Corporate Life-changing science Presentation February 2021 Overview

PYC is an RNA therapeutics company with an initial focus on diseases of the

§ RNA therapeutics have come of age But their ongoing success is impeded by inefficient or toxic delivery inside cells

§ PYC’s cell-penetrating peptide (CPP) delivery platform solves this ‘delivery’ problem PYC’s competitive advantage is getting more drug safely into the target cell

§ PYC is applying this advantage to develop drugs for eye disease: an area of unmet need PYC’s lead program is the first disease-modifying therapy for Pigmentosa type 11 - a USD1- 2B p.a. target market

§ PYC’s technology scales rapidly in the eye: same delivery tech for other RNA cargoes PYC has two other defined drug programs, each with blockbuster potential, addressing Diabetic and Autosomal Dominant Optic Atrophy

§ Building on its success in the eye, PYC is expanding the application of its technology The Company’s initial focus outside the eye is on neurodegenerative diseases

2 Corporate Snapshot (ASX: PYC)

Financial Information (29 January 2021, AUD) Share Price Performance (12 months) ASX website Share price $0.14

Number of shares 3,170M

Market Capitalisation $445M

Cash $57M

Debt Nil

Enterprise Value $388M

Board of Directors Alan Tribe – Chairman Sahm Nasseri– Chief Executive Officer (USA) Dr Rohan Hockings – Chief Executive Officer (Australia) Building out a US base to complement Australian discovery hub Dr Bernard Hockings – Non-Executive Director • Early discovery and candidate proof of concept development led by PYC Australia Top Shareholders (29 January 2021) % • Pre-clinical, clinical development and regulatory engagement to be led by PYC US Alan Tribe 30.11% • Corporate HQ shifting to US through 2021, in-line with corporate development activities David Sietsma 8.96% • Broaden Board of Directors to include US membership Dr Bernard Hockings 8.41% • Evaluating most appropriate corporate development path with a base-case approach of delivering a Anthony Barton and Associates 6.10% US-listing through ADR in next 12-18mths

3 Leadership team

Executive management

Sahm Nasseri, Chief Executive Officer US Kaggen Ausma, Chief Business Officer

Extensive experience in commercial drug development Previous roles in McKinsey & Co across Strategy, with Merck, incl. product leadership, investor relations Commercial, VC and PE, and public market finance and business development. Consultant with McKinsey with CLSA Asia-Pacific & Co prior to Merck.

Professor Sue Fletcher, Chief Scientific Officer Dr Rohan Hockings, Chief Executive Officer Australia

Leading global expert and pioneer in RNA therapeutics. Experience across both clinical and commercial Co-inventor of Exondys-51, Vyondys-53, and Casimersen, roles including Private Equity, Commercial Law, commercialised by Sarepta. Prof. Fletcher leads PYC’s and Strategy, prior to joining PYC discovery team and is the co-inventor of VP-001

Advisory Board

Dr Fred Chen Professor Judy Lieberman Asc. Professor Rakesh N. Veedu MBBS (Hons), PhD, FRANZCO MD, PhD MSc, PhD, MRACI Chair Ophthalmic Advisory Board Scientific Advisory Board Member Scientific Advisory Board Member

Retinal clinician, co-inventor of Leader and pioneer in the field of Extensive expertise in basic and VP-001 and leader of Ocular siRNA, Chair in Cellular and translational research in the field Tissue Engineering Laboratory at Molecular Medicine at Boston of oligonucleotide therapeutic Children’s Hospital, Professor of development Pediatrics at Harvard Medical School 4 PYC combines World-class RNA therapy design + Revolutionary delivery technology

World-class RNA drug design specialists, leveraging Delivery technology that enables RNA drugs to Antisense Oligonucleotides reach their target inside the cell

§ Team led by Chief Scientific Officer- Prof. Sue Fletcher – co- § The single greatest challenge for RNA drugs is the ability to cross inventor of two FDA approved RNA therapeutics with others in late- the cell membrane to reach their target stage clinical development § PYC’s delivery technology is based on a unique library of Cell § RNA drugs are precision therapeutics that act on the inside of cells Penetrating Peptides, nature’s solution to safely access cells § They occupy a unique position in the pharmaceutical landscape due § Cell Penetrating Peptides safely deliver the RNA drug: to their balance of durability and titratability § i) to the cell; and § PYC has the capability to identify highly valuable targets and § ii) across the cell membrane where it can engage its design tailored RNA intervention strategies to match intended target in the cell nucleus

5 Delivery remains the rate limiting step for RNA drugs PYC’s CPPs have a competitive edge in solving this problem

Delivery technology Companies Cargoes Tech dev. stage Technologies core mechanism of action

Naturally derived cell- PMO Pre-clinical § Utilise library of natural peptide to identify penetrating peptides peptide sequence driven uptake for delivery of cargoes into the cell Chemically derived cell- PMO Phase 1/2 § Utilise chemically derived, highly charge dense penetrating peptides and/or constrained peptides to enable delivery of cargoes into the cell

Antibody conjugates ASO and Pre-clinical § Utilise an antibody to bind to a cell surface siRNA receptor and transport to traffic cargoes into the cell

Ligand conjugates ASO and Marketed § Utilise a ligand to bind to a cell surface receptor siRNA and transport to traffic cargoes into the cell

Lipid conjugates siRNA Pre-clinical § Utilise a fatty acid to bind to a cell surface receptor and transport to traffic cargoes into the cell

Exosomes/LNP siRNA, ASO, Pre-clinical § Utilise exosomes to present or deliver ASOs plasmid using the exosomes trafficking ability

Chemically modified ASO Marketed § Modify the ASO backbone chemistry to improve backbone uptake and/or efficacy

6 PYC’s CPP-PMO technology offers several advantages over other genetic therapy modalities

PYC CPP-PMO advantages Why it matters AAV gene ASO siRNA therapies • PMOs do not bind or sequester positively charged Safe delivery of drug to splicing factors as do negatively charged ASOs, nucleus hence cause lower toxicity

• PMOs have higher resistance to intracellular Durability of drug within degradation vs. other ASOs which provides potential cell for longer duration of effect

• CPP-PMO is distributed broadly across tissue— Broad distribution within critical for treating diseases affecting tissue a target tissue structure and for accessing hard to reach cells

• CPP-PMO has potential applicability to a range of Effective delivery to a target tissues and cell types vs. other delivery range of target tissues modalities (e.g., GalNAc and antibodies)

• Like other ASO approaches, CPP-PMO allows precise Precise modulation of intervention to modulate cellular pathways to treat target gene multifactorial diseases

• Like other RNA therapies, CPP-PMOs avoid risk of over- Retention of endogenous expression of proteins which can cause additional cellular control disease, esp. in diseases caused by haploinsufficiency 7 PYC is applying our technology to create life changing treatments, with an initial focus on diseases of the eye

PYC is a multi-asset drug development company

Program overview Indication and stage of development Estimated market size

Lead Organ Program Target Discovery IND-enabling Clinical Marketed selection

Eye VP-001 PRPF31 Type 11 US$1-2 billion p.a.

