Interleukin-12 (IL-12) KOL Roundtable NASDAQ: PDSB | April 21, 2023

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The foregoing review of important factors that could cause actual events to differ from expectations should not be construed as exhaustive and should be read in conjunction with statements that are included herein and elsewhere, including the risk factors included in the Company’s annual and periodic reports filed with the SEC. The forward-looking statements are made only as of the date of this press release and, except as required by applicable law, the Company undertakes no obligation to revise or update any forward-looking statement, or to make any other forward-looking statements, whether as a result of new information, future events or otherwise. Versamune® is a registered trademark, and Infectimune™ is a trademark of PDS Biotechnology Corporation.KEYTRUDA® is a registered trademark of Merck Sharp and Dohme LLC, a subsidiary of Merck & Co., Inc., Rahway, NJ, USA.

Disclaimer PDS Biotech is hosting this roundtable Each panelist is speaking at the request of PDS Biotech Information presented is consistent with FDA guidelines

Introducing our Panel Dr. James Gulley Co-Director of the Center for Immuno-Oncology National Cancer Institute Dr. Jeffrey Schlom Co-Director of the Center for Immuno-Oncology National Cancer Institute

Today’s Agenda 5 Welcome and Introductions Dr. Lauren V. Wood History of IL-12 and NHS-IL12/PDS0301 Dr. James Gulley Preclinical and Mechanistic Studies of NHS-IL12/PDS0301 Dr. Jeffrey Schlom Clinical Studies of NHS-IL12/PDS0301 Dr. James Gulley Panel Discussion Moderated by Dr. Lauren V. Wood Closing Remarks Dr. Lauren V. Wood

History of IL-12 and NHS-IL12 / PDS0301 Dr. James Gulley

Investigations elucidate the mechanisms of IL-12 anti-tumor activity Modified from Trinchieri G, Nature Reviews Immunology 2003 DC IL-12 Antigen processing & presentation

1994: Early clinical development of IL-12 Day 1 Test dose 15 Cycle 1 19 35 Cycle 2 40 Tumor measurement 50 Schema of Phase 1: Day 1 Cycle 1 (dosed at MTD) 5 Schema of Phase 2: 500 ng/kg defined as the MTD Explanation: Mouse and monkey data show that the ‘test dose’ in the phase one trial reduced the toxicity of subsequent daily administrations – clinical trials allowed to resume… Severe toxicity in all patients; two patient deaths; trial stopped – Source: Leonard J et al, Blood 1997, Atkins M et al, Clin Ca Res 1997

IL-12 de-sensitization in patients is associated with counter-induction of IL-10 The first dose of IL-12 increases production of Th1 cytokines such as IFN-γ and TNF-α Frequent, repeated dosing was associated with declining IFN-γ and TNF-α levels, and a persistent elevation of the Th2 cytokine, IL-10 IL-10 is a negative regulator of IL-12 activity Repeated administration also increased serum levels of soluble IFN-γ receptor IL-10 1st dose 7th dose IFN-γ Source: Portielje J, Clin Can Res 2003

After well over a decade in the clinic, recombinant IL-12 has failed due to limited efficacy and toxicity Phase 2 Selected Phase I Limited efficacy observed in RCC and melanoma Promising activity against lymphomas Immunomodulatory effects clearly demonstrated Toxicities problematic, tolerability improved with s.c. delivery Frequent, repeated dosing causes a de-sensitization effect that limits efficacy…

Re-thinking IL-12 immunotherapy A strategy for success with NHS-IL12 (PDS0301): NHS-IL12 targets IL-12 delivery to the tumor, increasing exposure at the tumor site while reducing systemic exposure Further improved tolerability due to the reduced potency of NHS-IL12 NHS-IL12 is a large macromolecule (~250 kDa) with a longer PK than rIL-12, providing efficacious exposure with a single s.c. dose, eliminating the need for frequent dosing Administration by s.c. route will promote lymphatic absorption of the large NHS-IL12 molecule, promoting IL-12 effects at draining lymph nodes prior to systemic distribution Monitor the IL-10/IFN-γ axis to guide the establishment of optimal dose schedules in the clinic

NHS-IL12 - Molecule Overview Molecule Composition M9241 (NHS-IL12) is an immuno-cytokine comprised of two IL-12 heterodimers each fused to one of the H-chains of the IgG NHS76 (fully human) antibody It is a complex molecule with several glycosylation sites IL-12 has been genetically modified to eliminate a proteolytic cleavage site (p40 clipping resistant) The junction region between the IL-12 and NHS76 has been de-immunized. Molecule Characteristics NHS76 targets regions of tumor necrosis where cell membrane integrity has been lost and DNA has become exposed. It has affinity for both single- and double-stranded DNA Tolerability is further increased by administering NHS-IL12 by the s.c. route of administration to achieve a slow, sustained release into the bloodstream and enhance lymphatic absorption No ADCC or CDC activity in vitro

