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HARNESSING THE POWER OF PRECISION MEDICINE TO TREAT ALZHEIMER’S AND OTHER NEURODEGENERATIVE DISEASES

TorontoStockExchange(TSX)ticker:PMN.TOU.S.OTCQBticker:ARFXF

January23,2018

Forward Looking Statement: Safe Harbor

This slide deck may contain certain forward-looking information. Such information involves known and unknown risks, uncertainties and other factors that may cause actual results, performance or achievements to be materially different from those implied by statements herein, and therefore these statements should not be read as guarantees of future performance or results. All forward-looking statements are based on the Company’s current beliefs as well as assumptions made by and information currently available to it as well as other factors. Readers are cautioned not to place undue reliance on these forward-looking statements, which speak only as of the date of this slide deck. Due to risks and uncertainties, including the risks and uncertainties identified by the Company in its public securities filings available online at www.sedar.com. Actual events may differ materially from current expectations. The Company disclaims any intention or obligation to update or revise any forward-looking statements, whether as a result of new information, future events or otherwise.

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Investment highlights

• ProMIS is developing a portfolio of disease modifying therapies in neurodegenerative diseases, including Alzheimer’s disease, based on our proprietary discovery platform

- Neurodegenerative diseases a high priority area for large pharma licensing and acquisition

• ProMIS lead programs are following a “best in class” strategy targeting amyloid beta in Alzheimer’s disease, with advantages over ”first in class” therapy from Biogen (aducanumab)

• Listed on the TSX, ticker symbol PMN.TO. Listed on U.S. OTCQB, ticker symbol ARFXF and pursuing U.S. NASDAQ listing in 2018

• Highly experienced management team

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The potential value of Biogen’s aducanumab is gaining wide recognition…good news in Alzheimer’s…and a rising tide for ProMIS

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• Goldman Sachs Buy Biogen 08/16/17 “$12B peak sales estimate”

• Morgan Stanley Upgraded to OW Biogen 10/05/17 “Alzheimer’s Disease Remains a Must-Own Catalyst”

• RBC Initiate Biogen SP 09/14/17 “theoretical total market size could be $25B in U.S. alone...65% probability of success for aducanumab”

• Jeffries Initiates Coverage 07/10/17 “estimates odds of aducanumab success at 60%”

• Evaluate Pharma June 2017 “Aducanumab the highest NPV program in all industry” pipelines, Estimates NPV of $10B”

Biogen’s aducanumab is a good bet to be the first disease modifying therapy in Alzheimer’s…

• First ever amyloid beta targeted therapy with positive Phase 2 data, in December 2014

- ProMIS programs inspired by its success

• Biogen presented positive three year follow up data in November 2017 –still slowing disease progression

• Pivotal trials ongoing, data likely available in H1 2020

• ProMIS has generated scientific evidence supporting aducanumab’s superiority over prior failed therapies

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The three largest products in industry history were not first in class, but “best in class” – the inventors identified improvements to existing drugs

ProMISfollowingthe“bestinclass”playbook:

• Tookadvantageof“proofofbiology”developedbyearlierproducts:thescientificrationaleforaducanumab’ssuccess,whenallpriorprogramsfailed

• UsedProMIS proprietaryscienceplatformtodesignanimprovedproduct,whichmayyieldsuperiorclinicalresults

Lipitor Humira Sovaldi/Harvoni (Pharmasset)Cholesterol RA,Crohn’s HepatitisC1996 2003 2014

PeakSales$BB’s

$12BB$16BB

$25BB

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There is a scientific framework for understanding clinical performance of existing therapies…..and the rationale for ProMIS potential advantages

TherapeuticPotency

Drugdeliveredtothepathogen

Bindingtothepathogen?

