# EDGAR Filing Document

**Accession Number:** 0001614744
**File Stem:** 0001213900-25-112706
**Filing Date:** 2025-11
**Character Count:** 46776
**Document Hash:** 2556dbd4a1ffc450fd45a67a460218c5
**Contains OCR:** False
**Source Format:** 

## Filing Content

## Filing Summary
**0001213900-25-112706.hdr.sgml**: 20251119

**ACCESSION NUMBER**: 0001213900-25-112706

**CONFORMED SUBMISSION TYPE**: 6-K

**PUBLIC DOCUMENT COUNT**: 59

**CONFORMED PERIOD OF REPORT**: 20251119

**FILED AS OF DATE**: 20251119

**DATE AS OF CHANGE**: 20251119

**FILER**: 

**COMPANY DATA:**
- **COMPANY CONFORMED NAME:** PURPLE BIOTECH LTD.
- **CENTRAL INDEX KEY:** 0001614744
- **STANDARD INDUSTRIAL CLASSIFICATION:** PHARMACEUTICAL PREPARATIONS [2834]
- **ORGANIZATION NAME:** 03 Life Sciences
- **EIN:** 000000000
- **STATE OF INCORPORATION:** L3
- **FISCAL YEAR END:** 1231

**FILING VALUES:**
- **FORM TYPE:** 6-K
- **SEC ACT:** 1934 Act
- **SEC FILE NUMBER:** 001-37643
- **FILM NUMBER:** 251500092

**BUSINESS ADDRESS:**
- **STREET 1:** 4 OPPENHEIMER STREET
- **STREET 2:** SCIENCE PARK
- **CITY:** REHOVOT
- **STATE:** L3
- **ZIP:** 7670104
- **BUSINESS PHONE:** 97239333121

**MAIL ADDRESS:**
- **STREET 1:** 4 OPPENHEIMER STREET
- **STREET 2:** SCIENCE PARK
- **CITY:** REHOVOT
- **STATE:** L3
- **ZIP:** 7670104

**FORMER COMPANY:**
- **FORMER CONFORMED NAME:** Kitov Pharma Ltd.
- **DATE OF NAME CHANGE:** 20180125

**FORMER COMPANY:**
- **FORMER CONFORMED NAME:** Kitov Pharmaceuticals Holdings Ltd.
- **DATE OF NAME CHANGE:** 20140724

**UNITED STATES**

**SECURITIES AND EXCHANGE COMMISSION**

**Washington, D.C. 20549**

**FORM 6-K**

**Report of Foreign Private Issuer**

**Pursuant to Rule 13a-16 or 15d-16**

**of the Securities Exchange Act of 1934**

For the month of November 2025

Commission File Number: 001-37643

**PURPLE BIOTECH LTD.**

(Translation of registrant's name into English)

**4 Oppenheimer Street, Science Park, Rehovot 7670104, Israel**

(Address of principal executive offices)

Indicate by check mark whether the registrant files or will file annual reports under cover Form 20-F or Form 40-F.

Form 20-F ☒ Form 40-F ☐

**Purple Biotech**

On November 19, 2025, Purple Biotech Ltd. (the "**Company**" or the "**Registrant**") issued an updated Company presentation, "**Purple Biotech Corporate Presentation November 2025**", which is attached hereto as Exhibit 99.1.

---

| | |
|:---|:---|
| **Exhibit** |  |
| 99.1 | [Purple Biotech Corporate Presentation November 2025](ea026647401ex99-1_purple.htm) |

---

**SIGNATURES**

Pursuant to the requirements of the Securities Exchange Act of 1934, the Registrant has duly caused this report to be signed on its behalf by the undersigned, thereunto duly authorized.

---

| | | |
|:---|:---|:---|
| November 19, 2025 | **PURPLE BIOTECH LTD.** | **PURPLE BIOTECH LTD.** |
|  | By: | */s/ Gil Efron* |
|  |  | Gil Efron |
|  |  | Chief Executive Officer |

---

## Exhibit 99.1

**Exhibit 99.1**

![](ex99-1_001.jpg)

NASDAQ/TASE: PPBT November 2025 CORPORATE PRESENTATION

![](ex99-1_002.jpg)