PYC-001 VEGF >US$5 billion p.a.

Autosomal dominant optic VP-002 OPA1 ~US$1 billion p.a. atrophy

Multiple Undisclosed Discovery pipeline Multiples of programs

CNS Multiple Undisclosed Discovery pipeline Multiples of programs

PYC has 100% ownership of PYC-001 and 90% ownership of VP-001 and VP-002 (10% ownership by Lions Eye Institute, Australia) 8 VP-001 has already demonstrated a strong preclinical efficacy signal in vivo and in patient derived models

PYC has demonstrated delivery to the target cells, And shown upregulation of the target protein, PRPF31, in Retinal Pigmented Epithelium (RPE), for 28 days in patient iPSC derived RPE pathogenic mutations in PRPF31 the mouse %D7 RPE isolate (28 days) (each patients with a different mutation) 100

Exon 7 skipping in RPE1, Day 28 in the mouse eye post IVT PRPF31 protein levels2, RPE, 5µM treatment, (n=1 per patient) 80

2.5 Day 2 Day 5 Day 12 Untreated 60 60 d Treated e t (%) 2.0 a e

* r t n u

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Anticipated disease e

19.1 g correction threshold 1.0 n a h

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5.0 F 0.0 Exon Skipping 0 0.0 Patient 1 Patient 2 Patient 3 Patient 4 Patient 5 Vehicle 1.6µg 3.2µg 6.4µg Non-penetrant Penetrant g/eye) g/eye) g/eye) µ Leadµ CPP-PMOµ 1 Day 28 post intravitreal injection in mice. A readout of drug delivery, Exon-skipping of Survival of Motor Neuron (Smn) in the mouse across 3 dose cohorts (n=12 for each dose cohort, n=4 for vehicle) 2 For anticipated disease correction threshold see ‘Venturini, G. CNOT3 Is a Modifier of PRPF31 Mutations in Retinitis Pigmentosa with Incomplete Penetrance. PLOS Genetics November 2012’ 9 See ASX Announcement 22 July 2020; 7 October 2020 Vehicle control

Full-d-HPG0031-Ext2-3'SMN1Full-d-HPG0031-Ext2-3'SMN1Full-d-HPG0031-Ext2-3'SMN1 (1.6 (3.2 (6.4 The dose dependant response shows no increasing acute toxicity in the mouse

Dose dependant increase in effect … … and no increase in toxicity markers

Exon 7 skipping, Day 7 in the mouse eye Gfap expression,dd PDayC R7 info ther G mouseFAP eye ex pression in Neural Retina at D7 (n=12) Neural Retina 0.025 3.2µg/eye .

e 0.020 v 6.4µg/eye Smn a s

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l g g g Vehicle 1.6µg 3.2µg 6.4µg Vehicleo 1.6µµg 3.2µg 6.4µ g tr µ µ n .6 .2 .4 o 1 3 6 c 1 1 1 Lead CPP-ASO le N LeadN CPP-ASON ic M M M h -S -S -S e 2 2 2 Toxicity determined by treating mouse with 1.6 micrograms of an Antisense Oligonucleotide (ASO) delivered by each peptide and then measuring retinalV stress based on tlevels of Glial Fibrillaryt Acidic Protein (GFAP).t GFAP levels have been measured after retinal harvesting from mice at day 7 post intravitreal injection and normalised to a pool of ‘house-keeping’ genes. x x x 10 -E -E -E See ASX Announcement 22 July 2020 1 1 1 3 3 3 0 0 0 0 0 0 G G G P P P -H -H -H -d -d -d ll ll ll u u u F F F VP-001 has 2 fundamental advantages over AAV-gene therapies in inherited retinal disease

Advantage of an RNA 1. RNA therapies achieve an even 2. RNA therapies retain endogenous therapy approach cellular level distribution within the control of protein expression in the retina retina

Comparison to AAV-gene AAV-gene therapy engenders a patchy AAV-gene therapy leads to a 4-5 fold increase in therapy distribution in the target tissue due to PRPF31 expression variable cellular uptake – the consequence is a highly uneven drug distribution within the “In a highly specialized and organized tissue like target tissue the retina, it is particularly important to maintain endogenous gene regulation”2

Illustration in the “the rescue provided by AAV-derived PRPF31 PRPF31 gene therapy has the potential to context of RP11 (PYC’s may be limited to certain RPE functions, induce a disease phenotype in remaining lead program) while others like the barrier function cannot viable cells through overexpression of the be rescued”1 target protein3

Implication for patients Only RNA therapies currently have There is a risk to the remaining viable the ability to rescue the global cells in an RP11 patient’s of the function of the RPE monolayer – AAV-gene therapy that is avoided with protecting patients from confounding an RNA based approach macular oedema 11 1 Brydon. E. AAV-Mediated Gene Augmentation Therapy Restores Critical Functions in Mutant PRPF31+/− iPSC-Derived RPE Cells; 2 Bacchi. N. Splicing-Correcting Therapeutic Approaches for Retinal Dystrophies: Where Endogenous Gene Regulation and Specificity Matter; 3 Farkas. M. RNA-seq guided gene therapy for vision loss PYC’s CPP-PMO has demonstrated potential outside the eye and a clear delivery advantage

CPP-PMOs demonstrate strong uptake across high value CPP-PMOs show a clear advantage over naked tissues include heart and diaphragm ASOs in delivery to ‘hard to reach’ tissues

Exon 7 skipping (%) in tissue 1, Single I.V. injection in mice, Exon 7 skipping (%) in RPE/, Single day 2 IVT injection, day 5

50 (%)

