Purple Biotech Ltd.

Regulatory Filings • Dec 7, 2024

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 December 2024

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 ☐

On December 6, 2024, Purple Biotech Ltd. (the "Company" or the "Registrant") has made available an updated Company Presentation on its website. A copy of the updated Company Presentation is attached hereto as Exhibit 99.1 and may be viewed at the Company's website at www.purple-biotech.com.

Exhibit

99.1 Purple Biotech Corporate Presentation December 2024

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.

1

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.

December 6, 2024 PURPLE BIOTECH LTD.

By: /s/ Gil Efron

Gil Efron Chief Executive Officer

Forward-looking Statements and Safe Harbor

Cortain statements in this presentation that are forward-looking and not are froward-looking statements within the meaning of the safe tarbor provisions of the Private Securities Libration Reform Act of 195. Such forwards include, but are not initied on statements of historial fact and may be identified by words said as "believe", "expec", "phon", "nould", "could", "mien", "will", "wores", "will", "wones", "continu" or their negative or transions of these words of these words of these words ober commande works or by the fact that these strictly to historial maters. You should not there under criance on these forward-looking statements, which are not guarantees of future performance. For varient view, expectations, beliefs or intentions with respect to finance vents, and are solies to a number of assumplors. involve laryon and unknown risks, nany of which as well as uncertaining and other factors that may cases our actually performance or achievements to be significants different from any fittle werk or achievents expressed or implied by the forward-looking statements. Important factors that could cause or contribue to such differences inclu annong others, isls relains, strategies and objectives of management for fiture operations, podnet development for NT219, CM24 and M1240; the process by which such vary stage therapetic candidates could potentially long and subject o highly significant risks, particularly with respect to a joint development onlaboration, the fort that drug development and commercialization in olys a lengtin outome; our ability to successfuly develop and commercialize our pharmacentiel products, the expense, length, progress and results of any changes in regulation and legistation that could affect the phamnecutical industry; the difficulty in receiving the regulator approvals necessary in order the diffically of predicing of the U.S. Food and Drue Administration or any other applieded regulator of pharmaceuted products; the regulatory environment and regimes in the countries in which we operate; the uncertainly surrounding the actual market reeption to our pharmaceutical products one cleared for market; the introduction of competiters; patents obtained by competitor; dependence on the effectivers of our patent and other products; our ability to obtain, maintain and defent issued patents; the commencement of any patent interference or infingement other against our patents, and ou dolling to preval, obtainers in any such action; and the expresse to lingtion, including patent lingtion, and or regulatory actions; the inpect of the economic, publical and security situation in Israel, the U.S. and other countries in which we may operate or our business, and oler factors that are discussed in our Annual Report on Form 20-For 1, 2023 and in our other filings with the U.S. Securities and Exchange Commission ("SE"), including our cautonary discussion of risks and uncertains und Registration Statenents and Annual Reports. These are factors that we believe our actual results of differ materially form expected results. Other fised could also adversely affect us. Any foward-looking statement in this press relese spacks only as of the date which is i made. We disclaim any intention or oblickly update or revise any forward-looking satement or other information contained bevein, whether a a result of new information, future or otherwise, except as required by applicable law You and any additional disclosures we make in our reports o the SEC, which are available on the SEC's website, https://www.sec.gov.

Corporate highlights

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

• · Two First-in-Class clinical stage drugs
• · A preclinical tri-specific immuno-engagers platform
• · Lean & global operation
• Cash runway into 1H26 .

Purple Biotech (NASDAQ/TASE: PPBT)

As of September 30, 2024

• ADS Outstanding: 1.7 M ●
• Cash Balance: \$6.3 M .
• Additional \$4.0 M raised Dec 24 .