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 - looking statements include, but are not limited to, statements that are not statements of historical fact, and may be identified by words such as "believe", "expect", "intend", "plan", "may", "should", "could", "might", "seek", "target", "will", "project", "forecast", "continue" or "anticipate" or their negatives or variations of these words or other comparable words or by the fact that these statements do not relate strictly to historical matters . You should not place undue reliance on these forward - looking statements, which are not guarantees of future performance . Forward - looking statements reflect our current views, expectations, beliefs or intentions with respect to future events, and are subject to a number of assumptions, involve known and unknown risks, many of which are beyond our control, as well as uncertainties and other factors that may cause our actual results, performance or achievements to be significantly different from any future results, performance or achievements expressed or implied by the forward - looking statements . Important factors that could cause or contribute to such differences include, among others, risks relating to : the plans, strategies and objectives of management for future operations ; product development for NT 219 , CM 24 and IM 1240 ; the process by which such early stage therapeutic candidates could potentially lead to an approved drug product is long and subject to highly significant risks, particularly with respect to a joint development collaboration ; the fact that drug development and commercialization involves a lengthy and expensive process with uncertain outcomes ; our ability to successfully develop and commercialize our pharmaceutical products ; the expense, length, progress and results of any clinical trials ; the impact of any changes in regulation and legislation that could affect the pharmaceutical industry ; the difficulty in receiving the regulatory approvals necessary in order to commercialize our products ; the difficulty of predicting actions of the U . S . Food and Drug Administration or any other applicable regulator of pharmaceutical products ; the regulatory environment and changes in the health policies and regimes in the countries in which we operate ; the uncertainty surrounding the actual market reception to our pharmaceutical products once cleared for marketing in a particular market ; the introduction of competing products ; patents obtained by competitors ; dependence on the effectiveness of our patents and other protections for innovative products ; our ability to obtain, maintain and defend issued patents ; the commencement of any patent interference or infringement action against our patents, and our ability to prevail, obtain a favorable decision or recover damages in any such action ; and the exposure to litigation, including patent litigation, and/or regulatory actions ; the impact of the economic, public health, political and security situation in Israel, the U . S . and other countries in which we may operate or obtain approvals for our products or our business, and other factors that are discussed in our Annual Report on Form 20 - F for the year ended December 31 , 2024 and in our other filings with the U . S . Securities and Exchange Commission ("SEC"), including our cautionary discussion of risks and uncertainties under "Risk Factors" in our Registration Statements and Annual Reports . These are factors that we believe could cause our actual results to differ materially from expected results . Other factors besides those we have listed could also adversely affect us . Any forward - looking statement in this press release speaks only as of the date which it is made . We disclaim any intention or obligation to publicly update or revise any forward - looking statement or other information contained herein, whether as a result of new information, future events or otherwise, except as required by applicable law . You are advised, however, to consult any additional disclosures we make in our reports to the SEC, which are available on the SEC's website, https : //www . sec . gov . The trademarks, tradenames, service marks and logos included herein are the property of the owners thereof and are used for reference purposes only . Such use should not be construed as an endorsement of the products or services of the Company

![](ex99-1_003.jpg)

3 Purple Biotech develops promising first - in - class drug candidates to treat cancers with high unmet medical need Next generation tri - specific antibody platform • CAPTN - 3: Conditionally activated T - cell engager (TCE) enhanced by NK cell engager arm and a Tumor Associated Antigen engager Partnership and investment opportunities: Two Phase 2 first - in - class drugs • CM24, aCEACAM1 antibody: Unlocking personalized immunotherapy through biomarker - guided patient targeting; positive randomized Phase 2a results • NT219, I RS1/2 degrader and STAT3 blocker : Sensitizing the tumor & tumor microenvironment; Safety and anti - tumor activity demonstrated in Phase 1 Cash balance of $10.5M\* provides runway into 1H 2027 \*As of September 30, 2025

![](ex99-1_004.jpg)

4 Collaborator Value Drivers Phase III Phase II Phase I Pre - Clinical Indications Target Project FIH 2026 Solid Tumors Capped - CD3x5T4xNKG2A CAPTN - 3 Tri - specific Ab IM1240 Solid Tumors Capped - CD3xTROP2xNKG2A CAPTN - 3 Tri - specific Ab IM1305 Phase 2b Pancreatic Cancer (+ nivolumab+SoC) CEACAM1 mAb CM24 Interim data 2026 Head and Neck Cancer (+cetuximab/ pembrolizumab) IRS1/2 degrader & STAT3 blocker NT219 A pipeline dedicated to advancing oncology therapies

![](ex99-1_005.jpg)

CAPTN - 3: Conditionally - Activated Tri - Specific Antibody Platform

![](ex99-1_006.jpg)

6 Uniquely positioned: First - in - class dual conditionally - activated T and NK Cell Engagers on the same antibody \* B ased on publicly available information

![](ex99-1_007.jpg)

7 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 α TAA Abs a - NK binder Abs T - cell - binder a - CD3 Abs  CD3 masking moiety Tumor cell NK cell Cancer microenvironment Protease cleavage Removal of T cell engager ' s masking by proteases of the tumor microenvironment T and NK Cell activation restricted to selected tumors T cell • Multi - specific biologics are revolutionizing immuno - oncology, initial success in hematologic cancers • Solid tumors are the next frontier - novel formats enabling precise, potent targeting, limited toxicity, greater activity • Tarlatamab – first TCE approved for solid tumors (Small Cell Lung Cancer, 2024) • Notable activity in relapsed and refractory small cell lung cancer is a "gamechanger" • "Capped" or "Masked" CD3 TCEs have shown improved safety and activity in early clinical studies - Cytokine Release Syndrome (CRS) can be avoided Increased immune activation Increased therapeutic index Activating upon binding to TAA

![](ex99-1_008.jpg)

8 Plug & Play Tri - specific Scaffold Differentiated by Capped TCE with an NK Cell Activating Arm 8 Multiple opportunities for development and partnering Modular TCE architecture allows integration of multiple TAAs or NK - activating arms, enabling a robust pipeline of novel drug candidates. ▪  NKG2A ▪  NK2D ▪ Other NK cell engagers NK engager Cap - HSA CD 3 TAA ▪ α 5T4 ▪ α TROP2 ▪ α EGFR ▪ Other New  TAA anti - TAA Differentiated TCE platform – • Capped TCE design for enhanced activity, a better safety profile, improved PK and product stability (HSA) • Boosted by NK cell/T cell activation - synergy of CD 3 and NK arms for robust efficacy

![](ex99-1_009.jpg)

9 Plug & Play Platform Capabilities Demonstrated In - Vivo 9 CD3x 5T4 xNKG2A CD3x EGFR xNKG2A CD3x5T4x NKG2D CD 3 x TROP 2 xNKG 2 A Platform demonstrations Pipeline candidates Sustained tumor regression was presented for several tri - specifics, targeting various TAAs and NK receptors: Can we make these charts bigger Lindsey – maybe check w Vicki/Jess?