Avoidsideeffects,dosehigh

Avoidtargetdistraction

Aducanumab

PMN310

X ++ ++

+++ +++ +++

Sideeffect(ARIA-E)limitsdoselevel

Bindingtoplaqueormonomer“wastes”therapeuticammunition

Betterbindingtotoxicoligomersthanfailedclinicalprogrambapineuzumab

TargetProductProfile

Binding the right form of amyloid beta is critical: the toxic oligomer is the target

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Aducanumab• Phase2success• ARIA-Esideeffect

Solanezumab• Phase2failure• Phase3failure

Bapineuzumab• Phase2failure• Phase3failure• ARIA-Esideeffect

MONOMERS- bindingwastestherapeuticammunition

FIBRILS(Plaque)- bindingwastestherapeuticammunition- contributestoARIA-Esideeffect

OLIGOMERS- therighttarget

PMN310• Selectivebindingto

oligomers->Expectedimprovementin

efficacy&safety

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ARIA-E associated with both aducanumab & bapineuzumab; PMN310 lack of binding to Ab plaque deposits suggests a potential safety advantage*

Aducanumab PMN310

Plaquebinding

Vasculardepositbinding

Nobindingtoplaqueorvasculardeposits

*PMN310IgG4isotypealsocorrelatedwithlackofARIA-E

Not all oligomers are created equal… soluble low molecular weight toxic oligomers drive neurotoxicity and disease progression

• Recent findings from leading researchers show AD brain homogenates contain heterogeneous Ab aggregates dominated by high molecular weight species (>70kDa, or ~15+ “monomers”)1,2

• Neurotoxic activity resides primarily in the LMW (low molecular weight) fraction (<70 kDa)1

• This is consistent with reports from many oligomer researchers that a subset of the LMW oligomers are the most toxic oligomers (dimer, tetramer, dodecamer)1,3-7

• Importantly, purified oligomers from human brains are different and more potent than those synthesized in vitro2,4

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1Yang,Tetal,2017,JNeurosc;2EsparzaTJetal,2016,NatureScientificReports;3Shankar,GMetal,2008,NatMed;4Jin,Metal,2011,PNAS;5Cleary,JPetal,2005,NatureNeurosc;6Lesne,SEetal,2013,Brain;7Ferreira,STetal,2015,FrontiersinCellularNeuroscience

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HMWFraction

LMWFraction

Thyroglobulin670kDa

GammaGlobulin158kDa

Ovalbumin44kDa

Myoglobin17kDa

Evaluating soluble pooled brain extract from eight AD patients using SEC: the profile supports the existence of three main subsets of toxic oligomers

Abmonomer4.5kDa

Tetramer(4)~18kDa

Dodecamer (12)~56kDa

Dimer(2)~9.0kDa

--- ADSolubleBrainExtract

--- Molecularweightmarkers

Aducanumab is a more effective binder of “the real thing” than bapineuzumab, which may contribute to better clinical outcomes…PMN310 is best of all

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Humanize

d PMN310

Aducanumab

Bapineu

zumab

huIgG10

10

20

30

40

50B

indi

ng R

espo

nse

(RU

)

• Bindingofantibodiestothetoxicoligomer-enrichedLMWfractionofsolublehumanADbrainextractwasevaluatedbysurfaceplasmonresonance(SPR)

• Resultsrepresentativeof2SPRrunswithextractsfrom8differentADbrains

• huIgG1=Backgroundcontrol

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Alzheimer’s…the root cause

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The cause of Alzheimer’s: the progressive death of neurons in the brain

1 ReviewedinBloom2014,JAMANeurol

Healthy BrainBrain with

Mild Cognitive Impairment>15M Patients in US

Brain with AD1

>5M Patients in US

The number of AD patients and associated costs are rising rapidly

• By 2050, one new case of AD is expected to develop every 33 seconds in the U.S.

