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ProMIS Neurosciences Overview, updated July 29, 2020
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Toronto Stock Exchange (TSX) ticker: PMN OTCQB ticker: ARFXF
Forward looking statement: safe harbor
This slide deck may contain certain forward-looking information. Such information involves known and unknownrisks, uncertainties and other factors that may cause actual results, performance or achievements to bematerially different from those implied by statements herein, and therefore these statements should not beread as guarantees of future performance or results. All forward-looking statements are based on theCompany’s current beliefs as well as assumptions made by and information currently available to it as well asother factors. Readers are cautioned not to place undue reliance on these forward-looking statements, whichspeak only as of the date of this slide deck. Due to risks and uncertainties, including the risks and uncertaintiesidentified by the Company in its public securities filings available online at www.sedar.com. Actual events maydiffer materially from current expectations. The Company disclaims any intention or obligation to update orrevise any forward-looking statements, whether as a result of new information, future events or otherwise.
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ProMIS Neurosciences overview
• Unique technology platform, rapid, cost-effective value creation
• COVID serology test – current test among industry best, goal to create a 2nd iteration that can confirm immunity using ProMIS proprietary reagents
§ Expected need for MMs – 100’s of MM’s of accurate immunity tests
• Alzheimer’s and dementia mission and portfolio: Treat – Detect – Prevent§ PMN310 potential best in class therapy, scientific superiority to likely first in class Biogen’s aducanumab
§ Mid-2021 expected approval for aducanumab
• Entered rapidly growing AD/dementia screening and diagnosis market – JV with leading diagnostic lab
• Initial proof of concept for Alzheimer’s vaccine – ramping up vaccine development
• Numerous near-term catalysts
• Highly experienced management team and Boards
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Unique proprietary platform offers multiple opportunities for value creation: timelines contingent on availability of adequate capital
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Q3 2020 Q4 2020 Q3 2021Q1 2021 Q2 2021 Q4 2021
COVID-19 Serology/Immunity
Assay
PMN310 Best in class AD
antibody therapy
Neurodegenerative Disease
Diagnostics/Assays
Alzheimer’s Vaccine
Scientific evaluations and assay
developmentCOVID-19 Serology/Immunity Assay potential revenue – multiple sources
PMN310 IND enabling work (CMC – manufacturing; GLP Toxicology) PMN310 Phase 1 clinical trial in AD
patients – biomarker and clinical endpoints
Equipment purchase and assay validation
Neurodegenerative disease: potential detection assay revenue, potential diagnostic revenue
Develop vaccine using ProMIS proprietary peptide antigens, preclinical validation, initiate IND enabling work
Therapy Development Diagnostic Development Diagnostic Revenue
ProMIS unique technology platform: the key to unlocking value
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YAntibody
Conformational Epitope
Toxic Protein or virus
Antibodies bind to targets called EPITOPES ( )which have a specific conformation or shape
ProMIS unique technology platform: the key to unlocking value
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YAntibody
Conformational Epitope
Toxic Protein or virus
Antibodies bind to targets called EPITOPES ( )which have a specific conformation or shape
Peptide Antigen
Predict epitope including shape: Supercomputer Computations
Design and create an exact
replica
ProMIS has unique capability to predict epitopes including their shape and make precise replicas – peptide antigens
Highly Specific Peptide antigensMake “best in class”
- Antibody Therapies- Diagnostics- Vaccines
Y
ProMIS portfolio of therapies and diagnostics is based on the unique platform
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PMN310“Best in class” Alzheimer’s Tx
Conformational Epitope
Toxic Oligomers of amyloid
Epitopes for neutralizing antibodies
Serology Assaydetecting neutralizing
antibodies:Immunity
Alzheimer’s Disease
Coronavirus
RBD1 of spike
COVID Serology
1RBD = Receptor binding domain of spike protein
COVID-19 pandemic: need for serology assays that can confirm protective immunity
• Situation• Currently limited, evolving understanding of human immune response to COVID-19 exposure• Historically rapid vaccine development; vaccines will be approved with very little information about
variability and durability of immune response• Numerous existing serology assays provide accurate information about exposure to COVID-19,
including Roche, Siemens, ProMIS/BCNI• But exposure does not necessarily mean immunity, the ability to resist re-infection
• ProMIS approach to evaluation of protective immunity• ProMIS peptide antigens (n=18) identified on RBD of COVID-19 virus• Peptide antigens may represent targets for neutralizing antibodies• Test sera from patients exposed to COVID-19 for neutralizing activity in laboratory assays with live
coronavirus or pseudo-coronavirus• Goal: A high throughput, cost effective assay that accurately correlates with gold standard
tests of antibody-based immunity
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There is a way to measure antibody immunity…but much too expensive and cumbersome…ProMIS/BCNI are working to create a high volume, cost-effective assay
COVID-19 Immunity is complex• Cellular (T-cells) vs humoral (antibodies)• High variability• Quality of immunity after COVID infection• Quality of immunity after vaccination• Duration of immunity (months, years?)• Immunity in elderly, other subgroups• Infection may not lead to immunity from re-
infectionvProMIS assay to provide answers
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YY
YYY Y Y Y
Y Y Y YBlood sample
Do antibodies in the blood sample bind COVID-19 antigen?