![](ex99-1_010.jpg)

10 Unleashing both innate and adaptive immune response Dual activation of cytotoxic T - cells by CD 3 engagement & NKG 2 A inhibition Stimulates both helper (CD 4 +) and killer (CD 8 +) effector T cells via CD 3 targeting Dual mechanism: turns on killer T cells and blocks an immune " off switch " to unleash a stronger attack on tumors Activates NK cells by blocking the inhibitory NKG2A – HLA - E interaction

![](ex99-1_011.jpg)

11 • 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 CD 3 Cap inhibits T cell binding and cleavage restores activity: CAP advantages: improved safety, PK, and therapeutic window PBMCs mediated cytotoxicity assay Cytotoxic effect is restored following protease cleavage ELISA CD 3 binding assay Binding of CAPTN - 3 to CD 3 is dependent on protease cleavage (no proteases) CAPTN - 3 (no proteases) CAPTN - 3 +MMP9 CAPTN - 3 +UPA Ab Conc. (nM) % C y t o t o x i c i t y 0.000001 0.0001 0.01 1 0 20 40 60 80 100 ProTribody ProTribody + MMP9 TriBody (no proteases) CAPTN - 3 (no proteases) CAPTN - 3 +MMP 9

![](ex99-1_012.jpg)

12 Substantial contribution of the NKG 2 A arm was demonstrated: • in - vivo : IL 15 KI mouse model • in patient - derived explants (PDE) • in cell - based assays: • reinvigoration of exhausted T cells • NKG 2 A + gd 2 cell activation and anti - cancer activity • Blocking of NK arm function through mutation resulted in a substantial reduction in anti - cancer efficacy of CAPTN - 3 • The synergistic effect of the NK arm and the CD 3 arm was demonstrated Significant contribution of the NK and CD3 arms to the anti - tumor activity in vivo (EACR 2025) TNBC tumor growth inhibition in IL15 KI mice\* S ignificant effects of the NK and CD3 arms Contribution of the NKG2A arm (p = 0.002) Contribution of the CD3 arm (p < 0.0001) Tumor volume (mm 3) Tumor volume (mm 3) CAPTN - 3 1.5 mg/kg CAPTN - 3 (non - cleavable cap - CD 3) 1.5 mg/kg CAPTN - 3 0.75mg/kg CAPTN - 3 (mutated NKG2A) 0.7.5mg/kg \*Xenograft model of B - NDG IL15 KI mice inoculated with PBMC+MDA - MB - 231, treatments were QOD till end of study. The added value of the NKG2A arm was tested by comparing IM1240 activity to a capCD3x5T4xmutatedNKG2A (IM1340) at 0.75mg/kg dose. The added value of the CD3 arm was tested by comparing IM1240 activity to a non - cleavable capCD3x5T4xNKG2A (IM1242) at 1.5mg/kg dose.

![](ex99-1_013.jpg)

13 5 T 4 : a Novel Target in Oncology 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 /ajcr 0074519 5 T 4 is a Tumor Associated Antigen prevalent in several large indications Multiple 5T4 targeting programs are advancing with different modalities Kemper et al. LSA 2022;5:e202201481

![](ex99-1_014.jpg)

\| 14 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) Patient - derived explants (PDE) of 5 T 4 + NSCLC \*\* Synergistic effect of the CD 3 and NKG 2 A arms \*TNBC MDA - MB - 231 cells were s.c. inoculated 1:1 with PBMCs on day 0 . Treatments: IV QOD 1 mg/kg (non - capped) or equimolar dose 1.7 mg/kg (capped, 1240) till day 24 , 8 mice per group, Follow up 20 days following treatment completion \*\* 5 T 4 + NCSLC Patient - Derived Explant (PDE)\* at 10 nM concentration \*\*\* Ex vivo patient - derived tumor explants (PDE) involve the culture of resected tumor fragments that retain the TME native architec ture and immune cell array, tumor heterogeneity and the proliferative capacity (Golan 2023 , Powley 2020). Fresh NSCLC patient - derived biopsy was cultured as 250 um slices, treated for 96 hr, fixed, and H&E slides were blindly scored for response based on cell viability and damage to the cancerous tissue according t o p athological criteria. A scale of 0 – 100 was created with a score of 0 representing completely viable cancer tissue and a score of 100 representing no viable cancer cells. The analysis included functional (cell death) score of response (cResponse) using proprietary artificial intelligence (AI) algorithm (Curesponse). IM 1240 : In vivo efficacy and synergistic effect of the CD 3 and NKG 2 A arms Days following treatment initiation Treatment In vivo anti - tumor efficacy of IM1240 & IM1222\* Effective cleavage (p<0.0001) • Tumor regression by IM1240 is demonstrated . N o tumor recurrence observed • Similar effects for IM1240 (CD3 - capped) and IM1222 (CD3 - non capped) suggest efficient IM1240 efficacy following cap - cleavage • Disabling either the CD 3 or NKG 2 A arm diminished activity (score of 38 or 49), while the full tri - specific antibody drove powerful cancer cell killing (score of 94)

