Purple Biotech Ltd.

Foreign Filer Report • Sep 16, 2025

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 September 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 September 15, 2025, Purple Biotech Ltd. (the "Company" or the "Registrant") issued an updated Company presentation, "Purple Biotech Corporate presentation September 2025", which is attached hereto as Exhibit 99.1.

Exhibit

99.1 Purple Biotech Corporate presentation September 2025

Incorporation by Reference

This Report on Form 6-K, including all exhibits attached hereto, is hereby incorporated by reference into each of the Registrant's Registration Statement on Form S-8 filed with the Securities and Exchange Commission on May 20, 2016 (Registration file number 333-211478), the Registrant's Registration Statement on Form S-8 filed with the Securities and Exchange Commission on June 6, 2017 (Registration file number 333-218538), the Registrant's Registration Statement on Form F-3, as amended, originally filed with the Securities and Exchange Commission on July 16, 2018 (Registration file number 333-226195), the Registrant's Registration Statement on Form S-8 filed with the Securities and Exchange Commission on March 28, 2019 (Registration file number 333-230584), the Registrant's Registration Statement on Form F-3 filed with the Securities and Exchange Commission on September 16, 2019 (Registration file number 333-233795), the Registrant's Registration Statement on Form F-1 filed with the Securities and Exchange Commission on December 27, 2019 (Registration file number 333-235729), the Registrant's Registration Statement on Form F-3 filed with the Securities and Exchange Commission on May 13, 2020 (Registration file number 333-238229), the Registrant's Registration Statement on Form S-8 filed with the Securities and Exchange Commission on May 18, 2020 (Registration file number 333-238481), each of the Registrant's Registration Statements on Form F-3 filed with the Securities and Exchange Commission on July 10, 2020 (Registration file numbers 333-239807 and 333-233793), the Registrant's Registration Statement on Form S-8 filed with the Securities and Exchange Commission on April 4, 2022 (Registration file number 333-264107) and the Registrant's Registration Statement on Form F-3 filed with the Securities and Exchange Commission on March 23, 2023 (Registration file number 333-270769), the Registrant's Registration Statement on Form F-3, as amended, originally filed with the Securities and Exchange Commission on December 8, 2022 (Registration file number 333-268710), the Registrant's Registration Statement on Form F-1, as amended, originally filed with the Securities and Exchange Commission on October 30, 2023 (Registration file number 333-275216) and the Registrant's Registration Statement on Form F-1, filed with the Securities and Exchange Commission on July 22, 2024 (Registration file number 333-280947), to be a part thereof from the date on which this report is submitted, to the extent not superseded by documents or reports subsequently filed or furnished.

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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.

September 15, 2025 PURPLE BIOTECH LTD.

