Corporate PresentationJune 2020

Confidential to the Addressee Only

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2

Experienced leadership team

Serguei Nabirotchkin, PhD – Chief Biology Officer & Co-Founder

Xavier Paoli, MSc – Chief Commercial Officer

Susanne Dorn, MSc – Chief Regulatory Officer

François Chamoun, Master II Law, DJCE – Chief Legal Officer

Peter Collum – Chief Financial Officer & Chief Business Officer

Rodolphe Hajj, PhD – Chief Pharmacology Officer

Viviane Bertrand, PhD – Chief Preclinical Drug Development Officer

David Horn Solomon, PhD – Chief Executive Officer

Muriel Cottard, PhD – Chief Quality Officer

Philippe Rinaudo, PhD – Chief Data Science Officer

Overview

PLEOTHERAPYTM Platform

Maps disease networks and identifies

combination drugs to hit multiple highly

relevant disease targets

• Our PLEOTHERAPYTM discovery

platform is enabled by AI to help create

innovative combination therapeutics to

more effectively address pleiotropic

diseases

• Our platform has produced a phase III

program in CMT1A and a phase IIb

ready program in Alzheimer’s

PXT3003 (CMT1A) – Phase 3

PXT864 (AD) – Pre-Phase 2b

Over 20 additional indications mapped for further pipeline expansion

Collaborations

5

Pharnext is a late clinical stage biopharmaceutical company focused on advancing

innovative therapeutic candidates for orphan neurological disease with high unmet need

Proprietary Pipeline

Value Creation

5

PLEOTHERAPYTM AI platform scalable across multiple Tx areas

with combinations using both generics and NCEs

Superior targeting within disease network

Known safety profile of existing drugs

Discovery and development to pre-Phase II POC can be done in ~ 2.5

years

Phase III CMT1A program (~$1Bn WW sales potential)

Positive results from first Phase III and extension study

Large Potential

Opportunity

Enhancing

Probability of

Clinical Success

Capital Efficiency /

Speed to Approval

Advanced Lead

Program: PXT3003

Phase IIa data in AD

Ability to efficiently grow pipeline with PLEOTHERAPY platformAD Candidate Ph IIb

ready

PL

AT

FO

RM

PIP

EL

INE

Pipeline and Expected Milestones

6

PXT3003

PXT864

CMT1ASecond Phase III trial:

• Planned initiation (FPFD) – Q1 2021

Alzheimer’s

disease

Amyotrophic

lateral sclerosis

Phase IIb ready

Product Indication Preclinical Phase I Phase IIa Phase IIb Phase III Expected Milestone

Phase IIa ready

PXT3003 Overview

7

Charcot-Marie-Tooth Disease Type 1A

CMT1AChronic, severe, debilitating, inherited neuropathy

resulting from a duplication of the PMP22 gene,

causing demyelination of peripheral nerves

SYMPTOMS Muscle atrophy in extremities causing severe leg and

arm disabilities, pain, cramps and fatigue

DIAGNOSIS ~50% of patients have symptoms before the age of

20, confirmed by genetic testing

NATURAL

HISTORY

Genetic disease; symptoms starting in teenage

years, slowly declining through life, resulting in

braces, surgery and wheelchair

POPULATIONMore than 100,000 people affected with mild to

moderate CMT1A in US and EU5 (core market)

TREATMENT

OPTIONS

No approved drugs; only supportive care available

No other candidates in late stage clinical

development8

Chronic, Severe, Debilitating Inherited Neuropathy

PXT3003 Commercial Opportunity in CMT1A

▪ Complete unmet need with no approved drugs to treat chronic and debilitating disease

▪ No other mid/late-clinical stage programs in development for CMT1A

▪ Data from first Phase III study shows strong efficacy signal

▪ PXT3003 showed improvement over baseline

▪ Second Phase III study to initiate (FPFD) by 1Q 2021

▪ Revenue potential of approximately $1Bn worldwide

o More than 100,000 potential patients with mild-to-moderate CMT1A (US and EU5)