![](ex99-1_015.jpg)

15 Next Steps: IM 1240 and Other CAPTN - 3 Antibodies Non GLP tox • Q 4 25 GLP tox • H1 26 IND submission • mid 26 FIH – IM1240 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, NSCLC, pancreatic, ovarian, gastric adenocarcinoma and bladder cancers • Primary Objectives: to assess the safety, tolerability and MTD of IM1240 in patients, determine the RP2D of IM1240 • In a pre - IND meeting the FDA provided a clear roadmap for non - clinical and clinical development Initiate development of IM1305: capped - CD3xTROP2xNKG2A

![](ex99-1_016.jpg)

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

![](ex99-1_017.jpg)

17 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 cell - mediated cytotoxicity against tumors • CM24 binds to CEACAM1 on NETs and inhibits NET - related activities • CM24 shows benefits in combination with immuno - oncology treatments Demonstrated mechanism of action • 19 % reduction in risk of death (HR= 0. 81) and 2 5 % reduction in the risk of progression or death (HR= 0.7 5) and 25 % ORR, in metastatic PDAC as second - line treatment • Potential biomarkers: Serum CEACAM 1 and MPO, C EA CAM 1 + tumor cells and CPS PoC Clinical efficacy • Large opportunities to leverage the MoA in multiple indications (lung, colon, GI etc.) • Significant unmet medical need in pancreatic ductal adenocarcinoma (PDAC), the most common form of pancreatic cancer Sizable market potential

![](ex99-1_018.jpg)

18 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 creates a pro - angiogenic tumor microenvironment that supports tumor vessel maturation. Oncogene 30, 4275 – 4288 (2011) , \* Beauchemin N, Cancer Metastasis Rev 32, 643 - 671 (2013) CEACAM 1 expression on tumor and tumor - infiltrating immune cells in PDAC CEACAM 1 scoring in PDAC TMA vs normal tissues Representative examples of CEACAM 1 immunohistochemical images of pancreatic adenocarcinoma and normal tissues CD PDAC tumor cells Normal 80µm 80µm 80 µm 80 µm CEACAM 1 + CD 8 + CD CEACAM1 + NK cells Immune cells Tumor CD8+T & NK Cells CEACAM 1 CEACAM 1 CEACAM 1 CEACAM 5 CM24 Activating the immune response Making the tumor visible TME - Tumor Microenvironment

![](ex99-1_019.jpg)

19 CCAM 1 CM 24 CM 24 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. J Immunol. 2020; NETs Primed intercellular communication in cancer progression as a promising therapeutic target [Shang et al. Biomarker Resea rch (2023) 11:24] CEACAM 1 is a part of the Neutrophil extracellular traps (NET) structure MPO (green) DAPI (blue), CM 24 (red) CM 24 (red) CM 24 binds to CEACAM 1 on NETs NETs are web - like structures involved in: • Tumor immune evasion • Tumor progression • Metastasis • Cancer - associated thrombosis

![](ex99-1_020.jpg)

20 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 cancer. Therapeutic Advances in Medical Oncology. 2020;12. doi:10.1177/1758835920905408 4 . Wang - Gillam A, Hubner RA, Siveke JT, et al. NAPOLI - 1 phase 3 study of liposomal irinotecan in metastatic pancreatic cancer: Final overall survival analysis and characteristics of long - term survivors. Eur J Cancer. 2019;108:78 - 87. doi:10.1016/j.ejca.2018.12.007 .5. Calinescu et al, Journal of Immunology Research 2018: 7169081; Car cinoembryonic antigen - related cell adhesion molecules (CEACAM) 1, 5 and 6 as biomarkers in pancreatic cancer, DOI:10.1371/journal.pone.0113023 • ~ 60 K new cases/year in the US 1 ; 140 K new cases in EU in 2023 • 5 - year relative survival rate of 12 % 1 • 2 nd line chemo has 5 - year overall survival rate of 3 % 1 • 2 nd line Overall Survival of 6 to 8 months 2,3,4 • CEACAM 1 expression correlates with poor prognosis in pancreatic cancer 5 • Clinical and preclinical data support targeting patients based on CEACAM 1 levels • Synergy of CM 24 with currently marketed IO therapies Key PDAC Statistics Limited Treatment Options CM24 Opportunity Market opportunity in additional indications based on CEACAM1 expression pan - RAS inhibitor advancing in Phase 3 as second - line treatment Advanced PDAC PS 0 - 1 Bilirubin <1.5xULN No comorbidities PS 2 Bilirubin ≤1.5xULN PS 2 & KPS <70 Bilirubin >1.5xULN PS 3 - 4 FOLFIRINOX NALIRIFO X Gem/nab Nal - IRI/5FU/LV mFOLFOX6 Gem/nab Gem BSC Gem/nab 1 st L 2 nd L

![](ex99-1_021.jpg)