Well positioned to advance next clinical milestones

A pipeline dedicated to advancing oncology therapies

Clinical Benefit Demonstrated for CM24 & NT219

Advancing First-in-Class Oncology Therapies

CM24: an α-CEACAM1* mAb

Significant opportunity in multiple large indications with unmet medical need

Clinical POC achieved

*Carcinoembryonic Antigen Cell Adhesion Molecule

CM24: POC of a potential CEACAM1-targeting therapy

CM24 MOA (#1) Immune modulation

CM24 MOA (#2) Blocks NET oncogenic potential through CEACAM1 blockage

· Neutrophil extracellular traps (NETs) are web-like structures involved in:

• Tumor immune evasion (1, 3)

• Tumor progression (1, 2, 6)

• Metastasis (2, 3, 5, 6)

• Cancer-associated thrombosis (4)

• · CEACAM1 is a part of the NET structure
• · NETs are present in various types of

JRPLE

cancers (pancreatic, breast, GI, etc.)

CM24 binds to CEACAM1 on NETs, inhibiting NET-related activities

ession of Colon Carcinoma. J Immunol. 2020; ted from 'Chen, Q et al. Cancers 2021, 13, 2832'); Rayes RF, a
Primed intercellular communication in cancer progression as lular Trap-Associated CEACAM1 as a Put

18

CM24 MOA (#2 cont.) Blocks NET oncogenic potential thru CEACAM1 blockage

CM24 binds to CEACAM1 on NETs CM24 Inhibits NET-Induced CM24-Nivo treatment significantly reduced the migration of CEACAM1 expressing enhanced NET levels in patient's serum cancer cells 70% C1D1 PRE- Level of MPO in patient serum AUCo.24 (migrating cancer cells/time) 8,000 7,000 (% of Pre-treatment) 6.000 5.000 4,000 3,000 p = 0.034 p = 0.037 No treat No treat Isotype CM24 C1D1 = Cycle 1 Day 1; EOI = End of CM24 Infusion; C1D15 = Cycle 1 Day 15 with NETs No NETs Melanoma cell line

• · CM24 binds to CEACAM1 on NETs , inhibits NET-induced cancer cell migration, and reduces NET levels in patients' sera
• · MPO (myeloperoxidase) is a NET marker, an integral part of the NET structure
• · In the randomized P2, NET-related MPO was found as a potential predictive biomarker for CM24-based treatment

Significant opportunity in multiple large indications with unmet medical need

• · CEACAM1 is upregulated in different cancer indications: >90% in Colon and Bladder and >70% in Lung, Gastric, breast, and other 1
• · Elevated levels of neutrophil extracellular traps (NETs) have been observed in various cancers such as Lung, Breast, gastrointestinal cancers, and others2,3
• · Strong scientific rationale and supporting clinical data

CM24 opportunity in PDAC

• · Pancreatic Cancer accounts for ~60K new cases/year in the US alone; with a 5-year relative survival rate of 12. The 5-year overall survival rate with chemotherapy in 2nd line patients is 3%4
• · Two main interchangeable regimens are used worldwide in 200 line with limited benefit, OS ranging from 6 to 8 months5,6
• · CEACAM1 expression correlates with poor prognosis in Pancreatic cancer7
• · Clinical and preclinical data support synergy of CM24 with currently marketed IO therapies

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Phase 2 Combination Study Design (NCT04731467)

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

18 centers in the US, Spain & Israel

Each cohort was a separate study Patients were randomized after assignment to chemo regiment

A substantial rate of early discontinuation in the control arm of the gemcitabine/ Abraxane regimen created an imbalance between the two arms, leading to informative censoring. Consequently, the efficacy analysis of this regimen was deemed biased and uninterpretable.