MOA: Innate & Adaptive Immunity Driving Force Distinct Mechanisms for IL-12 as a Tumor Targeting Therapy Induces differentiation of naïve CD4+ T-cells to the Th1 phenotype Increases the proliferation and lytic capacity of CD8+ cytotoxic T cells and NK cells Promotes IFN-γ production via NK & T-cells Increases the production of IP-10 (interferon-inducible protein 10) and MIG (monokine induced by interferon gamma) which then mediates an anti-angiogenic effect Enhances antigen-presentation through paracrine upregulation of MHC class I and II expression Source: Lasek et al 2014

Effector programing of CD8+ T-cells dependent on APC in TME CD8+ T cells in tumor-draining lymph nodes maintain a TCF1+ stem-like program Tumor-specific CD8+ T cells migrate to the tumor in the stem-like state CD8+ T cells only acquire the canonical effector program within the tumor Effector program acquisition requires co-stimulation in the tumor microenvironment Source: Prokhnevska…Kissick et al. CD8+ T cell activation in cancer comprises an initial activation phase in lymph nodes followed by effector differentiation within the tumor. Immunity Dec 2022

Kinetic Analysis of Tumor Localization Following s.c. Administration of AF750-labeled NHS-muIL12 and BC1-muIL12 15 chTNT is a mouse/human chimeric Ab 131I-chTNT is a targeted radiotherapeutic Image at right shows biodistribution of 131I-chTNT in a patient with lung cancer. 131I-chTNT is licensed in China for advanced lung cancer treatment NHS-76 is a fully human 2nd generation TNT antibody 131I-chTNT targeting to lung tumor

Preclinical and Mechanistic Studies of NHS-IL12/PDS0301 Dr. Jeffrey Schlom

Components of Effective Cancer Immunotherapy Source: Schlom and Gulley. JAMA, 2018

Potential of IL-12 as an anti-cancer therapy: Bridges host innate and adaptive immunity Produced by activated APCs (macrophages, DCS, neutrophils, B cells) Drives Th1 differentiation of helper T cells Promotes IFN-γ production via NK & T cells Increases proliferation and lytic capacity of NK, NKT, and CD8+ T cells Stimulates further IL-12 production in DCs & enhances antigen presentation Upregulates IP-10/CXCL10 & MIG/CXCL9 - mediate an anti-angiogenic effect - drive infiltration of CD8+ T cells Clinically, recombinant human IL-12 has a narrow therapeutic index and its systemic administration can result in significant toxicity Image: Del Vecchio, et al. Cancer Res, 2020 Exploiting Immunotherapy Combinations With NHS-IL12/PDS0301

Tumor Localization Kinetics of AF750-labeledNHS-muIL12 and BC1-muIL12 (sc) MC38 LLC Antitumor Effect of NHS-muIL12 vs. muIL12 (sc) Fallon…Schlom, Greiner. Oncotarget, 2014; Greiner…Schlom. Immunotargets Ther., 2021

The Combination of PDS0101, NHS-IL12 and Bintrafusp alfa Reduced Tumor Volume and Increased T-cell Clonality in TC-1–bearing Mice Source: Smalley Rumfield…Schlom, Jochems. J Immunother Cancer. 2020

PDS0301 (NHS-IL12) Accumulates in Tumors and Promotes PDS0101 Induced CD8 and CD4 T Cell Infiltration and Expansion in Tumors – Maximum T Cell Accumulation in Tumor with All Three Agents 21 PBS Control PDS0301 (NHS-IL12) PDS0101 vaccine PDS0101 + PDS0301 PDS0101 + PDS0301 + checkpoint inhibitor

Hypothesis: Necrosis-inducing Agents Will Increase NHS-IL12 Targeting to the Tumor and Increase Immune Activation Day 17 Docetaxel causes necrosis in a dose-specific manner Tumoral NHS-IL12

Anti-tumor Activity of Docetaxel + NHS-IL12

Docetaxel and NHS-IL-12 Combination Therapy Independent of PD-L1 Tumor Expression MC38-PD-L1 KO: MC38 cells were co-transfected recombinant Cas9 and a RNA targeting murine PD-L1 PD-L1 negative cells were cloned and used in subsequent studies Model of Primary Checkpoint Resistance Cells made and characterized by Dr. Duane Hamilton