(%) 40

Smn 31 30 Smn

20

10 0 0 0 2 Exon 7 Skipping Skipping 7 Exon PS ASO PMO CPP-PMO

Exon 7 Skipping Skipping 7 Exon 10mcg/ey 1.6mcg/e 1.6mcg/e e ye ye

1 Day 2 post intravenous injection in mice. A readout of drug delivery, Exon-skipping of Survival of Motor Neuron (Smn) in the mouse tissue across 3 dose cohorts (n=2 for each dose cohort) 2 PS: Phosphorothioate backbone antisense oligonucleotide; 12 See ASX Announcement 14 October 2019 Major value catalysts in 2021 provide a strong foundation for corporate development

• VP001- lead program Multiple read-outs in 2021 across pipeline for additional Ocular programs and CNS programs (Retinitis Pigmentosa) • PYC001 and VP002 additional ocular programs • 1st CNS program expected early 2021 th th PYC001 and VP001 large PYC001 and • 4 and 5 ocular program Key internal expected in 2021 VP002 efficacy animal VP002 efficacy development Secured AUD data in patient (rabbit and data in animal VP001 IND catalysts 40M capital derived models NHP) tox models submission raise read-out (1H 2022)

4Q20 1Q21 2Q21 3Q21 4Q21 1Q22 2Q22

Potential US Potential US listing Corporate fundraising (in-line with IND development (post large submission) approach animal tox)

13 PYC is focused on delivering clinical proof-of-concept in our lead indication

PYC’s potential development pipeline in 2025 Milestones (2021 and 2022 highlighted in bold) Lead IND- Organ Program Discovery Clinical Marketed selection enabling

Ocular VP-001 Retinitis Pigmentosa type 11 § Large animal toxicity (Q1/2 2021) § IND (Q2 2022) § Human safety (H1 2023) PYC-001 Diabetic Retinopathy Revenue § Human efficacy (H1 2023 and 2024) generating § NDA/revenue generation (H1/2 2025) VP-002 Autosomal Dominant Optic Atrophy § Efficacy in patient derived models (H1 Ocular program #4 2021) § Efficacy in animal models (H2 2021) Ocular program #5 § IND toxicology/submission (H1/2 2023) § Human safety (2024) Discovery pipeline § Efficacy in patient derived models (H1 2021) CNS § Efficacy in animal models (H2 2021) Neurodegenerative disease #1 § IND toxicology/submission (H1/2 2023) § Human safety/efficacy (2023/2024) Neurodegenerative disease #2 § Multiple read-outs across pipeline for: Discovery pipeline § IP filing; § Efficacy milestones in animals and patient derived models § Safety read-outs in animals § Progression into clinical development

14 PYC’s Therapeutic Approach

15 PYC is in the right place at the right time

“In the long run, oligonucleotides are likely to become a major class of therapeutics, on par with small molecules and biologics1” Public RNA focused companies market capitalisation, USD B RNA therapy approvals

Drug RNA drug Approved 84 ASO2 1998

59 ASO 2013

43 ASO (PMO2) 2016

25 ASO 2016

11 ASO 2018

siRNA2 2018 2017 2018 2019 2020 Sep-20 ASO (PMO) 2019 Companies, # 7 8 11 12 12

siRNA 2019 Ave. valuation, USD B 1.6 3.2 3.9 4.9 7.0

1 Watts JK, Brown RH, Khvorova A. Nucleic Acid Therapeutics for Neurological Diseases. Neurotherapeutics. 2019;16(2):245-247 ASO (PMO) 2020 2 ASO: Antisense Oligonucleotide; PMO (phosphorodiamidate morpholino oligomer) are a chemical sub-class of antisense drugs; siRNA: small interfering RNA 16 Source: NASDAQ end of day quote 7 September 2020 PYC’s drug design team know how to choose the right approach for the target indication

Disease state

Exons – code for Protein Isoform A protein mRNA Pre-mRNA siRNA’s and ‘Gapmer’ ASOs can mark mRNA for ASOs can alter the exon selection degradation to prevent to change the protein. This can translation. This reduces the Intron – remove mutant sections or switch level of ‘unwanted’ protein non-coding, the protein’s function (from ‘bad’ regulatory to ‘good’)

Healthy DNA Pre-mRNA state

Protein Isoform B mRNA

Pre-mRNA

transcription splicing translation DNA pre-mRNA mRNA Protein Function

The cell transcribes the full gene – The cell then ‘cuts’ or splices the mRNA is then translated both protein coding and regulatory introns out to make mRNA by the cell into protein sequences 17 PYC’s drugs can access cells (and diseases) beyond the reach of competitive RNA technologies

The challenge for most RNA drugs The cell membrane has evolved over hundreds of PYC’s CPP-PMOs enable RNA therapeutics millions of years to keep foreign substances out to target the previously unreachable

Exon skipping (%) in mouse Retinal Pigment Epithelium/ Choroid Single IVT injection, day 5

50 40 31 30 20 10 0 0 0 PS ASO1 PMO CPP-PMO 10mcg/eye 1.6mcg/eye 1.6mcg/eye

PYC’s Cell Penetrating Peptides PYC’s proprietary Cell Penetrating Peptides (CPPs) can deliver RNA drugs, like PMOs, inside cells that are beyond the reach of competitive technologies

18 1 PS: Phosphorothioate backbone antisense oligonucleotide; PYC’s proprietary delivery platform is unique - leveraging nature’s solution to identify distinctive delivery vehicles

Microorganisms have evolved over millions of years to safely interact with the human body – PYC’s libraries leverage this pressure to screen for safe, highly effective delivery peptides

1 Genomes of microorganisms broken down 3 In vivo validation for each tissue and and expressed as short peptides cargo type – with a focus on delivery of ASOs

Smn exon skipping in mice, IV injection day 2 n=2

Screen and validate

2 Peptides screened and validated for cell-penetration properties (effective delivery to the nucleus) Created with BioRender.com 19 See ASX Announcement 14 October 2019 PYC has deep (and evolving) IP protection supporting our platform from discovery through to drug

Description Status Expiry

Libraries 2nd generation library construction and display Granted 2027

Screening Phenotypic screening of the peptide libraries Granted 2025

1st generation CPP Granted 2037 CPPs 2nd generation CPP (Ocular leads) Provisional TBD

VP-001 program lead and associated molecules PCT TBD ASOs PYC-001 and VP-002 leads and associated molecules Provisional TBD

Growing protection through IP coverage of the conjugate (CPP-ASO), new CPP’s for new targets, and new ASOs for new indications

20 Initial focus on eye disease applying CPP-PMO technology. CNS diseases next area of development

PYC is a multi-asset drug development company

Program overview Indication and stage of development Estimated market size

Lead Organ Program Target Discovery IND-enabling Clinical Marketed selection

Eye VP-001 PRPF31 Retinitis Pigmentosa Type 11 US$1-2 billion p.a.