By: /s/ Gil Efron

Gil Efron Chief Executive Officer

Forward-looking Statements and Safe Harbor

Certain statements in this presentation that are forwards of historical fiet are forward-looking statements within the meaning of the exte hadver provisions of the Private Se Ligation Reform Act of 1995. Such forward-look, but are not imied o, statements of historial fact, and may be identified by words such as "believ"," "exped", "intent", "plan", "thell", "twild", "twil", "terecs", "will", "typics", "forecas", "continue" or their agatives or waintions of these worls of the fiet that there stateners to not celate stickly to historial on these under eliance on these forward-looking statements, which are not grammanes of future performance. Forwar statements veller our current views, expect to fittere events, and are subject to a number of assumitions, involve known and unlarom risks, nany of visits are beyon our control, as well as uncertainies and other has could results, performance or achivements to be significantly different from any fitterents expressed or implied by the forward-looking stateners that could case or contribute to such differences include, annong other, siste reading to the plans, strangement for fiture operations: product do NT249, CM24 and IM240; the process by which such stage therapetic candidates could potenzials lead on an approved dong and subject to highly significant risks, particularly with research of that that that that that that that that involves a lengthy and expensive process with userations; our ability to successfilly develop and contral products; the expense, lengt, progress and essub of any changes in regulation and legishion and legishion tat could offect the plannaceutical in receiving the regulatory approvals secessary in order to commercialize on products, the U.S. Food and Dog Administration or any other of phamacential products; the regulatory environment and change in the counces in the counces in which we operate; the contries in which we operat survusion the attal narket reception to our cleared for marketing in ontivaler market, the introduction of competing products; patents obtained by competions; cheraders on the effectivenes of our protections for intrained with to obtain, mininan and deend issued processed of any patent interference of ally patent interference or infingence or i against our patents, and our ability to preceded any soch any soch action and the exposue to litigation, including patent lifigation, and or regulatory actions; the inport of the economic, publical and security situation in Issel, the U.S. and other commires in vicin we may operate or our podorts or our podorts or our posies, and other factors tha discussed in our Amad Report on For the year ended December 31, 2024 and in our other filings with the U.S.Commission ("SEC"), including on cantionary discussion of risks and uncertainies under "Risk Factors" in on Registerial and Amal Reports. These are actual cause our actual results of fifter materially from expected results. Ober fictors besides those we lased could also adversely affect in this press release speals only as of the date which it is nade. Ve discion any internation of obigation or obiga publicy update or revise any forward-boking statened beein, whether a a realt of new information, fitne events or othervise, exercy as required by appliadel w. You are advised, lovever, to consult any addical discoures ve nake in the SEC's website, http://www.e.gov. The tadenarks, tradeannes, tradeannes, service marks and logos included herein are the property of the owners there purposes only. Such use should not be constned as an endorsement of the products or services of the Company

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Purple Biotech develops promising first-in-class drug candidates to treat cancers with high unmet medical need

Project	Target	Indications				Collaborator
IM1240	Capped- CD3x5T4xNKG2A CAPTN-3 Tri-specific Ab	Solid Tumors			FIH 2026
IMI305	Capped- CD3xTROP2xNKG2A CAPTN-3 Tri-specific Ab	Solid Tumors
CM24	CEACAM1 mAb	Pancreatic Cancer (+nivolumab+SoC)			Phase 2b	University of Colorado Anschutz Medical Campus
NT219	IRS1/2 degrader & STAT3 blocker	Head and Neck Cancer (+cetuximab/ pembrolizumab)			Interim data 2026

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

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

Uniquely positioned: First-in-class dual conditionally-activated T and NK Cell Engagers on the same antibody

CAPTN-3: Tri-specific antibody activates innate and adaptive immune responses while increasing the therapeutic index

• · Multi-specific biologics are revolutionizing immuno-oncology, initial success in hematologic cancers
• Solid tumors 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

Unleashing both innate and adaptive immune response Dual activation of cytotoxic T-cells by CD3 engagement & NKG2A inhibition

CD3 Cap inhibits T cell binding and cleavage restores activity: CAP advantages: improved safety, PK, and therapeutic window

· CAPTN-3 uses multiple TME-specific proteases - increasing likelihood for cleavage by broad-

tumor types

Significant contribution of the NK and CD3 arms to the antitumor activity in vivo (EACR 2025)

5T4: a Novel Target in Oncology Expressed on Solid Tumors

IM1240: In vivo efficacy and synergistic effect of the CD3 and NKG2A arms

.

1984-1994 (1.1 min 1.1 minutes manus and manus and manus and and and and and and and and and and and and and and and and and and and and and and commendent commendent communi

Next steps IM1240 and Other CAPTN-3 Antibodies

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

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

CM24: Targeting CEACAM1expressing tumors

Attractive new target	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
Demonstrated mechanism of action	· 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
PoC Clinical efficacy	19% reduction in risk of death (HR=0.81) and 25% reduction in the risk of progression or death (HR=0.75) and 25% ORR, in metastatic PDAC as second-line treatment Potential biomarkers: Serum CEACAM1 and MPO, CEACAM1*tumor cells and CPS
Sizable market potential	Large opportunities to leverage the MoA in multiple indications (lung, colon, Gl etc.) Significant unmet medical need in pancreatic ductal adenocarcinoma (PDAC), the most common form of pancreatic cancer

CM24: Immune modulation of CEACAM1 expressing TMEs

CM24 blocks NET-related activities by CEACAM1 inhibition

CEACAM1 is a part of the Neutrophil extracellular traps (NET) structure

• Tumor immune evasion
• Tumor progression
• Metastasis

URPI

Cancer-associated thrombosis .

