Purple Biotech Ltd.

Regulatory Filings • Jul 21, 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 July 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 July 19, 2024, Purple Biotech Ltd. (the "Company" or the "Registrant") is announcing that it 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 July 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) and the Registrant's Registration Statement on Form F-1 filed with the Securities and Exchange Commission on October 30, 2023 (Registration file number 333-275216), 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.

July 19, 2024 PURPLE BIOTECH LTD.

By: /s/ Lior Fhima

Lior Fhima Chief Financial Officer

| 1 NASDAQ/TASE: PPBT July 2024 CORPORATE PRESENTATION

Forward-looking Statements and Safe Harbor

Certain statements in this presentation that are forward-looking and forward-ooking statements within the meaning of the safe harbor povisions of the Private Securities Litigation Refern Act of 1995. Such forwards include, but are not inited to, statements of historial fact, and may be ilentified by words schar "beleve", "sheed", "plan", "nay", "should", "might", "seek", "will", "project", "topinine" or "anticipat" or their negatives or various of these word or other compansion by the fact there statements on on relate stickly to historial matters. You should not plance on these forwards, which are not glarantees of fiture performance. Forwards reflect our curent views, expectations, belief or intentions with respect to fitture evers, and are subject to a number of assumpti involve known and unknown iss, nany of while as well as well as uncertaintes and other factors that news, performance or achievenents of be significanty differant from any finance or achievements expessed or implied by the forward-looking statements. Important factors that could cause or contribute to such differences include anong others, risks relains, stategies and objectives of nanzement for fiture opentions; poduct development for NT2.99, CM24 ach sage therapentic candidates could potentially lead to and subject to hights significant isks, particularly with respect on joint development collaboration, the fact that doughent and commercialization involves a legthy and expense; our ability to successfuly develop and commercialize our phamacetical poduct; the expense, length, progess and results of any changes in regultion and legistation that could affect the pharmacutical industry, the diffically in reeving the regulatory approvals neessary in order to commercialize of predicting actions of the U.S. Food and Drug Administration or any other applicable regulator of phamacentical products; the reglatory environment and regimes in the countries in which ve operate; the meetting survounding the actual maker reeption to our phamaceuical product one cleared for market; the introduction of competing products; patents obtained by competior; dependence of our patents and other protections for ability to obtain maintant defend issued patents; the commencement of any patent interference or infringenent on infringenent on patents, and or ability to preval, obtain a favored and the exposure to lingation, and the exposure to lingtion, and or regulators actions; the inpect of the economic public heath, policial and security situation in which ve nar opente or obtain approvals for our products or our products or our pusiness and other factors that are discussed in our Amal Report on Form 20-F for the year end the U.S. Securities and Exclange Commission ("SE"), including on cautionary discussion of isks and uneraining and Annual Reports. These are factors that we believe could case our actual results to differ materially from expected resuls. Other factors besided also adversely affect us. Any forward-boking statener in this press reless speaks only as of the date witch it is made. We disclaim any intention or obligation or public or revise any forward or other information contained herin, whether as a result of new information, fiture events or otherwise, except as required by applicable law. You 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

• Multiple data read-outs expected in 2024
• · Two First-in-Class clinical stage drugs
• · A preclinical tri-specific immuno-engagers platform
• Lean & global operation
• Cash runway into 1Q25 .

Purple Biotech (NASDAQ/TASE: PPBT)

As of March 31, 2024

• ADS Outstanding: 26.6 M
• Cash Balance: \$10.8 M
• Additional \$2 M raised in July 2024 .

Strong position to reach short and mid term value creating clinical data catalysts

A pipeline dedicated to advancing oncology therapies

| 4

Project	Target	Indications	Development Stage			Value Drivers
			Pre-Clinical	Phase I	Phase II	Phase III
CM24	CEACAM1 mAb	Pancreatic Cancer (+nivolumab * +SoC)					* Phase 2 interim analysis 2H24 * Phase 2 top line results 2H24
NT219	STAT3xIRS1/2 Dual Inhibitor	Solid tumors (monotherapy) Head and Neck ಹ Colorectal Cancer (+Cetuximab)					* Initiation of Phase 2 2H24
IM1240	CD3x5T4xNKG2A Tri-specific Ab	Solid Tumors
		*Clinical collaboration and supply agreement with: (1) Bristol Myers Squibb"
		Multiple data read-outs expected in the next 12 months