PYC-001 VEGF Diabetic Retinopathy >US$5 billion p.a.

Autosomal dominant optic VP-002 OPA1 ~US$1 billion p.a. atrophy

Multiple Undisclosed Discovery pipeline Multiples of programs

CNS Multiple Undisclosed Discovery pipeline Multiples of programs

PYC has 100% ownership of PYC-001 and 90% ownership of VP-001 and VP-002 (10% ownership by Lions Eye Institute, Australia) 21 CPP platform has demonstrated applicability outside the eye, with no systemic toxicity

Intravenous administration of CPP-PMO(Smn) into mice Systemic toxicity markers, 48hr post 32mg/kg n=2/dose injection in mice

Lead CPP – PMO

Linker 1 Linker 2 ALT Normal Normal Liver AST Normal Normal Pathology All score 0 All score 0 Urea Normal Normal Kidney Creatine Normal Normal Pathology All score 0 All score 0

22 See ASX Announcement 14 October 2019 PYC is exploring CPP-LNP conjugates to deliver other high value cargoes to hard to reach tissues and cells

PYC is currently in ‘proof of concept’ studies for a CPP-LNP conjugate delivery system to enable the effective and safe delivery of negative charged molecules (siRNA, DNA plasmids, Cas9 and others) in collaboration with the Peer Laboratory of Precision NanoMedicine at Tel Aviv University

siRNA-induced cell death after treatment with LNP-CPP conjugates PLK-1 siRNA Control siRNA CPP Safety Efficacy Safety Efficacy Safety Efficacy

CPP CPP 120 15nM 7.5nM * * 120 120 120 120 ** 15nM3.75nM 7.5nM1.87nM 120 120 ** 100 15nM **15nM7.5nM 7.5nM 15nM 7.5nM 15nM 15nM7.5nM** 7.5nM CPP ** 3.75nM 1.87nM **

100 3.75nM 3.75nM1.87nM 1.87nM 3.75nM 1.87nM 3.75nM 3.75nM1.87nM 1.87nM CPP 100 100 100 100 100 80

80 80 80 80 80 80 100% 60 CPP Lower values viability

CPP indicates 60 60 60 demonstrate 60 60 % Cell viability% 60 40 better PYC’s CPP % Cell viability% % Cell viability% % Cell viability% % Cell viability% Cell viability% % Cell viability% with the LNP 40 40 40 untreated) to (normalized 40 efficacy 40 40 20 is not toxic (normalized to untreated) to (normalized (normalized to untreated) to (normalized (normalized to untreated) to (normalized (normalized to untreated) to (normalized untreated) to (normalized (normalized to untreated) to (normalized 20 20 20 20 20 20 0 LNP CPP-LNP LNP CPP-LNP 0 0 0 0 0 0 OVACAR8 cellsLNP were treatedCPP-LNP for 72hrs with LNPs or CPP-LNPs LNPat differentCPP PLK1-LNP-siRNA doses. Cell viability was LNP CPP-LNP LNP CPP-LNP measured by XTT assay OVACAR8 cells were treated for 72hrs with LNPs or CPP-LNPs at different PLK1-siRNA doses. Cell viability was OVACAR8 cells were treated for 72hrs with LNPs or CPP-LNPs at different PLK1-siRNA doses. Cell viability was OVACAR8 cells were treated for 72hrs with LNPs or measuredCPP-LNPs byat XTTdifferent assay PLK1-siRNA doses. Cell viability was measured by XTT assay measured by XTT assay 23 See ASX Announcement 08 August 2020 VP-001 for the treatment of Retinitis Pigmentosa type 11

24 Executive Summary – VP-001 for Retinitis Pigmentosa type 11

1. Retinitis Pigmentosa type 11 (RP11) is a large target market with no disease-modifying therapies available for patients (nor in clinical development)

2. PYC’s lead drug program (VP-001) holds the promise of rescuing progressive cell death and blindness in patients with RP11 § PYC’s delivery technology can reach the target cell following intravitreal injection - conferring a major competitive advantage over therapies requiring sub-retinal administration (in vivo model) § VP-001 engages its target and achieves the desired exon skipping effect (patient derived model) § VP-001 corrects the deficiency of the target protein once inside the cell (patient derived model) § The increase in the target protein rescues the downstream functional consequences of RP11 (patient derived models)

3. PYC’s Cell Penetrating Peptide – Antisense Oligonucleotide conjugates show no evidence of toxicity in the retina (animal models)

4. VP-001 has an attractive path to market with small clinical trials and the potential for a single pivotal study

25 OVERVIEW There are a large number of patients with Retinitis Pigmentosa type 11 who have no available treatment options

Retinitis Pigmentosa is a genetic, blinding eye disease

§ VP-001 will treat Retinitis Pigmentosa Type 11 (RP11) ‒ Severe, progressive blinding eye disease ‒ Onset between the ages of 10 and 20 ‒ Leads to blindness between 40-50 years of age § There is no treatment in market or in clinical development

RP11 represents a 1-2B USD p.a. treatment market

§ 4,000-8,000 patients in the western world § ~250,000 USD p.a. orphan drug pricing § 1-2B USD p.a. market § Straightforward and low cost sales and distribution channel

26 OVERVIEW VP-001 will serve a 1-2B USD p.a. market

Retinitis Pigmentosa (RP) prevalence 1 in 2,500-4,0001 proportion of people in the population with RP

Proportion of RP that is autosomal dominant (adRP) 30-40%1 Inherited in a dominant pattern No competitors in market or Proportion of adRP that is RP11 1 in clinical Patients is a disease causing mutation in PRPF31 8-10% development Reimbursable RP11 patients Number of patients in the US, EU, and Japan 4,000-8,000 patients1

Median Rare Disease drug price Annual reimbursed cost for a rare disease drug US$250,000 p.a.2