Measurement of biomarkers: CEACAM1. NET marker (Myeloperoxidase-MPO), PDL1

Primary endpoint : OS

Secondary endpoints:

OS rate @ 6 & 12 months, PFS, PFS rate @ 3 & 6 months, ORR

Phase 2 final analysis

Intent to Treat (ITT) Population demographics and patient characteristics

	Nal-IRI/5FU/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)

Phase 2 final analysis

Safety Population the most frequent related Grade ≥3 TEAEs

Grade ≥3 TEAE	Nal-IRI/5FU/LV
	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)

( The CM24+nivolumab+Nal/IRI/5FU/LV regimen was well tolerated )

Phase 2 final analysis CM24+nivolumab+Nal-IRI/5FU/LV sub-study

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

Phase 2 final analysis CM24+nivolumab+Nal-IRI/5FU/LV sub-study

• Higher objective response rate (ORR) (25% vs 6.7%)

• Higher disease control rate (DCR) (62.5% vs 46.7%)

• Consistent and continuous decrease in CA19-9 was observed

% change in tumor size

Median CA 19-9 levels

Phase 2 final analysis-Efficacy summary

CM24+nivolumab+Nal-IRI/5FU/LV sub-study

Parameter		Nal-IRI/5FU/LV
	Experimental	Control
OS (median, m; 95% CI)	7.92 (4.14, 8.02)	5.55 (3.45, 7.56)
OS HR (95% CI)		0.81 (0.38,1.71)
6m OS rate (%)	53.6	46.7
PFS (median, m; 95% CI)	3.91 (1.84, 5.13)	1.97 (0.95, 3.78)
PFS HR (95% CI)		0.75 (0.35, 1.61)
3m PFS rate (%)	66.7	46.7
6m PFS rate (%)	26.7	13.3
ORR (%)	25.0	6.7
DCR (%)	62.5	46.7

Concordant and consistent improvement in the primary and all secondary efficacy endpoints

Phase 2 final biomarker analysis data Results for pre-treatment serum CEACAM1 level

Statistically significant results in patients with pre-treatment serum CEACAM1 level between 6K to 15K:

• 79% reduction in the risk of death (HR = 0.21) and > 90% reduction in the risk of progression or death (HR < 0.1)

• Prolongation of 5.1 months in median overall survival and 2.9 months in median progression-free survival

Phase 2 final biomarker analysis Results for pre-treatment serum CEACAMI or NET marker MPO levels

Statistically significant results in patients with defined pre-treatment serum CEACAM1 or MPO levels in the study:

• 61% reduction in risk of death (HR = 0.39) and 72% reduction in the risk of progression or death (HR=0.28)

• Prolongation of 2.4 months in median overall survival and 2.2 months in median progression-free survival

Phase 2 final biomarker analysis data Results for CEACAM1 and PDL1 levels in tumors

Statistically significant results for patients with High CEACAM1 (H-score>100) and Low PDL1 (CPS ≤ 1 ) expression in tumors:

• 90% reduction in risk of death (HR = 0.1) and 81% reduction in the risk of progression or death (HR = 0.19)

• Prolongation of 4 months in median overall survival and 2 months in median progression-free survival

Advancing First-in-Class Oncology Therapies

NT219: A Small Molecule Dual Inhibitor of IRS 1/2 and STAT3

Lead indication: Recurrent/Metastatic Head & Neck Cancer (SCCHN)

NT219, a new solution to improve treatment outcome for cancer patients

Innovative MOA	· NT219 is a First-in-Class, small molecule dual inhibitor of IRS1/2 and STAT3 · Covalently binds to IRS1/2 and leads to their degradation · 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 · Uniquely positioned to tackle resistance to cancer treatment such as EGFRi, MAPKi and ICI
Clinical Stage	· No DLTs in monotherapy or in combination · Early clinical activity demonstrated · RP2D determined at 100 mg/kg, Phase 1 concluded. Phase 2 initiation 1H25
Broad Market Potential	· Opportunity to establish a Standard of Care in 2L r/m SCCHN patients · Multiple market upsides in combination with major cancer treatments · NT219 is the only IRS inhibitor available for clinical investigations
		21

