Purple Biotech Ltd. · TASE:PPBT
Purple Biotech — Investor Presentation (August 2026)
45 slides from Purple Biotech's investor presentation, Aug 10, 2026
Slide 1: Corporate Presentation August 2026
CORPORATE PRESENTATION August 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 forward-lo
Slide 3: Snapshot: Company Highlights
| 3 2 Lead program expected to enter the clinic in 2027 IM1240 (cappedCD3x5T4xNKG2A), a first-in-class CAPTN-3 tri-specific antibody Second program, IM1305 (cappedCD3xTROP2xNKG2A) 1 CAPTN-3: differentiated tri-specific platform activating both innate and adaptive immune systems The only platform eng
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 tolerabili
Slide 5: CAPTN-3: A Tri-specific Platform Designed for Safer, Broader Tumor Killing
5 Solid tumors meet tri-specific antibodies: CAPTN-3 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 IMMUNE ATTACK
Slide 6: CAPTN-3: Built to Stand Out
| 6 CAPTN-3: Built to Stand Out Enhanced Efficacy with Improved Safety *Based on publicly available information •Masked TCE •Preclinical •$2.1b deal size 2026 • nondisclosed masked TCE •Preclinical •$850M deal size • PSMA masked TCE •Phase 1 •$1.7b deal size
Slide 7: Plug & Play Tri-specific Scaffold 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 NKG2A NKG2D Other NK cell engagers NK engager Cap-
Slide 8: Plug & Play Platform Capabilities In-Vivo Validation
| 8 Plug & Play Platform Capabilities In-Vivo Validation 8 CD3x5T4xNKG2D Pipeline and Platform Candidates Demonstrations Sustained tumor regression across multiple tri-specifics targeting TAAs and NK receptors CD3x5T4xNKG2A CD3xTROP2xNKG2A
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 (CD4+) and killer (CD8+) effector T cells vi
Slide 10: A CAPTN-3 Pipeline Dedicated to Advancing Oncology Therapies
10 PROGRAM INDICATION PRECLINCAL PHASE 1 PHASE 2 COLLABORATOR KEY 2026-27 MILESTONES IM1240 Capped-CD3x5T4xNKG2A Solid Tumors TOX, IND, Ph 1 Initiation IM1305 Capped-CD3xTROP2xNKG2A Solid Tumors Major Inflection Point Expected After Proof-of-Concept Study within Two Years : Comparables are +$1B A CA
Slide 11: IM1240 Non-Human Primate Data
11 IM1240 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 (IM1222) • Pharmacok
Slide 12: IM1240 Non-Human Primate Toxicology Data
12 IM1240 Non-Human Primate Toxicology Data: Dose-proportional pharmacokinetics and a broad therapeutic window • IM1240 demonstrated linear, dose-proportional pharmacokinetics in NHPs, with systemic exposure and Cmax scaling predictably with dose • Exposure levels associated with tumor regression an
Slide 13: IM1240 Synergy of CD3 and NKG2A Arms
13 5 38 49 94 0 20 40 60 80 100 Control IM1242 IM1340 IM1240 cResponse Score CD3x5T4xNKG2A (cleavable cap) IM1240 5T4xNKG2A (non-cleavable) capped CD3) 5T4xCD3 (cleavable cap; mutated NKG2A) Patient-derived explants (PDE) of PD1 resistant 5T4+NSCLC ** Synergistic effect of the CD3 and NKG2A arms *in
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 IM1240 IM1340 (non active NKG2A) Spatial plot IM1240 IM1340 Interaction Analysis • Tissue reorganization- IM1240 treatment, compared with NKG2A loss- of-function variant IM1340, induced pron
Slide 15: IM1240 Induces Apoptosis in Patient-Derived Biopsies from PD-1 Resistant Tumors
15 IM1240 Induces Apoptosis in Patient-Derived Biopsies from PD-1 Resistant Tumors Both the CD3 and NKG2A arms are required for full activity • Activity in resistant tumors: IM1240 induced apoptosis in patient-derived samples from PD1-resistlant metastatic HNSCC (n=6) and bladder cancer (n=1) • Both
Slide 16: Both CD3 and NKG2A Contribute to Anti-tumor Activity In Vivo
16 Both CD3 and NKG2A Contribute to Anti-tumor Activity In Vivo (EACR 2025) CD3 arm — primary driver IM1240 vs. IM1242 (no CD3) · 1.5 mg/kg NKG2A arm — significant benefit IM1240 vs. IM1340 (no NKG2A) · 0.75 mg/kg CD3 engagement drives tumor killing | NKG2A blockade adds meaningful benefit, consiste
Slide 17: NKG2A Blockade Amplifies Activity
| 17 A. NKG2A+ 2 T cell activation & contribution of NKG2A arm B. T cell-mediated anti-cancer activity & contribution of NKG2A arm • CD3 arm engagement is essential as capped CD3 (IM1240) and CD3-mutated (IM1353) variants show no cytotoxic activity in vitro • The bispecific CD3x5T4 (NGK2A-mutated, I
Slide 18: NKG2A is Relevant in the Targeted Patient Population
18 NKG2A is Relevant in the Targeted Patient Population Transcriptomic analysis of ~11,000 primary human tumors (TCGA) (ESMO-IO 2025) ➢ The Axis is Active - NKG2A and its inhibitory partner HLA-E are co-expressed across human tumors ➢ NKG2A expression strongly correlated to 5T4– NKG2A arm will be ac
Slide 19: 5T4: Sought-after Oncology Target Expressed on Solid Tumors
19 5T4: Sought-after Oncology Target Expressed on Solid Tumors 5T4 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 5T4 is a Tumor Associated Antigen prevalent in several large indications Kemper et a
Slide 20: 5T4: A Novel TAA with Renewed Therapeutic Potential