Total addressable market US$1-2bn p.a. Margins assumed at 90% due to low COGs 3

1 Daiger et al. ‘Genes and Mutations Causing Autosomal Dominant Retinitis Pigmentosa’ Cold Spring Harb. Perspect. Med. 5 (2014); Ellingford et al. ‘Molecular findings from 537 individuals with inherited retinal disease’ J Med Genet 53, 761-776 (2016); Sullivan LS, Bowne SJ, Birch DG, et al. Prevalence of disease-causing mutations in families with autosomal dominant retinitis pigmentosa: a screen of known genes in 200 families. Invest Ophthalmol Vis Sci. 2006;47(7):3052-3064. 2 Based on Luxturna pricing over 4 years (450k USD per eye). Luxturna is a gene therapy for treatment of a rare inherited retinal disease, approved in 2017, marketed by Spark Therapeutics. 27 3 Sarepta Therapeutics’ marketed Exondys 51 for a DMD subpopulation has margins which exceed 90% for a systemically delivered drug (much more product per dose) DEEP-DIVE VP-001 targets a down-regulator of the gene underlying RP11

Healthy eye Eye with RP11 PYC’s lead drug

We all have two copies of each gene in People with RP11 have only one healthy Our drug knocks down a protein that our chromosomes gene (and one mutated gene) down-regulates the RP11 target gene

Our body uses these genes to ‘code’ This leads to insufficient healthy protein This increases the amount of protein proteins in our cells being made by the cell from the healthy copy of the gene (haploinsufficiency)

These proteins help our bodies function, The lack of protein means the retinal The additional healthy protein restores including helping us to see cells in the eye don’t function correctly the eye’s ability to function properly and and start to die – causing blindness prevents further degeneration

28 DEEP-DIVE Insufficient PRPF31 protein drives RP11 and CNOT3 expression controls PRPF31 expression

PRPF31 expression levels determine if a patient suffers vision CNOT3 protein levels regulate PRPF31 expression loss § CNOT3 is a negative regulator of PRPF31 § RP11 patients have one healthy copy of PRPF31 and one mutated, § CNOT3 expression is higher in RP11 patients compared to non-functional copy of PRPF31 ‘asymptomatic’ family members with the same PRPF31 § For most patients this leads to insufficient PRPF31 protein for a mutations healthy retina (~50% the PRPF31 protein of a healthy person) § However, some patients have only one healthy copy of PRPF31, but late or no disease onset CNOT3 and PRPF31 expression in iPSC-derived § This is because their healthy gene produces ~1.2-1.4 fold more retinal pigment epithelium (RPE)1 protein than other patients

CNOT3 and PRPF31 expression in control patient fibroblasts1 Relative mRNA expression

Patients

1 RT-qPCR analysis of PRPF31 and CNOT3 mRNA expression normalised with TATA-binding protein (TBP) expression in iPSCs-derived retinal pigment epithelium from RP11, asymptomatic and wild type (WT) individuals. Bar chart represent mean±standard error of the mean (SEM) from three independent RT-qPCR. Expression of CNOT3 and PRPF31 transcripts in wild type was set to 1. *p<0.05 compared with wildtype. #p<0.05 compared with asymptomatic subject 29 See ASX Announcement 14 October 2019 DEEP-DIVE VP-001 uses an antisense oligo with a morpholino (PMO) backbone to reduce the functional effect of CNOT3 on PRPF31 expression

Schematic strategy of PMO-mediated CNOT3 exon skipping Without VP-001 With VP-001

PMO

Exon Intron Exon Intron Intron Exon Intron Exon Intron Intron Pre- Exon C Exon D Exon C Exon D mRNA A B A B

Exon Exon Exon Exon Exon C Exon D Exon D mRNA A B A B

Full length protein Truncated protein (non-functional)

Other domains (and some functions) remain Transcription Transcription intact Outcome PRPF31 PRPF31

VP-001 uses a PMO to remove in-frame exons encoding functional domains downregulating PRPF31 – the truncated CNOT3 isoform leads to an upregulation in PRPF31 expression levels 30 DEEP-DIVE PYC’s drug delivery technology can successfully deliver an RNA therapeutic into the nucleus of the target cell (the RPE) in mice

Delivery dose response (lead CPP with ‘reporter ASO’ targeting%D7 Smn RPEgene isolate after IVT (28 days) administration)1 100 %D7 NeuralNeuralNeural retina retinaRetina (28 days) RPE/ChoroidRPE Isolate 100 80

80 * 60 Smn

Smn 60 * * 40 40 28.2 26.0 19.1 20 13.7 20 10.0 Skipping Exon 5.0 Exon Skipping Skipping Exon 0.0 0.0 0 0

Vehicle 1.6µg 3.2µg 6.4µg Vehicle 1.6µg 3.2µg 6.4µg g/eye) g/eye) g/eye) µ µ µ g/eye) g/eye) g/eye) Lead CPP-ASO µ µLead CPP-ASOµ

Vehicle control Vehicle control 1 Day 28 post intravitreal injection in mice. A readout of drug delivery, Exon-skipping of Survival of Motor Neuron (Smn) in the mouse retina across 3 dose cohorts (n=12 for each dose cohort, n=4 for vehicle) 31 See ASX Announcement 22 July 2020

Full-d-HPG0031-Ext2-3'SMN1Full-d-HPG0031-Ext2-3'SMN1Full-d-HPG0031-Ext2-3'SMN1 (1.6 (3.2 (6.4

Full-d-HPG0031-Ext2-3'SMN1Full-d-HPG0031-Ext2-3'SMN1Full-d-HPG0031-Ext2-3'SMN1 (1.6 (3.2 (6.4 DEEP-DIVE VP-001 is the only disease modifying therapy in development that treats the entire retina

Treating the disease requires a delivery technology to reach Breadth of delivery is also required to treat the deepest cells at the back of the eye the entire eye

§ Cells degenerate across the entire retina causing CPP-PMO PMO it to ‘leak’ and the cells to die § An effective treatment must treat a majority of the cells to prevent significant vision loss

CPP-ASO treatment area (whole of the retina)

AAV treatment area

Target cell 31

PYC’s technology delivers the drug where others cannot – the cells 0 where treatment is needed CPP- PMO1 Affected cells PMO1 32 1 Exon 7 skipping of Smn at day 5 post 1.6mg Intravitreal administration in the mouse eye. DEEP-DIVE VP-001 achieves the desired exon skipping effect at the anticipated clinical concentration in patient derived models

We have proven that our drug modulates target gene expression in multiple patient derived models…

Exon skipping, retinal organoid Exon skipping, Retinal Pigment Epithelial Day 14, 2 treatments (n=2) Day 5, single treatment 70