• $500B Cost in the US, combining direct medical and indirect costs

• Fastest growing cause of death

Alzheimer’s disease: soluble toxic amyloid beta oligomers, not plaque, are the most neuropathogenic amyloid beta species

• SynapseabnormalitiesandmemoryimpairmentcorrelatepoorlywithplaqueburdeninhumanandmouseAD1,2

• Aβ monomersandAβ insolublefibrils(plaque)havelittleornodemonstrabletoxicityinvitroorinvivo3-5

• SolubleAβ oligomersshowthehighestdegreeofneurotoxicity6• Toxicityinprimaryneuronculturesandbrainslices3,5,7-9

• Inductionofcognitiveimpairmentinrodents3,4,10

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1Jacobsenetal,22006,PNAS;2Brieretal,2016,ScienceTransMed;3Shankaretal,2008,NatureMed;4Clearyetal,2005,NatureNeuroscience;5Hongetal,2016,Science;6Benilovaetal,2012,NatureNeuroscience- Review;7Lacoretal,2007,JNeuroscience;8Jinetal,2011,PNAS;9Laurenetal,2009,Nature;10Balduccietal,2010,PNAS

Synaptotoxicity ofhumanAb oligomersonhippocampalneuronsinvitro75min 6h 24h 24hcontrol

Monomers Oligomers Fibrils

Normal Monomers Oligomers Fibrils

Ab speciesinjected

InvivoimpairmentofrecognitionmemorybyAb oligomers,notmonomersandnotfibrils10

Current insight about Alzheimer’s biology: prion-like toxic oligomers are the disease pathogens

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AmyloidPlaque

AbMonomer

Ab Prion-likeneurotoxicoligomers

Non-toxicaggregates*

InductionofTauPrionFormation

&Disease

Progression

“Non-Toxic”Pathway

LowMolecularWeightOligomersDimer(2),Tetramer(4)

Dodecamer (12)

APP

Propagationofmisfolding

“Toxic”pathway

*Yangetal,2017,JNeurosc:HMWsolubleaggregatesinbrainhomogenatewithMWof70kDa– 600kDa(15– 140“monomer”equivalents)

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Dr. Eliezer Masliah, new head of US Nat’l Institute of Aging, stressed the need for therapies targeting the toxic oligomer at the AAN1 meeting in April 2017

• “A common mechanism underlies the top 3 neurodegenerative disorders, including Alzheimer’s: monomers aggregate into oligomers that are toxic to synapses and propagate in a prion-like fashion”

• Need to target oligomers of amyloid beta, tau, alpha-synuclein … [with therapy]

• Biogen’s aducanumab is showing promise, since it targets aggregated amyloid beta [oligomers]

1AmericanAcademyofNeurology

ProMIS used its proprietary technology platform to design antibodies with advantages over prior therapies

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Greater selectivity for the toxic oligomer (AβO)

• No monomer binding (like aducanumab), better efficacy

• No plaque binding (improvement over aducanumab), lower risk of brain edema side effect

• IgG4 (improvement over aducanumab) – lower risk of brain edema side effect

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Product Oligomer>MonomerBinding(SPR)

NoPlaqueBinding(IHC,Dotblot)

ADBrainExtract/CSFvsCTL(SPR)

Inhibitionofinvitro

propagation

Inhibitionofinvitroneurotox

Inhibition ofinvivoneurotox

PMN310✔ ✔ ✔ ✔ ✔ ✔

PMN330✔ ✔ ✔ ✔ ✔ ✔

PMN350✔ ✔ ✔ ✔ ✔ ✔

Firstleadproduct

Secondleadproduct

Thirdleadproduct

PMN310, PMN330 and PMN350 have all shown target-selective binding and functional performance

PMN310 blocks oligomer propagation and neurotoxicity in vitro

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Complete inhibition of oligomer propagation in vitro

0 1 0 2 0

0

2 ´ 1 00 5

4 ´ 1 00 5

6 ´ 1 00 5

I n c u b a t i o n T i m e ( h r s )

Re

la

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ve

F

lu

or

es

ce

nc

e

Un

it

s

A ß 4 2 + 3 0 5 - 6 1A ß 4 2

Incubationtime(hrs)