▪ IP protection through 2030, including composition of matter

▪ US orphan drug exclusivity and EU Orphan Drug Designation

▪ FDA Fast Track Designation

9

BACLOFEN

PXT3003 Novel Design and Mechanism of Action

Opioid/ Alcohol dependence

Spasticity

Constipation

CMT1A disease at-a-glance Network analysis Design of PXT3003

Current Indication

Opioid receptors

GABAreceptors

Muscarinic receptors

Current Dose

50mg

120mg

1.4mg

12mg

OPIOIDReceptors

MUSCARINICReceptors

GABAReceptors

420mg

15g

CMT1A - Axonaldysfunction andmuscle loss

NALTREXONE

SORBITOLNormal

10

Pharnext Dose

11

11

ATP/glutamate

pro-inflammatorycytokines

Musclecells

Neurons

Global effect

Immunecells

Musclecells

Neurons

SchwannCells

Lowering PMP22 overexpression improves signaling in CMT1A Schwann cells

Network controlling PMP22 gene expression

Naltrexone

Sorbitol

Baclofen

- genes mutated in CMT disease

- their functional partners

- therapeutic target of baclofen

- therapeutic target of naltrexone

- therapeutic targets of sorbitol

- activation

- inhibition

Mechanism of action of PXT3003 in CMT1APXT3003 Targets Are Ubiquitous Along The Peripheral Nerve

Mechanism of action of PXT3003 in CMT1APreclinical Data Demonstrate That PXT3003 Acts On Different Cell Types Of The Motor Unit In CMT1A

Increases number of myelinated

axons and axonal diameter in rats

Downregulates PMP22 in rats Improves Akt/Erk signaling dysbalance in rats

Schwann cell differentiation

*p<0.05, **p<0.01, ***p<0.001 vs placebo12

Num

ber

of to

tal m

yelin

ate

d

axons

Con

trol

Place

bo

PXT30

03

0

2000

4000

6000

8000

10000

12000

***

**

Con

trol

Place

bo

PXT30

03

3.0

3.5

4.0

4.5

5.0

5.5

Axon d

iam

ete

r (µ

m)

***

*

Con

trol

Place

bo

PXT30

03

100

110

120

130

140

150

160

PM

P22 m

RN

A e

xpre

ssio

n(s

cia

tic n

erv

e)

-31%

*

***

AT

P L

evel (A

.U)

Control Placebo PXT30030

500

1000

1500

2000

***

***

Improves global energy

expenditure in vitro

*p<0.05, **p<0.01, ***p<0.001 vs placebo

Mechanism of action of PXT3003 in CMT1APreclinical data demonstrate that PXT3003 acts on different cell types of the motor unit in CMT1A

(A,C,D) Morphology and number of neuromuscular junctions (black arrows in A)

(B,E) Innervation of neuromuscular junctions (white arrows in B)

AT

P L

evel (A

.U)

Control Placebo PXT30030

500

1000

1500

2000

***

***

Improves global energy

expenditure in vitro

*p<0.05, **p<0.01, ***p<0.001 vs placebo

Mechanism of action of PXT3003 in CMT1APreclinical data demonstrate that PXT3003 acts on different cell types of the motor unit in CMT1A

(A,C) Angular fiber phenotype (reflecting atrophy in CMT1A)(B,D) Muscle fiber type quantification (fast type IIb vs slow type IIa)

All Components of PXT3003 Synergistic to Activity in CMT1A

110

105

100

9 5

9 0

115

125

120

130M y e lin a t io

n

%Im

pro

ve

m e

nt

m y

elin

len

gth

S

S in g le D u o s

* * *

S

P la c e b

o

B C L + N L X B C L + S R B N L X +S R B P X T 3 0 0

3

4

5

6

7G r i p s t re n g t h a t e n d o f t r i a l

Gri

ps

tre

ng

th(N

)

(ch

an

ge f

rom

ba

se

lin

e)

***

###

#######

#

In CMT1A neurons on myelination in vitro In CMT1A animals in vivo

***p<0.001 vs CMT1A placebo/Control, ANOVA + Dunnett test#p<0.05, ###p<0.001 vs PXT3003, ANOVA + Dunnett test

S: synergy

BCL = Baclofen (GABA receptor)

NTX = Naltrexone (opioid receptor)

SRB = Sorbitol (muscarinic receptor)

15

Robust Phase II Results for PXT3003 in CMT1AExploratory multi-center, randomized, double-blind, placebo-controlled Phase 2 study

Low Dose n=21

High Dosen=19

PLACEBOn=19

Medium Dosen=21

NAL

BAC

SOR

n=80Mild to

Moderate Patients

• All doses safe and well

tolerated

• Effect achieved at 12 months with High Dose, which was used to design the Ph III study