CM24 (red)

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(adapted from 'Chen, Q.et al. Cancers 2021, 13, 2832'); Royes RF, et ol. Netropelity C.A.C.M1 co. Putchive Theropeut

Large market opportunity based on CEACAM1 expression in PDAC

ਹਰ

Completed Randomized Phase 2 Combination Study

(NCT04731467)

A randomized Bayesian study of CM24 in combination with nivolumab plus SoC chemotherapy in 2nd line PDAC patients*

Primary endpoint : OS

Exploratory biomarkers:

Secondary endpoints: PFS, ORR, DCR OS rate @ 6 & 12 months, PFS rate @ 3 & 6 months

Serum & tumor CEACAM1, NET marker (Myeloperoxidase-MPO), PDL1

*The other part of the study with gemcitabine/nab-pacitaxel regimen (n=32) was affected by informative censoring hence non interpretable

Demographics and patient characteristics (ITT)

	Nal-IRI/SFU/LV
Characteristic	Experimental (n=16)	Control (n=15)
Age (median)	66.0	68.0
Male (n. %)	10 (62.5)	8 (53.3)
Female (n. %)	6 (37.5)	7 (46.7)
Race/ white (n, %)	15 (93.8)	14 (93.3)
BMI (median)	23.4	23.1
0 ECOG (n. %)	5 (31.3)	3 (20.0)
1	11 (68.8)	12 (80.0)
Time from initial diagnosis (median, m)	17.8	17.6
Time from most recent disease progression (median, m)	1.0	1.0
BOR CR/PR to prior line (%)	6.3	33.3
BOR SD to prior line (%)	37.5	26.7
BOR CR/PR/SD to prior line (%)	43.8	60.0
Tumor M1 stage at study entry: N (%)	14 (87.5)	14 (93.3)
Pancreaticoduodenectomy	0 (0.0)	1 (6.7)

PDAC patients progressing on or after 1st line standard of care	1:1	Experimental arm CM24 + nivolumab & Nal-IRI/5FU/LV n=16
chemotherapy Randomized n=31		Control arm Nal-IRI/5FU/LV n=15

Safety- well tolerated

	Nal-IRI/5FU/LV
Grade ≥3 TEAE	Experimental (n=16) N (%)	Control (n=15) N (%)
Neutropenia	2 ( 12.5)	0 ( 0.0)
Diarrhea	4 ( 25.0)	1 ( 6.7)
Fatigue	2 ( 12.5)	0 ( 0.0)
Anaemia	0 ( 0.0)	0 ( 0.0)
Nausea	1 ( 6.3)	0 ( 0.0)
Vomiting	1 ( 6.3)	0 ( 0.0)
Thrombocytopenia	0 ( 0.0)	0 ( 0.0)
White blood cell count decreased	0 ( 0.0)	0 ( 0.0)

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Phase 2 Efficacy Proof of Concept demonstrated: Consistent efficacy across all endpoints

• 19% reduction in risk of death (HR=0.81) and 25% reduction in the risk of progression or death (HR=0.75)

• Prolongation of 2.3 months in median overall survival and 1.9 months in median progression-free survival

• 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

Post-hoc Phase 2 Biomarkers Analysis

· Represents a subgroup · Represents a subgroup · Support the rationale of the CM24/nivolumab of 52% of patients of 80% of patients combination · Consistent with CM24 · Suggests multifaceted MoA and the crosstalk MoA in targeting · Highlights potential in of the tumor with the CEACAM1 to modulate disease settings where TME and the whole immune evasion and immuno-oncology is less NET activities effective body	Patients with either Serum CEACAM1 or tumor CEACAM1+	Patients with either serum CEACAM1 or MPO (NET marker)	Patients with both tumor CEACAM1 and PD-L1 CPS