21 A randomized Bayesian study of CM 24 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) – Experimental arm CM24 + nivolumab & Nal - IRI/5FU/LV n=16 Control arm Nal - IRI/5FU/LV n=15 PDAC patients progressing on or after 1 st line standard of care chemotherapy Randomized n=31 1:1 \* The other part of the study with gemcitabine/nab - paclitaxel regimen (n= 32) was affected by informative censoring hence non interpretable Safety - well tolerated Exploratory biomarkers : Serum & tumor CEACAM 1 , NET marker (Myeloperoxidase - MPO), PDL 1 Demographics and patient characteristics (ITT)

![](ex99-1_022.jpg)

22 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 % reduction in risk of death (HR= 0. 81) and 2 5 % reduction in the risk of progression or death (HR= 0.7 5) » Prolongation of 2. 3 months in median overall survival and 1.9 months in median progression - free survival Overall Survival Progression Free Survival Experimental Control Experimental Control

![](ex99-1_023.jpg)

23 Post - hoc Phase 2 Biomarkers Analysis Patients with either Serum CEACAM 1 or tumor CEACAM 1 + • 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 CEACAM 1 or MPO (NET marker) • R epresents a subgroup of 80 % of patients • Consistent with CM 24 MoA in targeting CEACAM 1 to modulate immune evasion and NET activities Patients with both tumor CEACAM 1 and PD - L 1 CPS • Support the rationale of the CM 24 /nivolumab combination • Highlights potential in disease settings where immuno - oncology is less effective Baseline biomarkers tested to explore potential patient enrichment for greater clinical benefit

![](ex99-1_024.jpg)

24 Post - hoc analysis in serum or tumor CEACAM 1 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 0 . 22 , p 0 . 006) and 95 % reduction in the risk of progression or death (HR 0 . 05 , p 0 . 0003) » Prolongation of 3 . 7 months in median overall survival and 2 . 9 months in median progression - free survival » Higher objective response rate (ORR) (37 . 5 % vs 0 %) CEACAM 1 + Tumor cell H score 115 - 275 or Serum CEACAM 1 6 K - 15 K pg /mL Overall Survival HR = 0.22 (CI 0.07 - 0.7)  median= 3.7 m P = 0.006 Exp Cont Progression Free Survival HR = 0.05 (CI 0.01 - 0.44)  median =2.9m P = 0.0003 Exp Cont

![](ex99-1_025.jpg)

25 Results in serum CEACAM 1 or MPO enriched patients Significantly improved OS, PFS 6 K < sCCAM 1 < 15 K 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 results in patients with baseline serum CEACAM 1 or serum MPO levels representing 80 % of patients in the study : » 61 % reduction in risk of death (HR = 0 . 39 , p 0 . 039) and 72 % reduction in the risk of progression or death (HR = 0 . 28 , p 0 . 006) » Prolongation of 2 . 4 months in median overall survival and 2 . 2 months in median progression - free survival » Higher objective response rate (ORR) (30 . 7 % vs 0 %)

![](ex99-1_026.jpg)

26 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 - score> 1 00) and Low PDL 1 (CPS ≤ 1) expression in tumors : » 90 % reduction in risk of death (HR = 0 . 1 , p 0 . 013) and 81 % reduction in the risk of progression or death (HR = 0 . 19 , p 0 . 033) » Prolongation of 4 months in median overall survival and 2 months in median progression - free survival

![](ex99-1_027.jpg)

27 Planned 2 nd & 3 rd line PDAC Phase 2 b 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 CEACAM 1 /MPO within cutoffs of previous study Arm A SoC chemotherapy 1 Arm C CM 24 +SoC chemotherapy 1 Primary endpoints : ORR, PFS Secondary endpoints: OS, CA 19 - 9 R A rm B CM 24 +nivo+SoC chemotherapy 1 Arm A SoC chemotherapy 1 Arm C CM 24 + SoC chemotherapy 1 A rm B CM24+nivo+ SoC chemotherapy Stage 1 (n= 20 /arm) Stage 2 (n= 35 /arm) 1 – Study regimen will alternate and depend on prior regimen 2 – Continue to Stage 2 in either arm B or C, IF Arm B vs. Arm C ORR/DCR is different , the arm with lower ORR/DCR will be discontinued; if the difference is small or none – continue with both arms Simon 2 - Stage Interim analysis 2

![](ex99-1_028.jpg)

NT 219 : Small Molecule Degrader of IRS 1 / 2 and Blocker of STAT 3 Recurrent/Metastatic Head & Neck Cancer (R/M SCCHN)

![](ex99-1_029.jpg)

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 their degradation • Dual inhibitor of STAT 3 & IRS 1 / 2 , both required to overcome drug resistance • Affects both the tumor and the TME • Suppresses cancer stem cells Innovative MOA • Outstanding efficacy in various PDX models in monotherapy and in combination • Potential in EGFRi , MAPKi and ICI resistant cancers Robust preclinical package • No DLTs in monotherapy or in combination • Early clinical proof - of - mechanism • Activated IGF 1 R and STAT 3 identified as potential predictive biomarkers • RP 2 D determined at 100 mg/kg , Phase 1 concluded. Phase 2 initiated Clinical Stage • Opportunity to establish a Standard of Care in 2L r/m SCCHN patients • Multiple market upsides in combination with approved cancer treatments • NT219 is the only IRS degrader available for clinical investigation Broad Market Potential

![](ex99-1_030.jpg)

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 the biopsy tumor cells Activated STAT 3 in the TME SCCHN patient NT219+cetuximab Nuclear pSTAT3 H - Score Membranal IRS 2 H - Score pre - treatment Post treatment pre - treatment Post treatment Target engagement demonstrated in patients ' biopsies Dose - proportional increase in AUC and Cmax values