Advancing First-in-Class Oncology Therapies

CM24: an α-CEACAM1* mAb

Lead indication: Pancreatic Ductal Adenocarcinoma (PDAC)

*Carcinoembryonic Antigen Cell Adhesion Molecule

CM24: a new multi-functional CEACAM1inhibitor

CM24 MOA (#1) lmmune check point inhibitor

Concer Inmund Innunother 2010, Ortenberg et all, 200, 2009, U, 2003, Hung, 2015, Acharyo N, et d. Immother ppy Onr 8:e911-22, 2000, Gersel, D. et | 7 enic tumor n

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

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

• · CM24 binds to CEACAM1 on NETs , inhibits NET-induced cancer cell migration, and reduces NET levels in patient's serum
• · 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

Large Market Opportunity in Pancreatic Cancer

• Pancreatic Cancer accounts for ~60K new cases/year in the US alone; with a 5-year relative survival rate of 12%4
• Immuno-oncology approaches have been limited to patients with high microsatellite instability (MSI-H) or high tumor mutational burden (TMB-H)
• 5-year overall survival rate with chemotherapy in 2nd line patients is 3%4
• Two main interchangeable regimens are used worldwide in 2nd line:
  • Gemcitabine/Nab-paclitaxel³: OS 7.9 months, PFS 4.3 months (weighted average)
  • Irinotecan (or Nal-IRI)/5FU/LV4: OS 6.2 months, PFS 3.1 months

CM24 opportunity in PDAC

• · CEACAM1 expression correlates with poor prognosis in Pancreatic cancer2
• · Preclinical data support significant synergy of CM24 with currently marketed IO therapies;
• Combining nivolumab with CM24 in a clinical collaboration with Bristol Myers Squibb; Purple Biotech retains all worldwide rights to CM24

1. https://seer.cancer.gov/statfacts/html/pancreas.html
2. Calinescu et al, Journal of Immunology Research 2018 ryes: experior comments on one of comers of encomments (CEAM) 5 and on bionnies) (CACA) (LE) 2002.02.2012) war el 1920.02.2012 (LED 10.02.2020) wares in Media Crooke Media Cr oi:10.1177/175883592 n A Haber R, sivele II, et al. MOOL-1 posmal includes ance. Find oveal sunival analys and characterists of one em sunivor. Eur Cateer, 2010.000 (jeja.2002.00)

Phase 2 Combination Study Design (NCT04731467)

A study of CM24 in combination with nivolumab plus chemotherapy in patients with PDAC in the 2nd line The study is conducted in 18 centers in the US, Spain & Israel Primary endpoint :

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

Additional Interim analysis: 2H24 Top line data: 2H24 Measurement of CEACAM1 and other bio-markers is ongoing

Phase 2 interim data (cut off date - May 8, 2024) CM24+nivolumab+Nal/IRI/5FU/LV sub-study

• · 31 PDAC patients were randomized to the Nal- IRI/5FU/LV- based study regimen with a median follow up of 8.3 months.
• CM24+nivolumab+Nal/IRI/5FU/LV regimen was well tolerated
  • · Most frequent Grade≥3: diarrhea (19%), fatigue (19%) and anemia (6%).
• · An analysis of the gemcitabine/nab-paclitaxel study will be performed when the data is sufficiently mature

PURPLE

Characteristic	Experimental (n=16)	Control (n=15)
Age (median)	દિદ	68
Age 265 (n, %)	8 (50.0)	11 (73.3)
Male (n, %)	10 (62.5)	8 (23.3)
Female (n, %)	6 (37.5)	7 (46.7)
Race/ white (n, %)	15 (93.8)	14 (93.3)
BMI	23.4	23.1
ECOG (n, %) 0	5 (31.3)	3 (20.0)
1	11 (68.8)	12 (80.0)
Time from initial diagnosis (median, mo)	18	18
Time from most recent disease progression (median, mo)	0.94	0.89
CR/PR/SD to prior line (%)	43.8	60.0

Phase 2 interim data (cut off date - May 8, 2024) CM24+nivolumab+Nal-IRI/5FU/LV sub-study

ારાગા

26% reduction in risk of death (HR=0.74) and 28% reduction in the risk of progression or death (HR=0.72) > Prolongation of 2.1 months in median overall survival and 1.9 months in median progression-free survival

| 13

Phase 2 interim data (cut off date - May 8, 2024) CM24+nivolumab+Nal-IRI/5FU/LV sub-study