Relativ

eflu

orescenceun

its Ab42 Ab42+PMNMab

Inhibition of Ab oligomer toxicity in vitro

CTL AβO 5:1 1:1 1:2 5:1 1:1 1:240

50

60

70

80

90

100

110

120

Cel

l Via

bilit

y (%

of c

ontr

ol)

AbO + PMN mAb PMN mAb alone

(Thioflavin-based assay) (Primary mouse cortical neurons)

Normalpropagation

InhibitionbyPMNantibody

AbO +/- Mab

Novel Object Recognition Assay• Control mice remember a familiar object when re-exposed

to it and spend more time exploring a new object

• Oligomer-injected mice lose the ability to discriminate between known and novel objects and spend equivalent amounts of time exploring both

7 days

-0.2

0.0

0.2

0.4

0.6

Vehicle AβOPMN310+vehicle

PMN310+AβO

Discrim

inationInde

x

#

* *

Discriminationindex=(Timeexploringnewobject– timeexploringfamiliarobject)/totalexplorationtimeResultspressreleasedJanuary9,2017,www.promisneurosciences.com 21

N=12 per arm, *different from AβO (p < 0.05), #different from vehicle (p <0.05)

Administration of PMN310 to mice: prevents loss of short-term memory formation caused by toxic oligomers

THE RESULTSTHE EXPERIMENT

• Mice are tested for discriminating objects after brain injection of:

• Buffer (vehicle) - normal response • Toxic Aβ Oligomer• PMN310 and buffer (vehicle)• PMN310 and Aβ Oligomer

In vivo improvement of hippocampal synaptic and inflammation markers suggests cognitive benefit came from preventing neuronal death

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Decrease in hippocampal marker of inflammation

Vehicl

eAβ

O

PMN Mab

+ AβO

PMN Mab

+ Vehicl

e0.0

0.5

1.0

1.5

TNF-α

(pg/

ug to

tal p

rote

in) TNF-a

#

*

#* #*

Vehicl

eAβ

O

PMN Mab

+ Aβ

O

PMN Mab

+ Veh

icle

2

3

4

5

6

7

8

9

PSD

-95

(pg/

ug to

tal p

rote

in)

Vehicl

eAβ

O

PMN Mab

+ Aβ

O

PMN Mab

+ Veh

icle

0

5

10

15

20

25

SNA

P25

(pg/

ug to

tal p

rote

in)PSD-95 SNAP25

#

*

#

*#

#

*

#

#*

Preservation of hippocampal synaptic proteins

*DifferentfromVehicle(p<0.05);#DifferentfromAbO (p<0.05)

Biogen’s aducanumab is the first amyloid beta-targeted therapy with positive clinical efficacy results.. Likely first in class - PMN310 scientifically designed to be best in class

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Product Company Phase2Result

Phase3Result

MonomerBinding*

OligomerBinding*

Plaquebinding*

AntibodyIsotype

Solanezumab Lilly Failed,n=52 Failed,3trials +++ + None IgG1

Bapineuzumab J&J,Pfizer Failed,n=234 Failed ++ ++ +++ IgG1

Verubecestat Merck Noefficacyreadout,n=200

Failed DepletesMonomer

N/A N/A N/A

Crenezumab Roche Failed, n=450 Ongoing at4xdoseofPh2

+ ++ +++ IgG4

Gantenerumab Roche Failed Stoppedenrolling

+ ++ +++ IgG1

Aducanumab Biogen PositiveEfficacyn=166

Ongoing,expected2020

None +++ +++ IgG1

PMN310,330,350 ProMIS Ontrackfor2021

None +++ None IgG4

*Source:AndreUddin,MackieResearch

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There is a scientific framework for understanding clinical performance of existing therapies…..and the rationale for ProMIS potential advantages

TherapeuticPotency

Drugdeliveredtothepathogen

Strengthofbindingtothepathogen

Avoidsideeffects,dosehigh

Avoidtargetdistraction

Bapineuzumab

Aducanumab

PMN310

X

X

X

++

+

++

+++ +++ +++

Thisprofileledtofailure….