![](ex99-1_031.jpg)

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 treated with active doses (50 and 100 mg/kg): • 2 confirmed PRs; 3 SD • ORR: 25 %, DCR: 62.5 % Biomarker analysis at 50 mg/kg dose of NT 219 with cetuximab : • Significant differences in the activated pIGF 1 R and pSTAT 3 were revealed in the 2 responders (PR) compared to the 2 non - responders (PD), verified in the 100 mg/kg cohort. NT 219 : Activity in mono and combo dose escalation Numbers under horizontal line designate NT 219 dose in mg/kg; P = HPV positive; N = HPV negative -70 -60 -50 -40 -30 -20 -10 0 10 20 30 40 50 60 70 80 90 100 100 (N) 24 (N) 12 (N) 24 (P) 50 (P) 100 (N) 24 (P) 12 (P) 100 (N) 12 (N) 100 (N) 6 (N) 50 (N) 50 (N) 50 (N) Best % change from baseline NT 219 +cetuximab Waterfall for tumor size change

![](ex99-1_032.jpg)

32 Activated pIGF1R and STAT3, NT219 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) compared to the non - responders (PD,SD) • The findings at the 50 mg/kg were verified at the 100 mg/kg dosed patients Responders (PR) Non - responders (PD) Responders (PR) Non - responders (PD)

![](ex99-1_033.jpg)

33 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 mg/kg Q 1 W+ cetuximab 400 mg/m 2 - > 250 mg/m 2 n= 10 + 19 Simon 2 stage R 1 st Line ICI Naive 2 nd Line 3 rd Line Cohort 1 Cohort 2

![](ex99-1_034.jpg)

34 Purple Biotech develops promising first - in - class drug candidates to treat cancers with high unmet medical need Next generation tri - specific antibody platform • CAPTN - 3: Conditionally activated T - cell engager (TCE) enhanced by NK cell engager arm and a Tumor Associated Antigen engager Partnership and investment opportunities: Two Phase 2 first - in - class drugs • CM24, aCEACAM1 antibody: Unlocking personalized immunotherapy through biomarker - guided patient targeting; positive randomized Phase 2a results • NT219, I RS1/2 degrader and STAT3 blocker : Sensitizing the tumor & tumor microenvironment; Safety and anti - tumor activity demonstrated in Phase 1 Cash balance of $10.5M\* provides runway into 1H 2027 \*As of September 30 , 2025

![](ex99-1_035.jpg)

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. Rowinsky, MD Chairman of the Board Former CMO at ImClone, Stemline , Board member at Biogen Inc. Shai Lankry Chief Financial Officer Former CFO at Gamida Cell Ltd. (NASDAQ:GMDA)

![](ex99-1_036.jpg)

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

![](ex99-1_037.jpg)

Appendix A \| CAPTN - 3

![](ex99-1_038.jpg)

38 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 - fold • Safety factor # 2 : In the absence of 5 T 4 - expressing cancer cells, the non - capped variant showed a decreased IFN  release ~ 50 - fold

![](ex99-1_039.jpg)

Appendix B \| CM 24

![](ex99-1_040.jpg)

40 Confidential 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 CEACAM 1 as a putative therapeutic target to prevent metastatic progression of colon carcinoma " Ferri , 2020 Tsuzuki, 2020 Tsang, 2020 Blumberg, 2015 " C EACAM 1 regulates TIM - 3 - mediated tolerance and exhaustion " " CEACAM 1 regulates Fas - mediated apoptosis in Jurkat T - cells via its interaction with β - catenin " Shively, 2013 02 \| IMMUNE CELLS/ IMMUNE EXCLUSION 03 \| IMMUNO - ONCOLOGY " Immune - checkpoint molecules on regulatory T - cells as a potential therapeutic target in head and neck squamous cell cancers " " [Blockade] enhances natural killer cell cytotoxicity against tumor cells through blockade of the inhibitory CEACAM 1 / CEACAM 5 immune checkpoint pathway "

![](ex99-1_041.jpg)

41 CM 24 binds to CEACAM 1 on NETs CM 24 Inhibits NET - Induced migration of CEACAM 1 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 (red) Level of MPO in patient serum (% of Pre - treatment) p = 0.034 p = 0.037 C 1 D 1 = Cycle 1 Day 1 ; EOI = End of CM 24 Infusion; C 1 D 15 = Cycle 1 Day 15 Melanoma cell line

![](ex99-1_042.jpg)

42 Confidential 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 days post last CM 24 treatment Significant benefits as both single agent and in combination with α - PD - 1

![](ex99-1_043.jpg)

43 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 2 Cough 1 1 Abdominal pain aggravated 1 1 Alkaline phosphatase increase 1 1 Atrial flutter 1 1 C - Diff Colitis 1 1 GI bleed 1 1 Leukocytosis 1 1 Small bowel obstruction Study Design • As of March 8 th , 2022, a total of 13 patients were enrolled and 11 patients were evaluable for DLT determination (8 PDAC, 2 CRC and 1 PTC). • 9 patients had received 2 prior regimens for metastatic disease, 2 patients had one previous line. Phase 1 Doses: 10, 15, 20mg/kg q2wk + nivolumab (480mg q4w) 3+3 design, n=12 Indications: Pancreatic, CRC, Papillary Thyroid Carcinoma Phase 2 Expansion cohorts Safety • No DLTs were observed across all dose levels; no Grade 4 AEs or treatment - related deaths have been reported. • Grade 3 AEs were noted in 6/13 patients (46%).