• Higher objective response rate (ORR) (25% vs 7%)

• Higher disease control rate (DCR) (63% vs 40%)

• Consistent and continuous decrease in CA19-9 was observed

Phase 2 interim data (cut off date - May 8, 2024) Efficacy summary

Parameter	Experimental (n=16)	Control (n=15)
OS (mo, median; 95% CI)	7.72 (4.00-8.11)	5.62 (3.22 -7.89)
OS HR (95% Cl)	0.74 (0.31-1.77)
6 mo OS (%)	52.7	38.9
PFS (mo, median; 95% CI)	3.8 (1.8-5.0)	1.9 (0.9-3.6)
PFS HR (95% Cl)	0.72 (0.33-1.60)
3 mo PFS (%)	60.0	46.7
6 mo PFS (%)	19.0	10.0
ORR (%)	25.0	6.7
DCR (%)	62.5	40.0

Concordant and consistent improvement in the primary and all secondary endpoints

| 15

Interim biomarker analysis NET's marker as a potential predictive biomarker

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

• · NET-related serum MPO levels:

  • Enhanced levels were measured in >90% of the patients

  • NET-related mean MPO over 6-fold higher than healthy donors-

• Pre-dose NET-related serum MPO levels below the mean in the CM24-based therapy compared to the control suggests:

  • Median OS improvement of 3.6 mo (8.1 mo vs. 4.5 mo), HR 0.34 (95% Cl: 0.099-1.149)

NET-related serum MPO may serve as a predictive biomarker

| 16

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 2H24
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
		18

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

upl 1e56; Naolazu loki, Mapar Ghifari, Hatas Rever ine. 204; 14(2): 2827-283; Ramas etal, Charace Aranon, Clinical Great Previol, Clinical oncology 208; 35(4): 234-248. Iling 4394; Machado-Neto et al. Clinics 2018; 73;
ne 2016; 35(20):2675-80; 6Sanchez-Lopez et

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

NT219 re-sensitizes αPD1-refractory model

| 22 NT 219 combination with α PD 1 achieves a profound reprograming of the TME NT219 and PD1 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

dəl Data 2018: Headand Next Squana: Opertunity Aralysi and Forecast to 226; Internal best current estimates of patient umbers based on external research, major plobal errito

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

| 24

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

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

| 25

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

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 mitigate cytokine release syndrome and provide a wide therapeutic index
  • Carefully selected Tumor Associated Antigens allowing patient-centric development

CAPTN-3 Platform Technology Advantages

| 29

| 30 NK cells CD 4 + / CD 8 + T cells CD 8 + NKG 2 A + T cells NK cell activation by inhibition of HLAE - NKG2A/CD94 binding CD 4 + / CD 8 + T cells activation through CD 3 binding CD8 + NKG2A + T cells double activation through CD3 binding and NKG2A - HLA - E axis blocking 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 αCD3 and αNKG2A arms in suppressing 5T4*NCSLC Patient-Derived Explant (PDE)* at 10nM concentration

* E wir other tores reserce inn ring mark the Merelinter of minne et linns, and mane de aron, man her elenger, para her aller die are kaner and be since and be since and on representing no viable ancer cells. The and (cell death) score of response (Response) using proprietary artificial intelligence (Al) algorithm (Curesponse).

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

| 33 5T4: a Novel Target in Oncology 5 T 4 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

• Multiple data read-outs expected in 2024
• · Two First-in-Class clinical stage drugs
• · A preclinical tri-specific immuno-engagers platform
• Lean & global operation
• Cash runway into 1Q25 .

Purple Biotech (NASDAQ/TASE: PPBT)

As of March 31, 2024

• ADS Outstanding: 26.6 M
• Cash Balance: \$10.8 M
• Additional \$2 M raised in July 2024