Thisprofilewilllikelyleadtoapproval….

PMN310profilemayleadtosuperiorityand”BestinClass”

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Getting more antibody to the target: properties of PMN310 support improved therapeutic potency versus other Ab-directed antibodies

LMW ToxicOligomers

Plaque

Monomers

Aducanumab

HMW AggregatesBapineuzumab

• Greater specificity for toxic oligomers –> No target distraction, greater efficacy

• Reduced risk of ARIA-E –> Ability to dose higher

huPMN310

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ProMIS Neurosciences pipeline: Output of a highly productive discovery engine

ProductCandidate

Target Protein

Disease Area Focus Discovery Pre-Clinical Phase I

PMN310 Toxic Amyloid βOligomers Alzheimer’s1

PMN350 Toxic Amyloid βOligomers Alzheimer’s1

PMN330 Toxic Amyloid βOligomers Alzheimer’s1

In Process Tau Protein Alzheimer’s2

PMN110PMN120PMN130

Superoxide Dismutase-1 (SOD1)

Amyotrophic Lateral Sclerosis

(ALS)

Under Evaluation

TAR DNA-Binding Protein 43 (TDP43)

Amyotrophic Lateral Sclerosis

(ALS)3

In Process alpha synuclein Parkinson’s Disease4

ProMIS leadprograms:abestinclassstrategyinAlzheimer’s

1 PotentialuseinDownsyndrome2 Potentialuseinotherdementias,eg.chronictraumaticbraininjury3 Potentialuseinfrontotemporaldementia4 PotentialuseinLewybodydementia

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ProMIS value creation potential – medium term

2018 2019 H12020

Aducanumabpivotaldatapublic

PMN310ScientificDifferentiation;INDenabling PMN310Phase1SAD

Potentialpartnering– othertargets:TDP43,SOD1,alphasynuclein,tau

Diagnosticsdevelopment,collaborations

Aducanumab pivotaltrials

ProMIS Neurosciences: summary

• Developing “best in class” therapies targeting the root cause of Alzheimer’s and other neurodegenerative disease

• ProMIS proprietary technology platform is generating additional differentiated products in dementia, ALS, and Parkinson’s disease; potential partnering opportunities

• Numerous near term catalysts • Lead product PMN310 in Alzheimer’s disease on track to

• Further confirm differentiation from likely “first in class” Biogen’s aducanumab• Initiate clinical trials in 2019 and• Potentially superior clinical data vs aducanumab

ProMIS pursuing NASDAQ listing, likely in 2018

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Thank You

Eugene Williams, Executive Chairmaneugene.williams@promisneurosciences.com+1 (617) 460-0978

Website: www.promisneurosciences.comTwitter: https://twitter.com/ProMISincLinkedIn:https://www.linkedin.com/company/promis-neurosciences

We appreciate your interest in ProMIS Neurosciences and the exciting developments in AD therapeutics. Please feel free to contact us with any additional questions.

Elliot Goldstein, MD, CEOelliot.goldstein@promisneurosciences.com+1 (415) 341-5783

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Investor Relations Contact:Nick Rigopulos, PresidentAlpine Equity Advisorsnick@alpineequityadv.com+1 (617) 901-07856

Name

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Experienced leadership team

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Prior ExperienceTitle Years of Experience

Executive Chairman

CEO

Chief Science Officer

Chief Physics Officer

CFO

Chief Development Officer

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25+

25+

20

25+

25+

§ Former SVP at Genzyme, with senior roles integrating commercialization, drug development, and deal making

§ Recently the CEO of Dart Therapeutics, an Orphan Disease drug development company

§ Founder and director of Adheris, which became the largest company in the patient adherence/compliance area

§ Held positions as SVP of Strategic Product Development at SmithKline Beecham (now GSK)

§ Chief Operating Officer and Chief Medical Officer of Maxygen§ Chief Operating Officer at DART Therapeutics