Do neutralizing antibodies bind ProMIS peptide epitopes?
YESPatient has
been exposed
YESPatient is immune
PROMIS ASSAY
If results of neutralization assay based on ProMIS proprietary antigens are positive in Q4 2020, ProMIS may seek revenue in several ways
• Offer ProMIS unique peptide antigens in multiple non-exclusive licenses to multiple global diagnostics players (Roche, Siemens, etc) ; $2-$6 per test potential
• Deals with vaccine manufacturers for serology testing in clinical trials and post-marketing• Collaborate with a SPR instrument company (Danaher, Bruker), to seek EUA (Emergency
Use Authorization) approval for our assay on a high throughput SPR platform• Serology testing for large projects e.g. province of Ontario, BC• Potential revenue opportunity Q4/2020, 2021
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COVID serology testing opportunity
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Roche Abbott Siemens Ortho
- Major global players in current COVID serology, all sell test kits to diagnostics labs- Common to validate reagents on SPR (our platform), then sell reagents on a cost/test basis to them- Goal: create an assay that provides information about antibody immunity useful enough so thatnone of the four want to be left out
Abbott CEO Robert Ford in FORBES, July 17“As vaccines become available, we would anticipate continued surveillance testing to monitor and assess for both natural and vaccine related immune response, which would be followed by a steady state of ongoing monitoring and tracking of vaccineprotection…..that’s where I think we will see an increase in serology and antibody testing. I see that that’s going to be anopportunity for us and other companies that have the antibody test, I see that as being a real demand driver on the serology side”
Despite two active decades of clinical trials, there are not yet any approved disease modifying therapies → a pressing, unmet medical need
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Alzheimer’s disease profoundly impacts patients, caregivers and society
“Will Bankrupt Medicareif Therapy is not developed”
Direct and Indirect Costs Today in the US $500BB….
…. and the number is tripling by 2030….
AD characterized by brain accumulation of misfolded proteins:• Extracellular Amyloid Beta (Aβ), then• Intracellular Tau (Neurofibrillary Tangles)Toxic oligomeric species lead to:• Synaptic dysfunction and loss• Degeneration and death of neurons• Neuroinflammation• Brain atrophy
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ProMIS Neurosciences: an integrated strategy to address Alzheimer’s disease
TreatDetect Prevent
ProMIS/BCNI Joint Venture
Create state-of-the-art diagnostic
clinical platform for AD and other
neurodegenerative diseases
PMN310Provide best in class
anti-amyloid therapeutic
antibody that binds only toxic
oligomers, not monomer or plaque
Amyloid VaccineDevise safe, effective anti-amyloid and/or anti-tau vaccines to
induce a specific immune response
against toxic oligomers
Aβ accumulation is slow and protracted, taking 20 to 30 years before cognitive symptomsThis lengthy pre-symptomatic phase of AD provides a substantial opportunity to detect neuropathology,
prevent further brain abnormalities and treat patients before symptoms appear
Using ProMIS proprietary epitope prediction platform
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Billions of neurons are killed leading to the Alzheimer’s (AD) brain
1 Reviewed in Bloom 2014, JAMA Neurol
Healthy Brain Brain with Mild Cognitive Impairment
Brain with AD1
15 years pre-symptomatic 5 years MCI 10 years Alzheimer’s
Toxic oligomers of amyloid cause tau to become toxic, increase neuroinflammation, neurons and synapses die
Neurofilament light (NfL) increases as neurons die at faster rate, P-tau181 increases as amyloid oligomers increase toxic tau oligomers
Alzheimer’s disease: soluble toxic Aβ oligomers – not plaque or monomers – are the most neuropathogenic Aβ species
• Synapse abnormalities and memory impairment correlate poorly with plaque burden in human and mouse AD1,2
• Aβ monomers and Aβ insoluble fibrils (plaque) have little or no demonstrable toxicity in vitro or in vivo3-5
• Soluble Aβ oligomers show the highest degree of neurotoxicity6
• Toxicity in primary neuron cultures and brain slices3,5,7-9