Source: Attarian et al, Orphanet Journal of

Rare Diseases (2014),9:19916

20%

10%

0%

-10%

%IM

PR

OV

EMEN

Tin

ON

LS

PLACEBO

BASELINE 12 Mths

PHASE II DURATION: 12 MONTHS

Efficacy and dose-effect demonstrated with Overall Neuropathy Limitation Scale (ONLS)

Med Dose

High Dose

Low Dose

PLEO-CMT: First Pivotal Phase III Study Design and EndpointsInternational, randomized, double-blind, placebo-controlled

Primary endpoint: ONLS after 12 -15 months

▪ ONLS: a 12-point scale evaluating disability

▪ 90% of the patients scored 2-4 (mild-to-moderate)

▪ A 0.3-point ONLS difference vs. placebo was determined to be

meaningful

- Stabilizing or even improving disease versus placebo or natural

yearly evolution estimated at 0.1/0.2 point.

- 50% Placebo standard deviation (Cohen J., 1988)

▪ FDA and EMA agreed on using ONLS as the primary endpoint for

this study.

Secondary endpoints analysis include:

▪ 10-meter walk test (10-MWT)

▪ Nine-hole peg test (9-HPT)

▪ 2 subsets of CMTNSv2 (CMT Impairment Score)

(Clinical + Electrophysiological items = CMTNSv2)

- Sensory subset*

- Clinical subset = purely clinical items (CMTES)**

ONLS = Overall Neuropathy Limitation Scale

* Sensory subset of CMTNSv2: items 1,4 and 5

** CMTES is derived from CMTNSv2, items 1 to 7 excluding nerve conductions

17

PHASE III DURATION: 15 MONTHS

SOR

0.7 mg 6 mg 210 mg

PLACEBO

Low Dose

(Phase 2 highest dose)

High Dose

NAL

BAC

SOR

n=323Mild to

Moderate Patients

(age:16 – 65 y) 1.4 mg12 mg420 mg

PLEO-CMT: ONLS and 10MWT in SAP Primary Population

*, ** Dose 4 vs Placebo, ANCOVA with multiple imputation (Missing data implemented by multiple imputations following the placebo trend)

*** Average of 12 and 15 Month, or 12 Month if 15 Month is missing

18

p = 0.008

ONLS

p = 0.016

10mWT

Baseline 6 months 12+15 months*** Baseline 6 months 12+15 months***

Dose 4 (n=55)

Dose 3 (n=93)

Placebo (n=87)

Placebo n=101

Low Dose (Dose 3) n=109

High Dose (Dose 4) n=113

Phase 3 Study – CMC Event Interrupted High Dose Arm

19

Dec 2015

Study Start

Phase 3 Trial n=323 patients

per SAP*, ONLS (high dose) p=0.008

per original protocol*, ONLS (high dose) p=0.04

CMC event

*Original protocol adapted to account for “dropouts” due to CMC event (using ICH guidelines)

# DO classified as related or not related to treatment by a blinded adjudication committee (based on patient profile: efficacy + safety)

Statistical model not modified (ANCOVA) but adaptation of the dropouts (DO) considered

• Original protocol → primary population = FAS (n=323), all DO imputed like placebo for all study arms (conservative)

• SAP→ primary population = mFAS (n=235 = completers + DO related to treatment), DO related to treatment imputed like Placebo for all study arms, all other DO

excluded from analysis (considered at random)

80 completers

7 dropouts related to treatment#

July 2017

Germany stop ( all arms)

Sept 2017

High dose stop

Oct 2017: Variability

Nov 2017: Futility read

Mar 2018

Study End

Oct 2018

Study Read-out

14 dropouts unrelated

to treatment#

85 completers

8 dropouts related to treatment#

49 completers

6 dropouts related to treatment#

16 dropouts unrelated

to treatment#

58 dropouts unrelated

to treatment#

CMC Overview

▪ What happened?

▪ High dose solution in 100mL bottles exhibited a small amount of crystal precipitate (~ 2% by volume)

in some batches due to a reaction between baclofen and paraben

▪ How are we addressing?