§ Holds the Canada Research Chair in Neurodegeneration and Protein Misfolding Diseases,

§ Serves as the Director of the University of British Columbia ALS Centre,

§ Awarded the Jonas Salk Prize for biomedical research in 2000

§ Professor at UBC in the Department of Physics and Astronomy since 2001§ Appointed as the Canada Research Chair in Theoretical Molecular Biophysics§ Associate member of the Genome Sciences and Technology Program, the

Bioinformatics Program, and the Institute for Applied Mathematics at the University of British Columbia

§ Founding Managing Director of Danforth Advisors§ Served as the Chief financial officer of Homology, Inc, GenePeeks,

Inc., Transkaryotic Therapies, Inc., Cidara, Inc., Apellis, Inc. and Stealth BioTherapeutics, Inc.

§ Former VP of Research at Genzyme§ Associate Immunopathologist at SmithKline Beecham where she

established an Immunotoxicology program§ Her work has resulted in over 60 scientific publications and

multiple patents

Gene Williams

Elliot Goldstein

Neil Cashman

Steven Plotkin

Dan Geffken

Johanne Kaplan

NameAnthony Giovinazzo

Richard Gregory

Bill Wyman

Johannes Roth

Pat Kirwin

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Independent board of directors

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Prior ExperienceYears of Experience25+

25+

15+

§ President and CEO of Sunovion CNS Development Canada ULC

§ President, CEO and a Director of Cynapsus Therapeutics from 2009 to 2016 and one of the three original inventors and patent holders of the company’s Parkinson’s focused technology

40+

§ Chief Scientific Officer & Executive VP for Research at ImmunoGen

§ Held a variety of roles at Genzyme and Sanofi-Genzyme, including Vice President for Gene Therapy, Head of Corporate Research and Head of R&D

§ Co-founded the management consulting firm, Oliver Wyman & Co

§ Former President of the Management Consulting Group called Booz Allen and Hamilton

§ Founding director and partner at FiveT Capital Holding AG§ A board member of Insilico Biotechnology AG

§ Senior partner at Kirwin LLP§ Advises and represents businesses in a range of industries and

sizes from local to multinational30+

Name

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Scientific/business advisory board

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Prior ExperienceYears of Experience

ScientificAdvisoryBoard(SAB)

BusinessAdvisoryBoard

Todd Golde, MD, PhD.

Lary Walker, PhD.

Bill Mobley, MD, PhD.

§ Director of the Center for Translational Research in Neurodegenerative Disease at the University of Florida

§ Associate Professor of Neurology and Research Professor at Emory University Yerkes National Primate Research Center

§ Dean for Neurosciences Initiatives, Distinguished Professor of Neurosciences, and Florence Riford Chair for Alzheimer Disease at the University of California, San Diego

Mara Aspinall, MBA § Executive Chairman of GenePeeks§ Former President and CEO of Ventana Medical Systems, a division of

Roche Group, a worldwide leader in the development and commercialization of tissue-based cancer diagnostics

Nigel Burns, PhD. § CEO and Founder of SweetSpot Therapeutics Ltd§ Served as Senior Vice President of Cambridge Antibody Technology

Michael Higgins, MBA § Currently an Entrepreneur-in-residence at Polaris Partners§ Previously at Genzyme, served as Vice President of Corporate Finance

and Vice President of Business Development, and was involved with multiple business units, including Cell Therapy, Gene Therapy and Orphan Diseases

25+

20+

25+

25+

25+

20+

“Restart”July 2015

May 2016

Sep 2016

$25MM

$10MM

$2MM$2.5MM at $2MM Pre

$1MM at

$9MM Pre

$1.5MM at

$24MM Pre

Financial Status

• Cash life into H2 2018

• Common stock – 220,058,533

• Warrants – 24,708,098

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ProMIS has successfully raised $12.5MM in 5 rounds, at increasing values

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$2.7MM at

$26MM Pre

Feb 2017

$4.8MM At

$50 MM Pre

$50MM

Sep 2017