![](ex99-1_044.jpg)

44 Confidential 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 determine the RP2D • Safety was assessed according to CTCAE v5 and preliminary anti - tumor activity was assessed by the investigators according to RECISTv1.1 using CT/MRI • CM24 and CEACAM1 measurements in serum, biopsy specimens, and TILs, as well as tumor and TILs PD - L1 levels are being determined As of March 8th, 2022, a total of 13 patients were enrolled and 11 patients were evaluable for dose - limiting toxicity (DLT) determination (8 PDAC, 2 CRC and 1 PTC) • 9 patients had received 2 prior regimens for metastatic disease and 2 patients had one previous line. Demographics of patients treated with CM24 (10, 15, 20mg/kg) in combination with nivolumab (480mg) Prior Lines of Therapy, n (%) 65 (49 - 76) Median age, years (range) 2 (18 %) 1 Sex, n (%) 9 (82 %) 2 5 (45 %) Male Diagnosis , n (%) 6 (55 %) Female 8 (7 3 %) Pancreatic cancer Ethnicity, n (%) 1 (9 %) Papillary Thyroid cancer 10 (91 %) Not Hispanic or Latino 2 (18 %) Colorectal cancer 1 (9 %) Hispanic or Latino 2 3 (11 - 73) Median Time from Initial Diagnosis months (range) Race, n (%) ECOG, n (%) 10 (9 1 %) White 7 (64 %) 0 1 (9 %) Black or African American 4 (36 %) 1

![](ex99-1_045.jpg)

45 Confidential 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 Response: a fter initial treatment, the patient had a Partial Response of 40%, with a definite reduction of the para - tracheal adenopathy and liver lesions and 58% reduction in CA19 - 9 levels • Under treatment for 6 months, still under monitoring. 655 681 283 SCREENING FIRST VISIT - PREDOSE 2 MONTH VISIT - PREDOSE CA - 19 - 9 Levels

![](ex99-1_046.jpg)

46 Confidential 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 (PTC)) • Pharmacokinetic analysis of CM24 shows exposure is dose - proportional across the 3 doses in this study • Well tolerated with no Dose Limiting Toxicities (DLTs) and no grade ≥ 4 Adverse Events (AEs) • Median Overall Survival 4.5 months (95% CI 2.0 - 11.1) for 11 PDAC patients PR SD SD SD SD

![](ex99-1_047.jpg)

Appendix C \| NT219

![](ex99-1_048.jpg)

\| 48 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 STAT3 • Well - established transcription factor associated with the tumorigenic phenotype • Hyperactivated in many cancers • Promotes proliferation, survival, angiogenesis and metastasis • Critical player in tumor immune evasion Hadas Reuveni et al. Cancer Res 2013;73:4383 - 4394 ; Machado - Neto et al. Clinics 2018; 73,suppl 1 e566s; Naokazu Ibuki, Mazyar Ghaffari, Hadas Reuveni et al. Mol Cancer Ther. 2014; 13(12): 2827 - 2839 ; Rampias et al . Oncogene 2016; 35(20):2562 - 4; Flashner - Abramson, Reuveni Hadas, Levitzki Alexander et al. Oncogene 2016;35(20):2675 - 80 ; 6 Sanchez - Lopez et al. Oncogene 2016;35(20):2634 - 44. Zhao C et al. Trends Pharmacol Sci. 2016;37(1):47 - 6; Johnson, Daniel E et al. Nature reviews. Clinical oncology 2018; 15(4): 234 - 248. Zi Ying et al. J Cell Biochem . 2018;119:9419 - 9432. Binding kinetics to IRS1 (Octet) Dose - dependent inhibition pSTAT 3 STAT 3 NT219 (μ M) 0 1 3 10 NT219 triggers irreversible dephosphorylation of STAT3 STAT3 dephosphorylation following treatment No recovery following washout Phospho - STAT3 STAT3 Covalent binding of NT 219 leads to IRS degradation

![](ex99-1_049.jpg)

49 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 re - binding of IRS1/2 to the receptor CANCER CELL SURVIVAL CANCER CELL APOPTOSIS The proteasome degrades IRS1/2 IGF 1 IGF 1 R IRS AKT PI 3 K IGF 1 IGF 1 R IRS NT AKT IGF 1 IGF 1 R IRS pS pS AKT IGF 1 IGF 1 R AKT

![](ex99-1_050.jpg)

50 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 plays important roles in inhibiting the expression of crucial immune activation regulators and promoting the production of immunosuppressive factors • Targeting the STAT 3 signaling pathway has emerged as a promising therapeutic strategy for numerous cancers NT 219 demonstrates a durable and dose - dependent suppression of STAT 3 tyrosine phosphorylation, affecting both the tumor cells and the tumor microenvironment. Zou, S., Tong, Q., Liu, B. et al. Targeting STAT 3 in Cancer Immunotherapy. Mol Cancer 19 , 145 (2020). https:// doi.org / 10.1186 /s 12943 - 020 - 01258 - 7

![](ex99-1_051.jpg)