▪ For the upcoming Phase III study, we are delivering the high dose by dosing patients with 10mL of the

low dose concentration, which is equivalent to 5mL of the high dose, since the low dose concentration

does not have the issue with crystals

▪ This same approach was used for the prior Phase III extension study with the approval of regulatory

agencies

▪ We are also planning to use unit dose “stick packs” for better convenience and compliance

▪ Future

▪ In parallel, we are developing both a room temperature oral solution as well as a solid oral dosage

form which will better serve patients on a commercial basis20

PLEO-CMT: Safety and Tolerability

▪ Treatment emergent adverse events (TEAE) similar among three groups; majority mild

▪ TEAEs leading to treatment withdrawal similar in all three groups

▪ Single treatment-related serious TEAE occurred in lower dose group (gastroenteritis)

▪ Safe and well tolerated; showed a similar safety profile as in Phase 2

21

22

PLEO-CMT-FU Open Label Extension Study Design

PLEO-CMT Phase III Study PLEO-CMT-FU Study

15 monthsDouble blind – Placebo Controlled

9 monthsOpen Label – No Placebo**

High dose (D2)

Low dose (D1)

Placebo (P)

High dose (D2)

Low dose (D1)

187 Patients*

69 Patients

62 Patients

54 Patients

8 Patients

46 Patients

D2-D2

D1-D1

P-D2

P-D1

* 187 patients were enrolled, however 2 patients were excluded as outliers due to extraordinary circumstances, we considered unrelated to treatment

** Initial extension study design was blinded. Intercurrent event caused the extension study to be unblinded and therefore open label due to the change in dosing

for high dose patients switching to twice the low dose to equal the high dose amount of drug.

High dose (D2)

Low dose (D1)

23

ONLS Results for All Extension Study Participants(PLEO-CMT + Interruption + PLEO-CMT-FU Trials)

Intercurrent event caused an average 5-month treatment interruption between Phase III PLEO-CMT and extension study

All cohorts during extension vs placebo during PLEO-CMTestimate/year: -0.30 95%CI[-0.48; -0.12], p = 0.001

Placebo during extension vs placebo during PLEO-CMTestimate/year: -0.24 95%CI[-0.47; -0.01], p = 0.038

D2-D2 cohort from start of PLEO-CMT through extension –total of 25 months of study timeImproved by -0.26 points

Results must be cautiously interpreted because of open label extension PLEO-CMT-FU design

Large Commercial Opportunity in CMT1A

▪ Complete unmet need in CMT1A: no pharmacological treatments currently available; only supportive care

options (PT, surgery, pain management)

▪ No other candidates in mid/late-stage clinical development

▪ More than 100,000 potential patients in our core market, mild to moderate CMT1A (US and EU5)

▪ 25,000 potential patients already located via patient associations and market research

▪ 5 pricing /independent market research studies with consistent feedback on US and EU pricing, supporting

revenue potential of approximately $1Bn worldwide

24

Other PXT3003 Milestones and Anticipated Path Forward

Feb 2, 2019: FDA Fast Track Designation granted

Jan 6, 2020: Announced top-line results of extension study (PLEO-CMT-FU) of long-term safety

and efficacy of PXT3003

Mid 2020: Expect to finalize second Phase III trial protocol in CMT1A with FDA

1Q 2021: Expect to Initiate second Phase III trial (FPFD) in CMT1A

2020: Continued assessment of commercialization options for geographical areas within US, EU,

Japan and ROW; China commercialization rights are licensed to Pharnext & Tasly’s joint venture

25

PXT864 Overview

26

Novel AD Approach:Correcting chemical imbalance in the diseased brain

27

Glu GABA

PXT864 to break viciouscircle

Disease at-a-glance

GABAreceptors

Glutamatereceptors

Acamprosate

Baclofen

Healthy brain Diseased brain

Glu: Glutamate

Glu GABA

- +

GABA

Glu

GABA

Glu

Aβ -Tau

Vicious circle occurring in AD brain

(Govindpani 2017; Talantova 2013)

GABA

Glu

“Therapeutics that correct the E/I imbalance in early AD may prevent neuronal dysfunction, cell loss and cognitive impairments associated with later stages of the disease”

E/I imbalance = GLU excitation / GABA inhibition

Upstream of Aβ -Tau imbalanced cells overproduce each

28

Working memory: Combination

% A

lte

rnatio

n

Nor

mal

Con

trol

(Place

bo) AC

PBC

L

PXT864

45

50

55

60

65

70

75

******

S

Acamprosate BaclofenAcamprosate Baclofen

Working memory: Dose-response of single drugs

% A

ltern

ati

on

Nor

mal

A+

Place

bo

A+

ACP 0

.032

A+

ACP 0

.08

A+

ACP 0

.2

A+

ACP 0

.4

A+

ACP 0

.8

A+

ACP 1

.6

A+

ACP 8

.2

A+

ACP 4

1

A+

BCL

0.41

A+

BCL

0.48

A+

BCL

1.2

A+

BCL

2.1

A+

BCL

3

A+

BCL

10.3

45

50

55

60

65

70

75

***

PXT864 Demonstrates Synergistic Efficacy in AD Animals

(Chumakov et al., 2015)