FDA-approved HDACi Indication Vorinostat Cutaneous T cell lymphoma Romidepsin Cutaneous & peripheral T cell lymphoma Belinostat Peripheral T cell lymphoma Tucidinostat Cutaneous T cell lymphoma Panobinostat Multiple myeloma HDACi in solid tumors Exploiting Immunotherapy Combinations With HDAC Inhibition Source: Hontecillas-Prieto,et al. Front Genet., 2020

Exploiting Immunotherapy Combinations with NHS-IL12 ABSTRACT

Days Post-Tumor Implant Tumor Volume (mm3) EMT6 (BrCa) NHS-IL12 PBS ENT CR: 0/5 1/7 0/7 3/7 7/7 0/7 Days Post-Tumor Implant Tumor Rechallenge Survival Kristin Hicks ENT+NHS-rmIL12 rmIL-12 ENT+rmIL-12 Entinostat plus NHS-IL12 Source: Hicks…Schlom, Gameiro. Nat Commun, 2021 Exploiting Immunotherapy Combinations with NHS-IL12

79% TGI: 100% 63% Cures: 40% 100% 20% Can NHS-IL12 Plus Entinostat Overcome αPD-1/-L1 Refractory Tumors Due to Defects in APM/IFNγ Signaling? Source: Minnar...Schlom, Gameiro. J Immunother Cancer, 2022

M2 to M1 shift Activated CD8+ TILs Increased CD8/Tregs TC-1/a9 CMT.64 RVP3 TC-1/a9 TME NHS-IL12 Synergizes with Entinostat to Suppress αPD1/αPDL1 Refractory Tumors

Components of Effective Cancer Immunotherapy Source: Schlom and Gulley. JAMA, 2018

Clinical Studies of NHS-IL12 / PDS0301 Dr. James Gulley

Source: Clinical Cancer Research, 2019 Tumor targeted cytokine (binds DNA in areas of necrosis) Demonstrated safety and biologic activity MTD 16.8 mg/kg s.c. every 28 days NCI Phase 1: First in Human (FIH) Study NCT01417546

NCI Phase 1: FIH Study Phase I Study Design (Open Label) Assess the safety, PK and immune impact 3+3 dose-escalation in solid tumors (SAD & MAD portions) Dosing Schedule: Q4W s.c. administration 6 week DLT period Primary Objective MTD Secondary Objectives PK of subcutaneously administered NHS-IL12 Immunogenicity To determine immune response, including frequency of immune cell subtypes infiltrating tumor tissue (CD8 memory/effector cells, CD4 memory/effector cells, Tregs, NK cells, DCs), and activation of T lymphocytes against relevant tumor-associated antigens as measured by tetramer and/or ELISPOT analysis Dose Level* (mcg/kg) # of pts Tumor Types # of pts Treatment duration (MD), # of cycles Tumor Types 0.1 3 Kaposi, Breast, Transitional 0.5 3 CRC (n=2), Mesothelioma 1.0 4 CRC (n=4) 2.0 4 CRC (n=2), Rectal, Pancreatic 4 1, 1, 4, 5 NSCLC (n=3), Renal 4.0 3 CRC, Gallbladder, Lung 4 2, 2, 2, 9 Rectal, Pancreatic, Gallbladder, Prostate 8.0 3 Pancreatic, NEC lung, Esoph (sq) 3 3, 5, 6 CRC (n=2), Pancreatic 12.0 2 Adeno Ca (tongue), Breast 4 1, 3, 3, 14 Prostate (n=2), Thymoma, Anal 16.8 (MTD) 17 1, 1, 2, 2, 2, 2, 2, 2, 3, 4, 6 PDAC, Ovarian (n=3), Breast, Adeno Ca intestinal, Prostate (n=3), Chordoma (n=3), CRC (n=5), Cholangio Ca 21.8 6 1, 2, 2, 2, 3, 6 CRC (n=3), Rhabdomyosarcoma, Ovarian, Adeno Ca intestine 22 Total 37 Total *Doses are stated as exact dose in units (eg, mcg/kg) rather than as a percentage NCT01417546

NCI Phase 1 Study: PK Data Average PK from patients in the multidose cohort who received at least two cycles Average PK from both the single and multi-dose patients after the first cycle PK data: Trend for increased exposure with increasing dose with a high degree of inter-subject variability. New PK assay to be introduced in subsequent studies ADA testing to be conducted in Q2 2016 with new validated method NCT01417546

NCI Phase 1: INF-γ and IL-10 Response to NHS IL-12 Dose dependent systemic IFN-g release with trough levels going back to baseline Dose dependent IL-10 release with residual levels at Day 14 Average serum cytokine levels from patients in the multi-dose cohort who received at least two cycles Average serum cytokine levels from both the single and multi-dose patients after the first cycle IFNg IFNg IL-10 IL-10 NCT01417546