57

44

0 0 Untreated 5µM Untreated 2.5µM 5µM

PYC CPP-PMO PYC CPP-PMO treatment treatment

Exon skipping in patient retinal organoid models (n=2 patients with RP11), with and without PYC’s drug treatment. Organoids (4-6 organoids combined) were treated with 5µM of drug administered twice over a 14 day time period. Due to the successful delivery up to 71% of RNA molecules have been altered (skipped) by the PMO (n=1 sample per treatment) Exon skipping in patient derived RPE model (n=1), with and without PYC’s drug treatment. (n=2 per treatment) 33 See ASX Announcement 1 April 2020 DEEP-DIVE This exon skipping translates into an upregulation of the deficient protein at levels expected to rescue the disease

PRPF31 protein levels, RPE, 5µM treatment, (n=1 per patient)

2.5 Day 2 Day 5 Day 12 Untreated

d Treated e t 2.0 a e r t n u

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Anticipated disease e

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0.0 Patient 1 Patient 2 Patient 3 Patient 4 Patient 5

Non-penetrant Penetrant

For anticipated disease correction threshold see ‘Giulia Venturini, Anna M. Rose, Amna Z. Shah, Shomi S. Bhattacharya, Carlo Rivolta. CNOT3 Is a Modifier of PRPF31 Mutations in Retinitis Pigmentosa with Incomplete Penetrance. PLOS Genetics November 2012’ 34 See ASX Announcement 7 October 2020 DEEP-DIVE VP-001 has demonstrated the ability to correct important functional deficits associated with RP11

These results demonstrate VP-001’s ability to correct the structural deficiency in patient derived retinal cells that is one of the key causes of vision loss in RP11 patients1

1 Buskin A. Disrupted alternative splicing for genes implicated in splicing and ciliogenesis causes PRPF31 retinitis pigmentosa. Nat Commun. 2018 Oct 12;9(1):4234. 35 See ASX Announcement 16 December 2020 DEEP-DIVE Upregulation of the target protein rescues the functional deficits associated with the disease

Structure of the Retina Impact of RP11 Restoration Healthy RP11 Impact of RP11 with VP-001

§ Shorter ‘stunted’ connecting cilium in TBD the photoreceptors

§ Lower ‘phagocytosis’ of outer segments (lower ability of the RPE to dispose of the toxin)

§ Shorter and less frequent cilium on the RPE, showing poor RPE health

§ Short, less functional microvilli, which are the ‘arms’ that collect the outer segments during phagocytosis

§ RPE cells are not tightly joined and become ‘leaky’, causing retinal TBD degeneration

§ RPE loses polarity – or simply the cell TBD becomes ‘disordered’ 36 DEEP-DIVE RP11 patients experience lost functionality of Retinal Pigment Epithelial cells (RPE)

Structure of the Retina – target cells in the back Phagocytosis – the ‘self-repair’ process where RPE cells of the eye (RPE) ‘clear away’ debris from the photoreceptors. If outer segments are not phagocytosed, they build up and can become toxic, impairing the ‘visual cycle’

Ganglion cell layer

Inner nuclear layer

Outer nuclear layer

Photoreceptors

RPE

37 DEEP-DIVE VP-001 restores RPE functionality in patient derived models

Phagocytosis assay, 5µM 6hr timepoint

A) Green ‘specks’ are Phagocytosed outer-segments (more B) Intensity of phagocytosis per RPE cell green = improved functionality) p<0.01

Untreated PYC CPP-PMO

Un- PYC CPP- treated PMO

A) Phagocytosis in a patient with Retinitis Pigmentosa 11 with and without treatment with PYC’s lead drug (more green = more phagocytosis). Photoreceptor outer segments have been labelled with a fluorescent green ‘tag’ and the ability of the RPE (nuclei stained in blue) to self- repair (‘phagocytose’) the green outer segments has been assessed. The cells treated with 5uM of PYC’s drug demonstrate substantially greater ability to phagocytose the fluorescent green outer segments than the untreated cells. The Microscopic images taken 5 days post treatment at 10x magnification for both treated and untreated cells. These images are representative of a broader set of assays conducted across cells derived from multiple patients. B) Comparison of the level of phagocytosis in RPE cells (signal intensity of green florescent ‘tag’ per cell actively phagocytosing) derived from a patient with RP11, with and without treatment with PYC’s drug. Within 5 days, a single 5µM dose of drug (CPP-PMO, 2 samples) increased the phagocytosis ability of the diseased RPE cells by more than 1.5-fold (p=0.0083, two-tailed unpaired t-test) compared to untreated cells (4 samples). 38 See ASX Announcement 1 April 2020 DEEP-DIVE PYC’s lead drug is competitively differentiated in achieving this functional correction without causing toxicity in the retina

Retinal stress marker expression in mice Retinal thinning in mice Day 5 post single 1.6µg IVT injection Day 21 post IVT injection OCT imaging

PYC CPP-PMO – no thinning

Control CPP-PMO – severe thinning Higher expression toxicity more indicates

Toxicity determined by treating mouse retinas with 1.6 micrograms of an Antisense Oligonucleotide (ASO) delivered by each peptide and then measuring retinal stress based on levels of Glial Fibrillary Acidic Protein (GFAP). GFAP levels have been measured after retinal harvesting from mice at day 5 post intravitreal injection and normalised to a pool of ‘house-keeping’ genes. Notes i) PepK – a third-party delivery peptide that serves as the current benchmark for delivery peptides in clinical development (Red, n=6); ii) PYC’s delivery peptide (Green, n=2 ); and iii) a control group which received no treatment (Black, n=3). One-way ANOVA p values – PepK:naïve 0.1379; PYC CPP:naïve 0.9892 39 See ASX Announcement 8 April 2020 DEEP-DIVE The dose dependant response shows no increasing acute toxicity in the mouse

Dose dependant increase in effect … … and no increase in toxicity markers

Exon-skipping, Day 7 in the mouse eye Gfap expression,dd PDayC R7 info ther G mouseFAP eye ex pression in Neural Retina at D7 (n=12) Neural Retina 0.025 3.2µg/eye .

e 0.020 v 6.4µg/eye a Smn s

e o t n 0.015 e d g e

s K i l

H 0.010 a

f m o r o

Exon Skipping Skipping Exon 0.005 N

0.000

l g g g Vehicle 1.6µg 3.2µg 6.4µg Vehicleo 1.6µµg 3.2µg 6.4µ g tr µ µ n .6 .2 .4 o 1 3 6 c 1 1 1 Lead CPP-ASO le N LeadN CPP-ASON ic M M M h -S -S -S e 2 2 2 Toxicity determined by treating mouse retinas with 1.6 micrograms of an Antisense Oligonucleotide (ASO) delivered by each peptide and then measuring retinalV stress based on tlevels of Glial Fibrillaryt Acidic Protein (GFAP).t GFAP levels have been measured after retinal harvesting from mice at day 7 post intravitreal injection and normalised to a pool of ‘house-keeping’ genes. x x x 40 -E -E -E See ASX Announcement 22 July 2020 1 1 1 3 3 3 0 0 0 0 0 0 G G G P P P -H -H -H -d -d -d ll ll ll u u u F F F OVERVIEW The path to market for VP-001 has several major advantages over conventional clinical development pathways

