 Planned IM 1240 Phase 1 / 2 Study • Basket trial P 1 Dose escalation ( n~ 36 ) in expected 5 T 4 expressing sol

  24. Slide 24: T cell Engagers are Advancing: Solid Tumors Remain the Largest Unmet Need

    | 24 T cell Engagers are Advancing: Solid Tumors Remain the Largest Unmet Need Purple Biotech: CAPTN - 3 entering the clinic in 2027 $ 1 B+ Comparable masked TCE deals closed at preclinical stage 300x Higher dosing with minimal cytokine release Only tri - specific T and NK cell engager with conditio

  25. Slide 25: Snapshot: Company Highlights

    | 25 2 Lead program expected to enter the clinic in 2027 IM1240 (cappedCD3x 5T4 xNKG2A), a first - in - class CAPTN - 3 tri - specific antibody Second program, IM1305 (cappedCD3x TROP2 xNKG2A) 1 CAPTN - 3 : differentiated tri - specific platform activating both innate and adaptive immune systems The

  26. Slide 26: Leadership Team

    | 26 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.

  27. Slide 27: Contact Us / Thank You

    27 Contact Us: ir@purple - biotech.com THANK YOU

  28. Slide 28: Appendix: CAPTN-3

    Appendix: CAPTN - 3

  29. Slide 29: CD3 Cap inhibits T cell binding and cleavage restores activity

    29 • 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

  30. Slide 30: CAPTN-3 Induces Reinvigoration of Exhausted T cells

    30 CAPTN - 3 Induces Reinvigoration of Exhausted T cells Added value of the NKG2A arm IM 1222 induced reinvigoration of exhausted T cells; similar effect to fresh T cells Production of exhausted T cells by repeated stimulation Added value of the NKG 2 A arm IM1222 concentration ( nM ) CD 3 x 5 T 4 C

  31. Slide 31: Cytokine release is T-dependent and suppressed by the cap for improved safety

    31 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 -

  32. Slide 32: 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

  33. Slide 33: CM24: Targeting CEACAM1 expressing tumors

    33 CM 24 : Targeting CEACAM 1 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

  34. Slide 34: CM24: Immune modulation of CEACAM1 expressing TMEs

    34 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.

  35. Slide 35: CM24 blocks NET-related activities by CEACAM1 inhibition

    35 CCAM1 CM 24 CM 24 CCAM 1 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

  36. Slide 36: Large market opportunity based on CEACAM expression in PDAC

    36 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

  37. Slide 37: Randomized Phase 2 study of CM24 with nivolumab plus chemotherapy in 2nd line PDAC

    37 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 (NCT 04731467 ) – Experiment

  38. Slide 38: Phase 2 Efficacy Proof of Concept demonstrated

    38 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

  39. Slide 39: Phase 2 Biomarkers analysis in serum or tumor

    39 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

  40. Slide 40: 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)

  41. Slide 41: NT219: Novel IRS1/2 and STAT3 dual inhibitor for multiple indications

    41 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

  42. Slide 42: Dose escalation in combination with cetuximab: Well tolerated, responses observed

    42 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

  43. Slide 43: NT219: Activity in mono and combo dose escalation

    43 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

  44. Slide 44: Activated pIGF1R and STAT3, NT219 targets, as potential predictive biomarkers

    44 Activated pIGF 1 R and STAT 3 , NT 219 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) comp

  45. Slide 45: Phase 2: NT219 + pembro or cetuximab in patients with R/M HNSCC

    45 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

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