N=13 12 mcg/kg vs. 16.8 mcg/kg s.c. q 2 wk MTD not exceeded 11 evaluable for clinical activity 6/11 evaluable had stable disease as best response (with 5/11 having PD at first restaging) NCI Phase 1 NCT01417546

PT Dose Level (mcg/kg) Age Sex Cancer Type BOR Baseline % Change D14 vs Pre % Change D28 vs Pre IL-12 p70 (pg/ml) Non Classical Monocytes Immature NK DP NK Immature NK CD8 CM CD8 EM CD8 60 12.0 65 F Colon PD 0.3 3.8 -42 +130 -15 -10 -53 -30 67 16.8 44 F Cervical PD 0.5 4.9 -33 -18 -59 -39 -21 -37 69 16.8 64 F Cervical PD 0.7 5.5 +2 +23 70 16.8 51 F Colon PD 0.8 3.2 -46 -44 -53 +5 +4 0 71 16.8 71 M Prostate PD 0.3 6.0 -33 +13 -58 -36 -33 -44 63 12.0 35 F Cervical SD 0.5 1.1 +52 +342 +32 +22 +51 +35 64 12.0 72 M Prostate SD 1.9 2.1 +10 +211 +42 +25 +11 -7 65 12.0 56 M Prostate SD 1.7 2.2 +65 +98 +136 -21 -16 -22 66 12.0 79 M Prostate SD 1.0 3.3 +10 +516 -24 +31 +62 +49 68 16.8 54 F Vaginal SD 2.1 1.0 -32 +23 -43 +14 +20 +30 72 16.8 69 M Prostate SD 1.5 2.1 +32 +330 0 +19 -16 +57 Median PD 0.5 4.4 -33 +18 -53 -10 -21 -30 Median SD 1.7 2.1 +10 +211 0 +19 +11 +30 p-value 0.0173 0.0087 0.0087 0.0173 0.0381 0.0381 0.0381 0.0381 Patients treated with high exposure of NHS-IL12 (Q2 weeks) NCI Phase 1: Immune Status at Baseline and Early Changes in the Immune Profile After NHS-IL 12 Associated With Best Overall Response (BOR) Source: Gatti-Mays, et al. The Oncologist, 2023, Toney, et al. Int Immunopharm., 2023 NCT01417546 Low High

References: Gandhapudi SK, et al. 2019. Antigen priming with enantiospecific cationic lipid nanoparticles induces potent antitumor CTL responses through novel induction of a Type I IFN response. J Immunol. 202 (12): 3524-3536. Smalley Rumfield C et al. 2020. Immunomodulation to enhance the efficacy of an HPV therapeutic vaccine. J. for ImmunoTherapy of Cancer 8:e000612. Versamune® Platform Versamune® generates right type, potency and quantity of killer T cells

Versamune®-HPV (PDS0101) Phase 1 Clinical Trial: Confirmation of unique potential to induce rapid and strong CD4 and CD8 T-cell responses against a viral target (HPV16) 14 days post-vaccination Strong virus-specific CD8 T-cell responses were also confirmed by Granzyme-b ELISPOT (data not shown) Safe in all subjects: Mild transient vaccine site reactions without systemic toxicity 40 Source: Wood LV. et al, SITC 2019, (O19) Abstract ID 12533 Pre-treatment Post-treatment HPV-specific T-cell Response IFN-γ ELISPOT HPV-specific T-cell Response IFN-γ ELISPOT

Bintrafusp Alfa Source: Phase I: Strauss…Gulley. Clin Cancer Res. 2018

The combination of PDS0101, bintrafusp alfa and NHS-IL12 (PDS0301) resulted in tumor control in the HPV+ TC-1 syngeneic tumor model Source: Claire Smalley Rumfield et al. J Immunother Cancer 2020;8:e000612

NCI Triple Combination Study Design Patients with advanced HPV-related cancers received the combination of bintrafusp alfa at 1200 mg flat dose i.v. q 2wks, M9241(NHS-IL12/PDS0301) at 16.8 mcg/kg s.c. q 4 wks or 8 mcg/kg s.c. q 4 weeks and PDS0101 given as two separate 0.5 ml s.c. injections q 4 wks HPV genotyping was done with PCR based assays (BD Onclarity or Molecular MD) if testing not already done Population Cervical Anal P16+ oropharyngeal Other HPV-associated Endpoints Primary: ORRSecondary: safety Treatment until confirmed progression, unacceptable toxicity, or any criteria for withdrawal; treatment past progression was allowed 43