Stage IND-enabling Phase 1/2 Phase 2/3 Approval

Timeline 18 months 15 months 18 months 6 months

Higher Shorter time to Lower cost probability of market success § Orphan genetic drugs § Combined clinical trials § Lower patient numbers have a ~45% chance of and single pivotal § 2 planned clinical trials reaching market from § Favourable FDA § Favourable FDA Phase 1 pathways and Orphan pathways status

All numbers and timelines are estimates and are applicable to change and revision 41 PYC-001 for the treatment of Diabetic Retinopathy

42 PYC has the capability to rapidly scale its technology in the retina

Right Biology Does the drug Do we Does the drug alter the disease progress to engage the Right Indication in a functional IND- target safely? model? enabling studies? Right Commercials

PYC’s ‘RNA hub’

~3 months ~6-12 months 3-6 months 43 Advancing our lead program into the clinic will validate our drug delivery platform for retinal disease

The Retina is a high value target Proven Delivery in the Eye Develop Further Applications

1.6ug IVT injection in mice % Exon 7 Skipping Smn Diseases primarily affecting the Photoreceptors § 57 § Usher Syndrome § Rhodopsin RP (most prevalent adRP in the US) § >10 commercially viable Inherited Retinal Diseases 0 Neural retina/ photoreceptors CPP-PMO PMO

60 Diseases primarily affecting the RPE § Diabetic retinopathy § Wet age-related (wAMD) § Dry age-related macular degeneration (dAMD) 0 § >5 commercial Inherited Retinal Diseases CPP-PMO PMO RPE (21 days post- (5 days post-IVT) IVT)

44 PYC-001 – PYC’s second drug development program

§ Diabetic Retinopathy (DR) is the leading cause of vision loss in adults aged 20–74 years

§ Current treatment options for DR are limited due to a lack of response to first line anti-Vascular Endothelial Growth Factor (VEGF) therapies and the need for longer acting drugs

§ In addition, there is a growing body of evidence suggesting that prolonged VEGF inhibition is responsible for the death of sensitive nerve cells in the retina

§ PYC has leveraged the unique advantages of its RNA therapeutics technology to create a modified VEGF therapy that addresses these shortcomings – this drug promises to: – Retain the ability of the current generation of drugs to stop blood vessels destroying the retina; – Add a ‘pro-survival’ effect to help protect sensitive neurons from dying; and – Significantly extend the dosing interval between treatments for patients

§ The drug leverages all of the intracellular delivery work undertaken for PYC’s lead program (a treatment for a blinding disease of childhood called Retinitis Pigmenotsa) and, as a result, is expected to have a rapid development pathway into the clinic

45 Common eye diseases are linked through dysfunction of blood vessels in the eye

46 Image: Mayoclinic.com Inhibiting new blood vessel growth (VEGF-inhibition) has been a major step forward in the management of these diseases

Global ocular anti-VEGF sales, USD B

10 9 8 7 6 5 4 3 2 1 0 2014 2015 2016 2017 2018 2019

47 Source: Roche, Regeneron annual reports and financial statements But… Inhibition of VEGF is known to cause retinal ganglion cells to die and is also suspected of being linked to macular atrophy

“VEGF inhibition increased Retinal Ganglion Cells apoptosis and neuronal damage in diabetic retinopathy”1

“A majority of patients show Macular Atrophy after long-term anti-VEGF treatment” 2

“An association between anti-VEGF treatment and atrophy development has been observed” 3

1 Mechanisms behind Loss in Diabetes and Therapeutic Approach. Int. J. Mol. Sci. 2020, 21, 2351; doi:10.3390/ijms21072351 2 Munk MR, Ceklic L, Ebneter A, Huf W, Wolf S, Zinkernagel MS. Macular atrophy in patients with long-term anti-VEGF treatment for neovascular age-related macular degeneration. Acta Ophthalmol. 2016 Dec;94(8):e757-e764. doi: 10.1111/aos.13157. Epub 2016 Jul 15. PMID: 27417506. 3 SriniVas R. Sadda,Robyn Guymer,Jordi M. Monés,Adnan Tufail,Glenn J. Jaffe. Anti–Vascular Endothelial Growth Factor Use and Atrophy in Neovascular Age-Related Macular Degeneration Systematic Literature Review and Expert Opinion. :48 Journal of the American Academy of Ophthalmology Diabetic patients with higher VEGFA165a to VEGFA165b show lower penetrance of Diabetic Retinopathy

Diabetes patients without retinopathy display proportionally more expression of the b isoform

Distribution of growth factors (VEGF) among cases and controls, pg/ml Mean and SEM

VEGFA165a VEGFA165b (VEGFA165a) – (VEGFA165b)

250 209 200 158 124 150 109 100 61 46 56 52 50 27 0 Control Diabetic Diabetic Control Diabetic Diabetic Control Diabetic Diabetic control retinopathy control retinopathy control retinopathy

Paine SK, Mondal LK, Borah PK, Bhattacharya CK, Mahanta J. Pro- and antiangiogenic VEGF and its receptor status for the severity of diabetic retinopathy. Mol Vis. 2017 Jun 22;23:356-363 49 There is an alternative method of inhibiting new blood vessel growth without the negative effects of VEGF inhibition

PMO

Exon Exon Exon VEGFA pre-mRNA Exon 7 7b 8a 8b

PYC’s drug ‘switches’ from the 165a to the 165b isoform of VEGF VEGFA-165a mRNA VEGFA-165b mRNA

Exon Exon Exon Exon Exon 1-5, 7 Exon 1-5, 7 7b 8a 7b 8b

Increase leaky new The current generation of VEGF inhibitors cause Decrease leaky new blood blood vessel growth the loss of the ‘pro-survival’ signal that is likely vessel growth the link between sustained exposure to these drugs and retinal cell death – PYC’s drug Pro-survival overcomes this issue Pro-survival