20 5T4: A Novel TAA with Renewed Therapeutic Potential IM1240 first 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 -> overcomes immune
Slide 21: TROP2 is Broadly Expressed Across Solid Tumors
21 TROP2 is Broadly Expressed Across Solid Tumors Supports its appeal as an oncology target CESC, cervical squamous cell carcinoma and endocervical adenocarcinoma; BLCA, bladder urothelial carcinoma; PRAD, prostate adenocarcinoma; LUAD and LUSC, NSCLC; ESCA, esophageal carcinoma; THCA, thyroid carci
Slide 22: IM1305: Dose-Dependent, Sustainable Efficacy
22 IM1305: Dose-Dependent, Sustainable Efficacy Capped CD3xTROP2xNKG2A In vivo Proof of Concept In-vivo Tumor Regression by IM1305 & IM1302* Vehicle IM1305-0.4mpk Q2D IM1305-0.8mpk Q2D IM1305-1.6mpk Q2D IM1302-1mpk Q2D 0.0 0.1 0.2 0.3 Tumor Weight (g) Mean ± SEM ✱✱✱✱ • Sustained tumor regression by
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 H1 2027 End of P1 DE H1 2028 P1 Expansion cohorts H2 2028 Planned IM1240 Phase 1/2 Study • Basket trial P1 Dose escalation (n~36) in expected 5T4 expressing solid tumors (TNB
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 $1B+ Comparable masked TCE deals closed at preclinical stage 300x Higher dosing with minimal cytokine release Only tri-specific T and NK cell engager with conditional ac
Slide 25: Snapshot: Company Highlights
| 25 2 Lead program expected to enter the clinic in 2027 IM1240 (cappedCD3x5T4xNKG2A), a first-in-class CAPTN-3 tri-specific antibody Second program, IM1305 (cappedCD3xTROP2xNKG2A) 1 CAPTN-3: differentiated tri-specific platform activating both innate and adaptive immune systems The only platform en
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. Ro
Slide 27: Contact Us / Thank You
27 Contact Us: ir@purple-biotech.com THANK YOU
Slide 28: Appendix: CAPTN-3
Appendix: CAPTN-3
Slide 29: Protease Cleavage of the CD3 Cap Restores Activity
29 • Binding to CD3 and cytotoxic effect is retained following protease cleavage of the CD3 cap • CAPTN-3 uses multiple TME-specific proteases – increasing likelihood for cleavage by broad- tumor types CD3 Cap inhibits T cell binding and cleavage restores activity: CAP advantages: improved safety, P
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 IM1222 induced reinvigoration of exhausted T cells; similar effect to fresh T cells Production of exhausted T cells by repeated stimulation Added value of the NKG2A arm IM1222 concentration (nM) CD3x5T4 CD3x5T4xNKG2A
Slide 31: Cytokine Release is 5T4-Dependent and Suppressed by the Cap
31 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 • Saf
Slide 32: 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 33: CM24: Targeting CEACAM1 Expressing Tumors
33 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
Slide 34: CM24: Immune Modulation of CEACAM1 Expressing TMEs
34 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 cr
Slide 35: CM24 Blocks NET-Related Activities by CEACAM1 Inhibition
35 CCAM1 CM24 CM24 CCAM1 CM24 CM24 blocks 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 Progression of Colon Carcinoma. J Im
Slide 36: Large Market Opportunity Based on CEACAM1 Expression in PDAC
36 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 pancreatic ca
Slide 37: Randomized Phase 2 Study of CM24 with Nivolumab plus Chemotherapy in PDAC
37 A randomized Bayesian study of CM24 in combination with nivolumab plus SoC chemotherapy in 2nd 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 ar
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 CA19-9 Median CA 19-9 levels % change in tumor size ➢19% reductio
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 CEACAM1 levels (6K-15K pg/mL) or tumor CEACAM1 expression (H-score 115-275) ➢ 78% reduction in risk of death (HR 0.22, p 0.006) and 95% reduc
Slide 40: 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 41: NT219: Novel IRS1/2 and STAT3 Dual Inhibitor for Multiple Indications
41 NT219: Novel IRS1/2 and STAT3 dual inhibitor for multiple indications • Covalently binds to Insulin Receptor Substrate IRS1/2 and leads to their degradation • Dual inhibitor of STAT3 & IRS1/2, both required to overcome drug resistance • Affects both the tumor and the TME • Suppresses cancer stem
Slide 42: Dose Escalation in Combination with Cetuximab
42 Dose escalation in combination with cetuximab: Well tolerated, target exposure reached, responses observed • NT219 was well tolerated as monotherapy and in combination with cetuximab; No DLTs reported • Human Equivalent Dose exposure was reached at 50 mg/kg • RP2D determined at 100 mg/kg IRS2 in
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 8 treated with
Slide 44: Activated pIGF1R and STAT3 as Potential Predictive Biomarkers
44 Activated pIGF1R and STAT3, NT219 targets, as potential predictive biomarkers 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 responders (PR) compared to the n
Slide 45: Phase 2: NT219 + Pembro or Cetuximab in R/M HNSCC
45 Phase 2: NT219 + 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 N219 100mg/kg Q1W+ pembro 200mg Q3W n=10 +19 Simon 2 stage N219 100mg/kg Q1W+ cetuxi