PLEODIAL: Exploratory Phase 2a Trial Design

• 45 mild naïve AD patients treated by 3 doses:

• Clinically diagnosed but low mean Log Abeta 42/40

• 7 centers in France

• Assessed at 0,3,6,9 months

• 9 clinical endpoints, open label, single blind

• Biomarker: Plasma Aβ42/40 assessed by Quanterix

Memory Orientation Language Attention Visuospatial Executive function speed Daily activity Social interaction

Adas Cog

CDRSB

IADL

TMT A

TMT B

ZAZZO

Apathy Inventory

DSST

ISAAC

Functions assessed by each endpoint

29

p = 3e-13 Highest drug exposure versus historical placebo

p = 0.013 All patients versus historical placebo

PXT864: CDR-SB Analysis Based on Plasma Drug ExposureHigher Dose Could Rapidly Generate Partial Recovery Vs Less Decline With No Safety Concerns

***

***

*

*

Acamprosate Baclofen

Approved dose 2000 mg 80 mg

Ingested dose 3 40 mg 24 mg

Next dose to be tested 400 mg 24 mg

Imp

rove

me

nt

30

Biogen EMERGE : 9 months high dose Aducanumab: ̴ 0,7 pts decline

Both analyses with patients with sufficient exposure (increasing dose limited by safety concerns)

Biogen ENGAGE : 9 months high dose Aducanumab: ̴ 0,5 pts decline

Plasma Aβ42/40 Analysis Based on Plasma Drug ExposureImprovement at 3 and 6 Months, but a Higher Dose Could Rapidly Generate Sustained Effect

Drug exposure = Cmax for both drugs

(n=45)(n=10)(n=10)(n=25)

Imp

rove

me

nt

31

Plasma Aβ42/40 3-Month Improvement Correlates With Clinical Improvement at 9 Months:

Suggests a Delayed Effect “From Molecular To Clinical”

32

Biomarker 3-Month improvement Biomarker 3-Month improvement

3-M

on

thC

DR

-SB

imp

rove

men

t

3-M

on

thC

om

po

site

sco

re (

CS)

* im

pro

vem

ent

9-M

on

thC

DR

-SB

imp

rove

men

t

9-M

on

thC

om

po

site

sco

re (

CS)

im

pro

vem

ent

* Composite score of all clinical endpoints.

PXT864 in Alzheimer’s Disease Overview

Higher doses of PXT864 have potential to demonstrate a sustained therapeutic effect on

Alzheimer’s Disease, due to the following advantages:

▪ Strong safety profile

▪ Can be co-administered with already approved drugs in AD

▪ Can be synergistic with other NCEs to create a powerful novel new entity

33

PLEOTHERAPYTM AI Platform Overview

34

PLEOTHERAPYTM Universal R&D PlatformStarting with Big Data

In Silico AI & Expert System

Disease

Network

Knowledge

Integration

Virtual

Repositioning

Preclinical

2,000+

approved drugs50

candidate drugs(filtered for PK, toxicity, safety, IP)

6 months ≈ 2 years

1

Pleodrug™

In Vitro

Screening

Clinical

≈ 7 years

Phase 1(not always mandatory)

Phase 2A/B

Phase 3

In Vivo

Test

ApprovalDisease

25 Positive Drugs

4 synergistic combos

35

Human geneticsGWAS ( Genome Wide Association Study )

Virtual Repositioning Step 1 Disease Associated Molecular Network

A Fraction of the Whole Interactome

BIG DATA

36

Genome Wide Association Studies(GWAS) e.g. from AD patients

Protein – Protein Interaction

Known Drug-Targetrelationships

Literature

EXPERTS AI

e.g. AD Associated Molecular Network

Virtual Repositioning Step 2 Identifying Candidate Drugs from Drug Data Base and Disease Associated Molecular Network

BIG DATA

37

Genome Wide Association Studies(GWAS) e.g. from AD patients

Protein – Protein Interaction

Literature

EXPERTS AI

e.g. AD Associated Molecular Network

Known Drug-Targetrelationships

Candidate drugs Experimental

Testing

RALBP1

metabolite

metabolite

metabolite

metabolite

metaboliteGRM5

mTOR

metabolitetransport

metabolite

metabolite

PITPNC1

PITPNC1

SNCA

PLD1

metabolite

THEM2

metabolite

metabolite

ACHE

metabolitePLD1/2

PLD2

NFĸB1

metabolite

metabolite

metabolite

metabolite

SGPP2

PPARγ

PDGF

metaboliteeffect

PLA

?