Strong position to reach short and mid term value creating clinical data catalysts

| 35 Contact Us: ir@purple - biotech.com THANK YOU

Appendix A | CM24

CEACAM1 Plays a Key Role in Cancer Biology

02| IMMUNE CELLS/

IMMUNE EXCLUSION

01| ADHESION

URPLE

Horst, 2011	Tsuzuki, 2020	Blumb
Oncogene		117
"CEACAM1 creates a pro-angiogenic tumor microenvironment that supports tumor vessel maturation"	"Immune-checkpoint molecules on regulatory T-cells as a potential therapeutic target in head and neck squamous cell cancers"	"CEA TIM-3 exhau
Ferri, 2020	Tsang, 2020	Shivel
4 Immunology "Neutrophil extracellular trap- associated CEACAM1 as a putative therapeutic target to prevent metastatic progression of colon carcinoma"	Cancer Biotherapy. "[Blockade] enhances natural killer cell cytotoxicity aqainst tumor cells through blockade of the inhibitory CEACAM1 / CEACAM5 immune checkpoint pathway"	"CEAl apop interc

03 | IMMUNO-ONCOLOGY

erg, 2015

ture

CAM1 regulates 3-mediated tolerance and ustion"

ly, 2013

xperimental

ell Research

CAM1 regulates Fas-mediated tosis in Jurkat T-cells via its action with в-catenin"

| 37

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%). .

AE Term	Total	Grade
		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

| 39

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) on with nivolumab (480mg) in cor

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.

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

| 45 0 200 400 600 800 1000 1200 0 5 10 15 20 Tumor volume (mm 3 ) Days following treatment initiation Control (n=3) NT219 (n=3) Keytruda (n=3) Keytruda + NT219 (n=3) Autologous PBMCs ( 2.1 M/mouse) NT 219 Re - sensitizes Tumors Refractory to α - PD 1 PDX Model Humanized PDX of GastroEsophageal Junction (GEJ) Cancer (refractory to pembrolizumab) Drug Pembrolizumab (Keytruda®) * Double autologous model - Tumors & PBMCs are from the same patient (#RA 236 ) | Keytruda - 6 mg/kg IP, NT 219 - 60 mg/kg IV

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.

Simultaneous Blockade of STAT3 and AKT Pathways are Required to Overcome Resistance to EGFRi

Selected Publications

NT219 Suppresses β-Catenin activity in CRC Cells and Inhibited CRC Brain Metastasis

Colon cancer LS-513 cells overexpressing IRS2 demonstrate enhanced ß-catenin activity. Targeted inhibition of IRS2 by NT219 or IRS2-SH RNA, suppresses the increased ß-catenin activity and inhibit LS-513 cell viability. Combination of 5-FU and NT219 significantly inhibited the growth of CRC turnors in brain, using intracranial model anice survival.

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

NT219 | Highly effective anti cancer activity exhibited by NT219 Pancreatic Cancer in combination with Gemcitabine in Combination Pancreatic cancer (Patient A) PDX Pancreatic cancer (Patient B) PDX with Gemcitabine 3.0 Tumor volume (cm³) 로 선 일 업 2.0 Tumor volume (cm³) ​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​ (n=15) NT219 (n=7) ដ ដ +NT219 0.9

0.6 -81 03
0 PDX model NT219 (n=5) Days o 5 10 15 20 20 25 30 Dav 10 15 20 0 Pancreatic Cancer Pancreatic cancer (Patient C) PDX Pancreatic cancer (Patient D) PDX Tumor volume (cm³) នដកដដ 1.4 Tumor volume (cm³) 1.2 1.0 0.8 0.0
0.4 0.6 Drug ﻪ.0 ﺍ 9 (n=5) Gemcitabine (Gemzar®) 02
0 0.2 (n=5) NT219 0 1 Days 0 5 10 15 20 10 | 50

RNA Sequencing| Reduced expression of IRS1, Ki67, FOXM1 & TGFb is 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% 17% Control NT219 Gemzar Gemzar Pancreatic Cancer Control NT219 Gemzar Gemzar +NT219 +NT219 FOXM1 TGFbeta (EMT Driver) 01% Drug Gemcitabine (Gemzar®) Gemzar Control NT219 Gemzar Control NT219 Gemzar Gemzar +NT219 +NT219

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

NT219 overcomes resistance to KRASG2D inhibitors and synergizes with MRTX1133 to combat pancreatic cancer

URPLE

Higher sensitivity of mKRAS(GI2D) resistant PDAC with MRTX133. a MRTX133-resistant PDC clone was eveloped. Inhibito of mknos 6120.
sensive (APC-MRTX1133-R) by NT21 (2D cell p monotherapy and in combination with MRTX1133 in colory formation and resistant PDAC cell ines (B). Synergiste effect (ClcL) of NT219 and MRX1133 ws 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

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