NT219 blocks 2 critical signalling pathways at once

IRS1/2

• · Scaffold proteins, mediating mitogenic, metastatic, angiogenic and antiapoptotic signals from IGF1R, IR, IL4R and other oncogenes, overexpressed in multiple tumors
• · Regulates major survival pathways such as the PI3K/AKT, MEK/ERK and WNT/βcatenin
• · Activated as a feedback response to anti-cancer therapies
• IRS plays an important role in promoting a tumor-protective microenvironment, by mediating upregulation of TAMs and CAFs

STAT3

• Well-established transcription factor associated with the tumorigenic phenotype
• · STAT3 is broadly hyperactivated in many cancers, promoting proliferation, survival, angiogenesis and metastasis
• · STAT3 pathway is required for TGFBinduced EMT and cancer cell migration and invasion
• · STAT3 is a critical player in tumor immune evasion, suppressing immune stimulators and enhancing immunosuppressive factors

al Revell e L C one: P 2013 203 409, Mondoleta e 4 Circuit 2014, Mare Grile, Mar Rever E. Mal Care, 2014, 2022 2022 2022 2022 20:20 Parker at Corgane at Chicanon,
williat

NT219 restores sensitivity to EGFRi in PDX models

Lung Cancer

Non-small cell lung cancer (NSCLC) Exon 19 deletion EGFR and T790M, biopsy of bone marrow metastasis, patient previously progressed on afatinib and osimertinib

Head & Neck Cancer

Recurrent/metastatic squamous cell carcinoma of the head and neck (R/M SCCHN) metastasis, patient progressed on chemoradiation, several chemotherapies and pembrolizumab

Osimertinib 5 mg/kg, NT219 65 mg/kg, mean tumor volume at the end point, 3 mice/group;

Treatments on days 0, 3 and 10, cetuximab - 1mg/mouse, 3 mice/group; PBMCs (1.4M 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

| 24 NT219 re - sensitizes PD1 - refractory model 6 8 10 12 14 16 18 20 22 0 500 1000 1500 2000 Control α-PD-1 NT219 NT219+α-PD-1 Days post tumor challenge T u m o r v o l u m e ( m m 3 ) Days following tumor challenge PD 1 - resistant melanoma cells (FACS analysis) PDL1 expression (MFI) NT219 ( M) treatment in culture 0 1 10 NT 219 + PD 1 reverse resistant tumors NT 219 induces PDL 1 expression (n=10) (n=10) (n= 10 ) (n=10) * Collaboration with Prof. Bareli and Prof. Curran, M.D. Anderson cancer center ; presented at AACR 2023

| 25 NT 219 combination with α PD 1 achieves a profound reprograming of the TME NT 219 and PD 1 combination converted immuno - suppressive TME to immuno - reactive * Collaboration with Prof. Bareli and Prof. Curran, M.D. Anderson cancer center, presented at AACR 2023 Activated cytotoxic T cells (% CD8 + GZMB + ) Activated NK cells (% NK 1.1 + 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 CD 45 + )

First Market Opportunity

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

Targeting the unmet medical need

• SCCHN is the 6th most common cancer type ; 175k new cases/year are expected by 2024
• 1L standard of care has shifted from chemotherapy towards immuno-oncology + chemotherapy
• · < 20% of R/M SCCHN patients respond to Pembrolizumab
• Market size forecasted to >\$5b in 2030

Phase 1 dose escalation in combination with cetuximab: Well tolerated, target exposure reached, patient's responses observed

• · No DLTs reported, NT219 was well tolerated as monotherapy and in combination with cetuximab
• · Dose-proportional increase in AUC and Cmax values
• · Human Equivalent Dose exposure was reached at 50 mg/kg
• · Target engagement demonstrated in patients' biopsies
• · RP2D determined at 100 mg/kg

Post-treatment

Phase 1 Dose Escalation (cont.): Anti-tumor activity at target exposure level, 2 confirmed responses in SCCHN patients

Efficacy overview of monotherapy arm:

· 20 evaluable patients (all doses): 2 PR (confirmed-GEJ, unconfirmed-PDAC), 5 SD