• Induction of cognitive impairment in rodents3,4,10
151Jacobsen et al, 22006, PNAS; 2Brier et al, 2016, Science Trans Med; 3Shankar et al, 2008, Nature Med; 4Cleary et al, 2005, Nature Neuroscience; 5Hong et al, 2016, Science; 6Benilova et al, 2012, Nature Neuroscience - Review; 7Lacor et al, 2007, J Neuroscience; 8Jin et al, 2011, PNAS; 9Lauren et al, 2009, Nature; 10Balducci et al, 2010, PNAS
Synaptotoxicity of human Ab oligomers on hippocampal neurons in vitro7
5min 6h 24h 24h control
Monomers Oligomers Fibrils
Normal Monomers Oligomers Fibrils
Ab species injected
In vivo impairment of recognition memory by Ab oligomers, not monomers and not fibrils10
PMN310: an anti-Aβ-oligomer antibody with strong potential to demonstrate best-in-class characteristics
Biogen’s aducanumab EMERGE study validates the amyloid hypothesis
Aducanumab and BAN2401 are only partially selective for amyloid oligomers
• Aducanumab (phase 3) and BAN2401 (phase 2) showed modest but meaningful efficacy in reducing cognitive worsening
• Both significantly bind amyloid plaque → ARIA-E (patchy brain swelling)• Neither bind monomer (the physiologic amyloid species)
PMN310 is a next-generation, best-in-class anti-amyloid therapy• Highly selective for only toxic oligomers• Dose will not be limited by off-target binding or side effects
• Does not bind monomer• Does not bind plaque → likely no ARIA-E
• All dosed PMN310 will focus on neutralizing toxic oligomers → potential greater clinical efficacy
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Aβ amino acids 13-16 (HHQK)A unique, Aβ oligomer specific epitope targeted by PMN310
There are three forms of amyloid, choosing the correct target is critical….
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Monomer – Important for brain health
Plaque – usually present, but no significant role in
disease
Toxic oligomers –thousands of scientific
studies showing neurotoxicity
Two drugs: Biogen’s aducanumab and EISAI’s BAN2401 partially selective FOUR OUT OF FOUR POSITIVE*(Two Phase 2 trials, one Phase 3 program*)!!! DOSE-LIMITING TOXICITY side effect ARIA-E** due to plaque binding !!!
* Using Biogen’s presentation of patients consenting to V4 amendment, receiving 10mg dosing** ARIA-E (Amyloid Related Imaging Abnormality- Edema) also known as brain swelling
Monomer – Important for brain health
Plaque – usually present, but no significant role in
disease
Toxic oligomers –thousands of scientific
studies showing neurotoxicity
Monomer – Important for brain health
Plaque – usually present, but no significant role in
disease
Toxic oligomers –thousands of scientific
studies showing neurotoxicity
Monomer – Important for brain health
Plaque – usually present, but no
significant role in disease
Toxic oligomers –thousands of scientific
studies showing neurotoxicity
4 programs/13 phase 2 and 3 clinical trials non-selectively targeting all forms of amyloid, wasted too much ammunition on abundant monomer to be effective
All negative
10 programs/25 phase 2 and 3 clinical trials targeting monomer
All negative
Forms of Amyloid
AmyloidBinding
profile of clinical
programs
Four positive trials…partially selective antibodies…higher dose over long duration leads to better outcomes, but all limited by patchy brain swelling (ARIA-E)
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Biogen Ph1b “PRIME” December 2014
Eisai BAN2401 Phase 2July 2018
Biogen pivotal EMERGEDec 2019*
Biogen pivotal ENGAGEDec 2019**
* Final Intent-to-treat data set ** Post-protocol version 4 data set
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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
ProMIS following the “best in class” playbook with PMN310• Improved selectivity for toxic
oligomers• No binding to plaque = Lower
risk of ARIA-E = Better safety• Ability to safely dose higher• No “waste of ammunition” on
non-toxic amyloid -> Greater efficacy
Lipitor Humira Sovaldi/HarvoniCholesterol RA, Crohn’s Hepatitis C1996 2003 2014
PeakSales $BB’s
$12BB$16BB
$25BB
Binding the right form of toxic oligomer is critical……
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Aducanumab (Biogen)• Phase 2 & 3 success• ARIA-E side effect
Solanezumab (Eli Lilly)• Phase 2 failure• Phase 3 failure