Post-hoc analysis in serum or tumor CEACAM1 enriched patients Significantly improved OS, PFS

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% 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%)

CEACAM1*Tumor cell H score 115-275 or Serum CEACAM1 6K-15K pg/mL

Results in serum CEACAM1 or MPO enriched patients Significantly improved OS, PFS

Statistically significant results in patients with baseline serum CEACAM1 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%)

Overall Survival

Combination of CEACAM1 and PDL1 as predictive biomarkers

Opportunity to treat patients currently not eligible for PD1 inhibitors

Statistically significant results for patients with High CEACAM1 (Hscore>100) and Low PDL1 (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

Planned 2nd & 3rd line PDAC Phase 2b study design

To demonstrate enhanced efficacy in enriched population and contribution of parts

• 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

NT219: Small Molecule Degrader of IRS 1/2 and Blocker of STAT3

Recurrent/Metastatic Head & Neck Cancer (R/M SCCHN)

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

Innovative MOA	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 cells
Robust preclinical package	· Outstanding efficacy in various PDX models in monotherapy and in combination • Potential in EGFRi, MAPKi and ICI resistant cancers
Clinical Stage	· No DLTs in monotherapy or in combination · Early clinical proof-of-mechanism • Activated IGF1R and STAT3 identified as potential predictive biomarkers RP2D determined at 100 mg/kg, Phase 1 concluded. Phase 2 initiated
Broad Market Potential	• 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
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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

NT219: Activity in mono and combo dose escalation

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)
• •
• · 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 50mg/kg dose of NT219 with cetuximab:

• Significant differences in the activated pIGF1R and pSTAT3 were revealed in the 2 responders (PR) compared to the 2 nonresponders (PD), verified in the 100mg/kg cohort.

Numbers under horizontal line designate NT219 dose in mg/kg; P = HPV positive; N = HPV negative

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 non-responders (PD,SD)
• · The findings at the 50mg/kg were verified at the 100mg/kg dosed patients

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

Purple Biotech develops promising first-in-class drug candidates to treat cancers with high unmet medical need

Leadership Team

Appendix A | CAPTN-3

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 IFNy release > 150-fold
  • Safety factor #2: In the absence of 574-expressing cancer cells, the non-capped variant showed a decreased IFMy release "50-fold

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Appendix B | CM24

CEACAM1 Plays a Key Role in Cancer Biology

PURPI

02| IMMUNE CELLS/ оз | IMMUNO-ONCOLOGY 01 | ADHESION IMMUNE EXCLUSION Tsuzuki, 2020 Horst, 2011 Blumberg, 2015 ល្វិត

ប្រិស្វាន់ Oncogene nature "CEACAM1 creates a pro-angiogenic "Immune-checkpoint molecules on "CEACAM1 regulates tumor microenvironment that regulatory T-cells as a potential TIM-3-mediated tolerance and therapeutic target in head and neck supports tumor vessel maturation" exhaustion" squamous cell cancers" Shively, 2013 Ferri, 2020 Tsang, 2020 @ ™Journal』
Immunology Cancer Biotherapy&&
Radiopharmaceuticals Experimental "Neutrophil extracellular trap-"[Blockade] enhances natural "CEACAM1 regulates Fas-mediated associated CEACAM1 as a putative killer cell cytotoxicity aqainst apoptosis in Jurkat T-cells via its therapeutic target to prevent tumor cells through blockade of the interaction with в-catenin" metastatic progression of colon inhibitory CEACAM1 / CEACAM5 carcinoma" immune checkpoint pathway"

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Confidential

CM24 binding/efficacy can be predicted by MPO levels

CM24 Reduces Tumor Burden & Synergetic with α-PD-1

Phase 1 Dose Escalation Interim Results CM24 is Safe and Well Tolerated in Combination with Nivolumab

Study Design

• 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.