50 A very subtle change in the ratio of protein regulated by this ‘switch’ is required to correct the disease process

VEGF-A a causes RPE tight junction breakdown 165 VEGF-A165b prevents VEGF-A165a -induced changes in tight junctions

Worse outcome

Ved N, Hulse RP, Bestall SM, Donaldson LF, Bainbridge JW, Bates DO. Vascular endothelial growth factor-A165b ameliorates outer-retinal barrier and vascular dysfunction in the diabetic retina. Clin Sci (Lond). 2017 Jun 1;131(12):1225-1243 51 The therapeutic value of this approach has been recognised

“This switch changes what would be otherwise mild effects from activation by VEGFA165b, to stronger activation of retinal endothelial cells. Isoform switching from VEGFA165a to VEGFA165b would be an excellent target for therapeutic development”

1 Kenneth P Mitton; Wendy A Dailey; Megan Moore; Alvaro E Guzman; Jennifer Felisky; Kaylee Moyer; Nahrain Putris; Peter Chen; Austen Knapp; Anju Thomas; Regan Miller; Brandon Metcalf. VEGFA Isoform Switching in Diabetic Retinopathy and52 ROP is a Significant Factor in the Activation of Human Retinal Endothelial Cells. Investigative Ophthalmology & Visual Science July 2019, Vol.60, 2669. The program is expected to progress into Investigational New Drug enabling studies in 2021

Evaluation in patient cells Evaluation in animal models and/or patient derived models

Expected 4Q 2020 Expected 3Q 2021

IND-enabling decision in 2021 53 VP-002 for the treatment of Autosomal Dominant Optic Atrophy (ADOA)

54 Executive summary – PYC’s third drug development program

§ Autosomal Dominant Optic Atrophy (ADOA) caused by mutations in the Optic Atrophy 1 (OPA1) gene affects >8,000 patients in the Western World

§ ADOA is a ‘monogenic’ disease (a disease caused by a mutation in a single gene) where the mechanism of disease is caused by haploinsufficiency (insufficient protein levels caused by a loss of function mutation in one of the two copies of the OPA1 gene)

§ PYC has designed an oligonucleotide capable of correcting the OPA1 protein haploinsufficiency in cells derived from ADOA patients (>100% protein upregulation in patient fibroblasts)

§ PYC has filed for intellectual property protection over this drug program

§ The Company will now create a drug through conjugation (joining) of this oligonucleotide to one of PYC’s proprietary Cell Penetrating Peptides (CPP) and validate this drug in more sophisticated ADOA patient disease models before deciding whether to progress the candidate into clinical development

§ This drug development program will benefit from a number of synergies with PYC’s lead drug program and is expected to have a rapid development pathway

55 Autosomal Dominant Optic Atrophy

ADOA is caused by the cells (retinal ganglion cells, RGCs) losing their ability to transmit visual signals to the brain § This can cause severe vision loss in the patient

§ Vision loss often starts before the age of 10 Healthy Healthy Light retina RGCs Affects approximately 1 in 30,000 people § ~70% of all ADOA is caused by mutations in mutation in one gene, OPA1 Signal to brain § ~75% of cases caused by OPA1 mutations are due to low levels of the OPA1 protein

Dying Retina Light RGCs with optic atrophy

Reduced signal to brain 56 Created with BioRender.com This increase has been replicated in ADOA patient fibroblasts

Change in OPA1 protein levels, 50µM PMO treatment, patient fibroblasts

For upregulation benchmark see poster ‘Antisense oligonucleotide mediated increase of OPA1 expression using TANGO technology for treatment of autosomal dominant optic atrophy’ Fig.6 at https://www.stoketherapeutics.com/wp- 57 content/uploads/ASGCT2020_final.pdf PYC’s path to validating a therapeutic for ADOA

Validate CPP-PMO conjugate in multiple human cell models

Validate leads in ADOA patient-derived target cell models for target engagement

Validate leads in ADOA patient-derived target cell models for functional readouts

Complete preliminary toxicology and QC studies

Determine if there is an appropriate in vivo efficacy model

58 OPA1 upregulation may play a role in numerous mitochondrial- driven diseases

Glaucoma ‘Overexpression of Optic Atrophy Type 1 Protects Retinal Ganglion Cells and Upregulates Parkin Expression in Experimental Glaucoma’1

‘Harnessing the protective role of OPA1 in diabetic Cardiomyopathy cardiomyopathy’2

‘OPA1 overexpression ameliorates mitochondrial Neurodegeneration cristae remodelling, mitochondrial dysfunction, and neuronal apoptosis in prion diseases’ 3

Hu X, Dai Y, Zhang R, Shang K, Sun X. Overexpression of Optic Atrophy Type 1 Protects Retinal Ganglion Cells and Upregulates Parkin Expression in Experimental Glaucoma. Front Mol Neurosci. 2018;11:350 Patten D, Harper ME, Boardman N. Harnessing the protective role of OPA1 in diabetic cardiomyopathy. Acta Physiol (Oxf). 2020 May;229(1) 59 Wu, W., Zhao, D., Shah, S.Z.A. et al. OPA1 overexpression ameliorates mitochondrial cristae remodeling, mitochondrial dysfunction, and neuronal apoptosis in prion diseases. Cell Death Dis 2019 10, 710 Disclaimer

The purpose of this presentation is to provide an update of the business of PYC Therapeutics Limited (ASX:PYC) [‘PYC’]. These slides have been prepared as a presentation aid only and the information they contain may require further explanation and/or clarification. Accordingly, these slides and the information they contain should be read in conjunction with past and future announcements made by Phylogica and should not be relied upon as an independent source of information. Please contact PYC and/or refer to the Company's website for further information.

The views expressed in this presentation contain information derived from publicly available sources that have not been independently verified. No representation or warranty is made as to the accuracy, completeness or reliability of the information.

Any forward looking statements in this presentation have been prepared on the basis of a number of assumptions which may prove incorrect and the current intentions, plans, expectations and beliefs about future events are subject to risks, uncertainties and other factors, many of which are outside PYC’s control. Important factors that could cause actual results to differ materially from assumptions or expectations expressed or implied in this presentation include known and unknown risks. Because actual results could differ materially to assumptions made and PYC’s current intentions, plans, expectations and beliefs about the future, you are urged to view all forward looking statements contained in this presentation with caution.

This presentation should not be relied on as a recommendation or forecast by PYC. Nothing in this presentation should be construed as either an offer to sell or a solicitation of an offer to buy or sell shares in any jurisdiction.

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