Best Overall Response Active Against Diverse HPV16 Cancers Effective Translation from Preclinical to Human: PDS0101 + PDS0301 + Checkpoint Inhibitor Shows Clinical Activity 44 *HNSCC – head and neck squamous cell carcinomas Higher PDS0301 Dose Cervical Vaginal/Vulvar Anal HNSCC* Reference: Strauss J. et al. Phase II evaluation of the triple combination of PDS0101, M9241, and Bintrafusp alfa in patients with HPV 16 positive malignancies. Presented at: American Society of Clinical Oncology 2022 Annual Meeting; June 3-7, 2022; Virtual. Abstract: 2518. Best Overall Response is defined by RECIST 1.1 Checkpoint inhibitor refractory patients Efficacy data in HPV16-positive patients: Objective response in optimal dose group (high dose PDS0301) - 5/8 (62.5%)1,2 Median overall survival (OS) is 21 months (all dose groups n=29)3 Checkpoint inhibitor naive patients Interim data: Objective response - 7/8 (87.5%)4 Percent of patients alive at median follow-up of 27 months – 6/8 (75.0%)5 Safety results (CPI Naïve and Refractory) 24/50 (48%) of patients experienced grade 3 and higher adverse events 2/50 (4%) experienced grade 4 adverse events Phase 2 Trial Correlates with Preclinical Results Demonstrating Improved Shrinkage of HPV16+ Tumors with the Triple Combination in Multiple Types of HPV-Associated Cancers

Effective Translation from Preclinical to Human: PDS0101 + PDS0301 + Checkpoint Inhibitor Shows Clinical Activity 45 *HNSCC – head and neck squamous cell carcinomas Reference: Strauss J. et al. Phase II evaluation of the triple combination of PDS0101, M9241, and Bintrafusp alfa in patients with HPV 16 positive malignancies. Presented at: American Society of Clinical Oncology 2022 Annual Meeting; June 3-7, 2022; Virtual. Abstract: 2518. Best Overall Response is defined by RECIST 1.1 Checkpoint inhibitor refractory patients Efficacy data in HPV16-positive patients: Objective response in optimal dose group (high dose PDS0301) - 5/8 (62.5%)1,2 Median overall survival (OS) is 21 months (all dose groups n=29)3 Checkpoint inhibitor naive patients Interim data: Objective response - 7/8 (87.5%)4 Percent of patients alive at median follow-up of 27 months – 6/8 (75.0%)5 Safety results (CPI Naïve and Refractory) 24/50 (48%) of patients experienced grade 3 and higher adverse events 2/50 (4%) experienced grade 4 adverse events Phase 2 Trial Correlates with Preclinical Results Demonstrating Improved Shrinkage of HPV16+ Tumors with the Triple Combination in ICI Naïve and Refractory Patients Best Overall Response Active in ICI Naïve and Refractory Patients Best Overall Response Active in ICI Naïve and Refractory Patients ICI Naive Higher PDS0301 dose ICI Refractory

NCI Publications Involving NHS-IL12 Tumor-targeted interleukin-12 synergizes with entinostat to overcome PD-1/PD-L1 blockade-resistant tumors harboring MHC-I and APM deficiencies. J ImmunoTher Cancer. 2022 Cure of syngeneic carcinomas with targeted IL-12 through obligate reprogramming of lymphoid and myeloid immunity. JCI Insight. 2022. Tumour-targeted interleukin-12 and entinostat combination therapy improves cancer survival by reprogramming the tumour immune cell landscape. Nat Commun. 2021. NHS-IL12, a tumor-targeting immunocytokine [review]. Immunotargets Ther. 2021. Efficient tumor clearance and diversified immunity through neoepitope vaccines and combinatorial immunotherapy. Cancer Immunol Res. 2019. Temporal changes within the (bladder) tumor microenvironment that accompany the therapeutic effects of the immunocytokine NHS-IL12. J Immunother Cancer. 2019. Enhanced antitumor effects by combining an IL-12/anti-DNA fusion protein with avelumab, an anti-PD-L1 antibody. Oncotarget. 2017. First-in-human phase I trial of a tumor-targeted cytokine (NHS-IL12) in subjects with metastatic solid tumors. Clin Cancer Res. 2019. A phase 1 single arm study of bi-weekly NHS-IL12 in patients with metastatic solid tumors. The Oncologist. 2023. Immune correlates with response in patients with metastatic solid tumors treated with a tumor targeting immunocytokine NHS-IL12. Int Immunopharm. 2023.

Panel Discussion

Closing Remarks Dr. Lauren V. Wood