Efficacy overview of combination arm in SCCHN patients *:

• · 15 evaluable patients (all doses 6, 12, 24, 50, 100 mg/kg)
• · Median follow-up of 9.4 months (95% Cl: 3.4-10.0)
• · Out of 7 treated with 50&100 mg/kg:
  • . 2 confirmed PR
    • 3 SD
    • ORR:29%, DCR: 71% .
• * Interim data analysis, cut-off date Jan 25, 2024

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

In preparation of a phase 2 study of NT219 in combination with cetuximab w/wo chemotherapy in 2L R/M SCCHN

Activated IGF1R and STAT3 as potential predictive biomarkers

Biomarker analysis at the 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 non-responders (PD)

Advancing First-in-Class Oncology Therapies

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

Lead candidate: IM1240 (CD3x5T4xNIKG2A)

A Novel Mechanism of Action Tri-Specific Antibody

• · Multi-specific biologics is an expanding class of drugs getting a lot of interest in the industry
• · After initial success in hemato-oncology, new formats are being investigated in solid tumors
• · Technology displays several distinctive features:
  • · Dual engagement of T cells and NK cells to mount an optimal anti-tumoral immune response
  • · A tumor-restricted activation through a cleavable capping system designed to provide a wide therapeutic index
  • · Carefully selected Tumor Associated Antigens allowing patient-centric development

CAPTN-3 Platform Technology Advantages

Cleavage site (

anti-NK

HSA

Cap

inti-hCD3

anti-TAA

CAP / cleavage site:

• · Safety: Activation only in the TME
• · Efficacy: better PK

αΝΚ cell arm:

· NK cell engager

· Checkpoint inhibitor Enhancement of immune response

All in one:

• · Proximity increased local concentration
• · Synergistic effect
• · Molecule size similar to mAb (~170 kDa)

Human Serum Albumin (HSA)

· Improved stability in blood circulation

αCD3 arm: · T cell engager · T cell activation Efficient anti-tumor effect

aTAA arm:

· Tumor Associated Antigen Targeted activation against tumor cells 32

| 33 Unleashing both innate and adaptive immune systems

POC: αNKG2A arm contributes substantially to tumor cell killing and synergizes with the CD3 Arm

• Tribody induces cytotoxicity at pM EC50 against NSCLC . A549 cells
• Up to 20-fold more potent than the bi-specific CD3x5T4 .
• . Cell killing validated on multiple 5T4+ cell lines (MDA-MB-231, HCT116, NCI-H226)

· Synergistic effect of the o.CD3 and o.NKG2A arms in suppressing 5T4*NCSLC Patient-Derived Explant (PDE)* at 10nM concentration

* E wive patient-derived umor explants (PDE) invested tunor fragments that retain the TME native architecture and immune cell argy tumor het one the polycative capcir) (Gol. Fealts). Frent eined ing wos calterd on Streat (o 96), free and Mac site since brocosoner on orocores on
cel violity on danceres isse accornity by

Cleavable capping leads to improved in vivo efficacy

• · Sustained tumor regressions in TNBC xenograft model (MDA-MB-231) in CD34 engrafted humanized mice
• · The Pro-Tribody, Capped-CD3x5T4xNKG2A, performed better than the uncapped variant
• PK analysis in normal mice showed 3-fold higher exposure of the capped tribody compared to the non-capped

· No change in body weight

* Study conditions: dose regimen-0.2mg/kg capped, equimolar 0.1mg/kg non capped, daily IP administration

Improved safety profile: Cytokine release is 5T4-dependent and suppressed by the cap

· The capped variant vs the non capped, showed a decreased IFNy release > 150-fold (Safety factor #1).