ADCY2

DRD2

ANXA3

DRD5

metabolite

ASAH1

metabolite

metabolite

metabolite

PRIMA1

metabolite

metabolite

PLAUST14

Virtual Repositioning Step 1 Example of Alzheimer’s Disease – Associated Sub Network

metabolite

Proteins

encoded by

genes with

statistical

association

with

Alzheimer’s

Disease

Proteins

encoded by

genes without

statistical

association

with

Alzheimer’s

Disease

32

RALBP1

metabolite

metabolite

metabolite

metabolite

metaboliteGRM5

mTOR

metabolitetransport

metabolite

metabolite

PITPNC1

PITPNC1

SNCA

PLD1

metabolite

THEM2

metabolite

metabolite

ACHE

metabolitePLD1/2

PLD2

NFĸB1

metabolite

metabolite

metabolite

metabolite

SGPP2

PDGF

metaboliteeffect

?

ANXA3

DRD5

metabolite

ASAH1

metabolite

metabolite

metabolite

PRIMA1

metabolite

metabolite

PLAUST14

metabolite

Genetic association

Drugged Target

Virtual Repositioning Step 2 Crossing Drug Data Base And Alzheimer’s Disease – Associated Sub Network

Candidate drugs ready for experimental screening

33

AI

con

tin

uu

m

Human (computer assisted)Computer (human assisted)

2007

2007

40

2021

2021

2017

2017

Other omics

Platform Status 2017-2021

1. New generation GWAS module: machine learning &

deep learning-based imputation (by end 2019) +

disease risk prediction (projected 2020)

2. Other Omics data (Big Data)

3. Network building powered by AI, learned from

Pharnext’s existing networks and methods

4. Network analysis powered by AI (ex: synergy

prediction)

• And other ML projects …Network construction

module

DiseaseNetworks

Genetic Data

(GWAS)

GWAS analysis module

LiteraturePatents

Other databases (proteins, pathways,

other PPI, etc.)

IngenuityReaxys

databases

Experts*2

* 1

* 3

* new

ML tools

* 4

AI assisted

Virtual Repositioning Powered by AI and Big Data with New Machine

Learning (ML) ToolsProcess reduced from 1 year to 1 quarter - now aiming to reduce to only a few weeks

5-year plan for automation 34

BACLOFEN

Discovery of PXT3003

72 Drugs selected to screen

2,000+ drugs

Virtual screening

Down-regulation of Pmp22 in

Schwann cells 16 positive drugs (22%)

3 prioritized, 1 selected

NALTREXONE

SORBITOL

In CMT1A, excess Pmp22

protein is produced, leading

to instability and loss of

myelin

41

42

33 Drugs selected to screen

2,000+ drugs

Virtual screening

Protection of:

- Neurons

- Synapses

- Vessels25 positivedrugs (76%)

91 combinations tested

In AD, excess of β-Amyloid

is produced, leading to

neuronal/glial dysfunction

and cell death

Discovery of PXT864

Acamprosate Baclofen

Aβ-induced toxicity

32 positivecombos

4 combos prioritized, 1 selected

Value Creation and Milestones

43

PXT3003

• Phase III for CMT1A

• Phase III data showing strong

efficacy and safety

• ~$1B WW potential revenue

opportunity / IP through 2030

PXT864

• Phase II for AD

• Strategy to out-license to

commercial partner

- Novel mechanism, upstream

of Aβ and tau

- Validates PLEOTHERAPY AI

platform network

pharmacology approach

- Promising potential in

combination with an NCE

PLEOTHERAPYTM AI

• Potential to produce

pipeline across all

therapeutic areas

- Can go from

discovery and

development to

pre-Phase II POC

in ~ 2.5 yrsPhase IIIFPFD in 1Q 2021