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%).

		Grade
AE Term	Total	1	2	3	4/5
Diarrhea	5	4		1
Abdominal pain	4	1	3
Fever	4	2	2
Headache	4	3	1
Fatigue	4	4
Nausea	3	1	2
Creatinine increased	3	2	1
Hypokalemia	2			2
Dyspnea	2	1		1
Constipation	2	2
Cough	2	2
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	1			1

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)

Median age, years (range)		65 (49-76) Prior Lines of Therapy, n (%)
Sex, n (%)		1	2 (18%)
Male	5 (45%)	2	9 (82%)
Female	6 (55%)	Diagnosis , n (%)
Ethnicity, n (%)		Pancreatic cancer	8 (73%)
Not Hispanic or Latino	10 (91%)	Papillary Thyroid cancer	1 (9%)
Hispanic or Latino	1 (9%)	Colorectal cancer	2 (18%)
Race, n (%)		Median Time from Initial Diagnosis months (range)	23 (11-73)
White	10 (91%)	ECOG, n (%)
Black or African American	1 (9%)	0	7 (64%)
		1	4 (36%)

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: after 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.

PREDOSE

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Confidential

CM24 Phase 1 Dose Escalation Results Encouraging 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% Cl 2.0-11.1) for 11 PDAC patients

Appendix C | NT219

NT219 targets 2 critical signalling pathways simultaneously leading IRS1/2 to degradation and blocking STAT3

Novel MOA: IRS Degradation By NT219 Blocking IGF1R-AKT Pathway¹

Novel MOA Signal Transducer and Activator of Transcription 3 (STAT3) Înhibition

• 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 STAT3 signaling pathway has emerged as a promising therapeutic strategy for numerous cancers

NT219 demonstrates a durable and dose-dependent suppression of STAT3 tyrosine phosphorylation, affecting both the tumor cells and the tumor microenvironment.

Zou, S., Tong, Q., Liu, B. et al. Targeting STAT3 in Cancer In py. Mol Cancer 19, 145 (2020). https://doi.org/10.1186/s12943-020-01258-7

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NT219 re-sensitizes a.PD1-refractory models and restores sensitivity to EGFRi

Head & Neck Cancer Recurent/metastatic squanous care (R/M SCHN) metastasi, patient progressed
chemoradation, several chembrapies and pembrunal, Tretments on de Janer - Imery

Non-small cell ung cancer (NSCLC) Exon 19 deletion EGFR and T790M, biopsy of bone marcov metatasis, patient previously
progressed on afatinib and Osimertinib 5 mg/kg, MT219

52 NT219 combination with α PD1 achieves significant reprograming of the TME NT219 and PD1 combination converted immuno - suppressive TME to immuno - reactive • Immune profiling of the ICB - resistant melanoma tumors following treatment of the mice with the NT219 + αPD1 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 (% CD8 + GZMB + ) Activated NK cells (% NK1.1 + GZMB + ) NT219+ PD1 leads to a significant increase in cytotoxic effector cells (T & NK cells) NT219+ PD1 leads to a significant reduction in myeloid derived suppressor cells (MDSC) % Mo - MDSC (out of CD45 + ) % Gr - MDSC (out of CD45 + )

Selected Publications

NT219 inhibits the IRS to ß-Catenin pathway and synergizes with 5FU to suppress CRC tumor growth in mouse brain

overcomes chemo-resistance, and inhibits LS-513 cell viability and tumor growth in intracranial model.

AACR Anual Meeting, April 2021, AACR Virtual Special Corference on Epigenetics and Metabolism, Oct 2020, Ido Wolf, MD, Head of Oncology Division, Tel Aviv Sourcsky Medical Center

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Market Opportunity

Recurrent or Metastatic Squamous Cell Carcinoma of Head and Neck (R/M SCCHN)