In the absence of 5T4-expressing cancer cells the non-capped variant showed a decreased IFNy release ~50-fold (Safety factor #2).

| 37 5 T 4 : a Novel Target in Oncology 5T4 is highly expressed on certain tumors and correlates with poor prognosis Am J Cancer Res 2018 ; 8 ( 4 ): 610 - 623 www.ajcr.us /ISSN: 2156 - 6976 /ajcr 0074519 5 T 4 is a Tumor Associated Antigen prevalent to several large indications Opportunity of patient stratification strategy ( 5 T 4 + )

Corporate highlights

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

• · Two First-in-Class clinical stage drugs
• · A preclinical tri-specific immuno-engagers platform
• · Lean & global operation
• Cash runway into 1H26 o

Purple Biotech (NASDAQ/TASE: PPBT)

As of September 30, 2024

• . ADS Outstanding: 1.7 M
• Cash Balance: \$6.3 M .
• Additional \$4.0 M raised Dec 24 .

Well positioned to advance next clinical milestones

Appendix A | CM24

CEACAM1 Plays a Key Role in Cancer Biology

03 | IMMUNO-ONCOLOGY 02| IMMUNE CELLS/ 01 | ADHESION IMMUNE EXCLUSION Horst, 2011 Tsuzuki, 2020 Blumberg, 2015 త్రి, 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 supports tumor vessel maturation" therapeutic target in head and neck exhaustion" squamous cell cancers" Ferri, 2020 Shively, 2013 Tsang, 2020 @ Immunology Cancer Biotherapy. < Experimental

Cell Research "Neutrophil extracellular trap-"[Blockade] enhances natural "CEACAM1 regulates Fas-mediated associated CEACAM1 as a putative killer cell cytotoxicity against apoptosis in Jurkat T-cells via its therapeutic target to prevent tumor cells through blockade of the interaction with 8-catenin" metastatic progression of colon inhibitory CEACAM1 / CEACAM5 carcinoma" immune checkpoint pathway"

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

• · As of March 8th, 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 ﺓ ﺍﻟ 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%).

AE Term	Total	Grade
		1	2	3	4/5
Diarrhea	5	4		1
Abdominal pain	র্যা	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 (480r

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%

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.

SCREENING FIRST VISIT - PREDOSE 2 MONTH VISIT -PREDOSE

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 B | NT219

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

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

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 Annual Meeting, April 2021, AACR Virtud Special Corference on Epigenetics and Metobolism, Oct 2020, Ido Wolf, MD, Head of Oncology Division, Tel Aviv Sourasky | 53 Medical Center

Reduced expression of IRS1, Ki67, FOXM1 & TGFb is RNA Sequencing | exhibited by pancreatic cancer treated with NT219 alone and Analysis of Tumors in combination with gemcitabine Following Treatment IRS1 Ki67 (Proliferation marker) PDX model 17% Control NT219 Gemzar Gemzar Pancreatic Cancer Gemzar NT219 Control Gemzar +NT219 +NT219 FOXM1 TGFbeta (EMT Driver) 01% Drug Gemcitabine (Gemzar®) Control NT219 Gemzar Gemzar Control NT219 Gemzar Gemzar +NT219 +NT219

NT219 suppresses cancer stem cell (CSC)-mediated resistance to KRAS02C inhibitors and synergizes with sotorasib to combat NSCLC

NT219 overcomes resistance to KRAS02D inhibitors and synergizes with MRTX1133 to combat pancreatic cancer

Higher sensitivity of mKRAS(G12D) resistant PDAC and MRTX133. a MRTX1133-resistant PDAC clone was developed. Inhibition of mKRAS G12Dsensitive (AsPC1) and resistant (AsPCI-MRTX113-R) by NT219 (2D cell prolferation) shows 8-fold lower (AJ. NT219 is effective both as monotherapy and in combination with MRTX133 in colory formation assay of sensitive and resistant PDAC cell ines (B). Synergistle effect (CCC) of NT219 and MRTX133 was demonstrated in 2D growth (C) and in spheroid 3D growth (D) of HPAC PDAC cells.

Collaborationn with Dr. Azmi, Karmanos. Presented at AACR Annual Meeting 2024

JRPLE