51 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) Control (n= 6) Erlotinib (n= 8) Erlotinib+NT 219 (n= 6) Erlotinib+Ruxolitinib+Buparlisib (n= 8) STAT 3 IRS EGFR MEK Tumor Regression ERK PI 3 K AKT Tumor Survival Tumor Survival Buparlisib Ruxolitinib Erlotinib NT 219 NT 219 JAK By blocking both STAT 3 and IRS resistance pathways, NT 219 re - sensitizes tumors to anti - cancer therapies

![](ex99-1_052.jpg)

52 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 center; presented at AACR 2023 NT 219 +  PD 1 reverse  PD 1 - resistant melanoma in a syngeneic mouse model\* Tumor Volume (mm 3) Tumor Volume (mm 3) Biopsy and PBMC are from a GEJ cancer patient who progressed on keytruda . Mice were treated 3 times (d ays 0,5,10); Keytruda - 6 mg/kg IP NT 219 - 60 mg/kg IV TGI= 71 % P = 0.0056 SCCHN PDX model Head & Neck Cancer Recurrent/metastatic squamous cell carcinoma of the head and neck (R/M SCCHN) metastasis, patient progress ed on chemoradiation, several chemotherapies and pembrolizumab . Treatments on days 0 , 3 and 10 , cetuximab - 1 mg/mouse, 3 mice/group; PBMCs (1.4 M cells/mouse) were injected on day 6 . \*\* p< 0.01 , \* p< 0.02 based on one - way ANOVA with post hoc Tukey ' s HSD test Lung Cancer PDX model Non - small cell lung cancer (NSCLC) Exon 19 deletion EGFR and T 790 M, biopsy of bone marrow metastasis, patient previously progressed on afatinib and Osimertinib. Osimertinib 5 mg/kg, NT 219 65 mg/kg, mean tumor volume at the end point, 3 mice/group;

![](ex99-1_053.jpg)

53 NT 219 combination with α PD 1 achieves significant reprograming of the TME NT 219 and  PD 1 combination converted immuno - suppressive TME to immuno - reactive • Immune profiling of the ICB - resistant melanoma tumors following treatment of the mice with the NT 219 + αPD 1 revealed significant reprograming of the TME, while none of the monotherapies had an effect (n= 10 mice per group, analysis on day 13 following 5 treatments) • Collaboration with Prof. Bareli and Prof. Curran, M.D. Anderson cancer center, presented at AACR 2023 Activated cytotoxic T cells (% CD 8 + GZMB +) Activated NK cells (% NK 1.1 + GZMB +) NT 219 +  PD 1 leads to a significant increase in cytotoxic effector cells (T & NK cells) NT 219 +  PD 1 leads to a significant reduction in myeloid derived suppressor cells (MDSC) % Mo - MDSC (out of CD 45 +) % Gr - MDSC (out of CD 45 +)

![](ex99-1_054.jpg)

54 NT 219 +  PD 1 Converted Immuno - suppressive to Immuno - reactive TME Zou et al. Molecular Cancer (2020) 19:145 ; Rampias et al. Oncogene (2016) 35:2562 ; Flashner, Reuveni, Levitzki et al. Oncogene (2016) 35:2675 ; Sanchez - Lopez et al. Oncogene (2016) 35:2634  PD 1 + NT 219  PD 1 + NT 219  PD 1 + NT 219  PD 1 + NT 219  PD 1 + NT 219  PD 1 + NT 219  PD 1 + NT 219

![](ex99-1_055.jpg)

55 Selected Publications Michael Karin Alexander Levitzki Menashe Bar - Eli Michael Cox

![](ex99-1_056.jpg)

56 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 IRS 2 by NT 219 or IRS 2 - shRNA, suppresses the increased  - catenin activity, overcomes chemo - resistance, and inhibits LS - 513 cell viability and tumor growth in intracranial model. NT 219 inhibits the IRS to β - Catenin pathway and synergizes with 5 FU to suppress CRC tumor growth in mouse brain Chemo - resistance Immune evasion Brain Metastasis Tumor Growth epithelial - mesenchymal transition (EMT) IRS  - Cat IRS IRS 2 NT 219 downregulates IRS 2 and suppresses the  - catenin activity Silencing IRS 2 inhibits  - catenin activity In Vitro LS 513 sh - NS LS 513 sh - IRS 2 DAPI β - catenin IRS 2 Merge 1 0 μ m 1 0 μ m 1 0 μ m 1 0 μ m 1 0 μ m 1 0 μ m 1 0 μ m 1 0 μ m In Vivo C. A. B. D.

![](ex99-1_057.jpg)

57 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/   catenin pathways, are known to be involved in cancer stem cell renewal, immune evasion, metastasis and highly involved in drug resistance to  PD 1 and cetuximab • SCCHN is the 6 th most common cancer type • 175 k new cases/year are expected by 2024 • 1 L standard of care has shifted from chemotherapy towards immuno - oncology + chemotherapy • EGFR and PD(L) - 1 are the only clinically validated targets in SCCHN • < 15 % of R/M SCCHN patients respond to cetuximab in 2 L • < 20 % of R/M SCCHN patients respond to Pembrolizumab in 1 L • New compounds currently in P 3 1 L Targeting the unmet medical need α - PD - 1 + Chemo 1 L 60 K pts NT 219 Cetuximab 2 L 48 K pts NT 219