Bapineuzumab (Pfizer)• Phase 2 failure• Phase 3 failure• ARIA-E side effect
MONOMERS- binding wastestherapeutic ammunition
FIBRILS (Plaque)- binding wastestherapeutic ammunition- contributes to ARIA-Eside effect
OLIGOMERS*- the right target
PMN310• Selective binding to
oligomers-> Expected improvement in
efficacy & safety
* Synthetic oligomers
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ARIA-E associated with aducanumab, BAN2401 & bapineuzumab; PMN310 lack of binding to Aβ plaque strongly suggests a potential safety advantage
Aducanumab PMN310
Plaque binding
Vascular deposit binding
No binding to plaque or vascular deposits
Most likely no ARIA-E*
* ARIA-E (Amyloid Related Imaging Abnormality- Edema) also known as brain swelling
Humanize
d PMN310
Aducanumab
Bapineu
zumab
huIgG10
10
20
30
40
50B
indi
ng R
espo
nse
(RU
)
PMN310 shows superior binding to toxic oligomers from human AD brains vs other antibodies directed against amyloid-beta
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• Binding of antibodies to the toxic oligomer-enriched LMW fraction of soluble human AD brain extract was evaluated by surface plasmon resonance (SPR)
• Results representative of over 10 SPR runs with extracts from 11 different AD brains
• huIgG1 = Background control
Source for comparative reagents: Creative Biolabs
AbO +/- MabNovel 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
Dis
crim
inat
ion
Inde
x
#
* *
Discrimination index = (Time exploring new object – time exploring familiar object) / total exploration timeResults press released January 9, 2017, www.promisneurosciences.com 23
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, by saving mouse neurons
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
PMN310: potential for value-creating clinical data in the near term - likely positive market developments could amplify PMN value
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ProMIS Final IND enabling work
2020
AD in Down Syndrome - prevention, treatment, or both: Biomarker and
clinical endpoint readout
Sporadic AD Phase 1: 3 month Pbo control, 9 month extension, MAD design
2021 2022
Potential Approval Path:AD in Down Syndrome
AducanumabFiling
AducanumabApproval
Aducanumab Launch and Market Development- Reimbursement, Med Ed: ARIA-E screening
BAN2401 Ph 3 data
• Recent advances in blood-based biomarkers may allow ProMIS to detect an objective treatment signal as early as Phase 1, potentially providing rapid & cost-effective proof-of-concept
ProMIS plans to use biomarkers in its first clinical study, which could show a disease modifying treatment effect at a cost of $5MM-$10MM
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BloodNfL
100*
* 100 = patient baseline value
Months1260
Placebo/ Large natural history dataset
3 mg/kg
10 mg/kg
20 mg/kg
40 mg/kg
80 mg/kg
Placebo dataset as an historical control
Potential for meaningful datain 6-12 months from trial start…
Potential biomarkers:
NfL – Neuronal Loss
P-tau181 - tau toxicity
Others
Dose escalation design: 3-month placebo-control, then 9-month open-label extension
Alzheimer’s/Dementia screening, diagnosis, and disease monitoring
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Historical: AD diagnosis at autopsy
Recent advance:A/T/N
Amyloid PET
Tau PET
Cortical MRI
$10,000 - $15,000
Future Vision A/T/N
NfLBlood based
P-tau181Blood based
~$100
…Plus proprietary assays
TDP43 , Alpha Synuclein- Differential diagnosis
Other assays – overall algorithm
ProMIS/BCNI Joint Venture to build a diagnostic revenue base
• Significant progress over past several yrs. to advance a more precise diagnosis of AD• Introduction of A/T/N (amyloid/tau/neurodegeneration) criteria 2 years ago offered an unbiased approach for
objective biological diagnosis of AD • However, the A/T/N diagnostic approach, until recently, required either costly PET and MRI scan assessments or
invasive lumbar puncture to measure specific biomarkers in cerebrospinal fluid (CSF)
• Blood levels of NfL (neurofilament light chain) and P-tau181 (phosphorylated tau181)• Provide equally precise A/T/N characterization as imaging or CSF measurements, and can thus offer convenient, cost-
effective and objective detection and monitoring of the AD process
• JV/collaboration to first offer existing blood-based assays for NfL and P-tau181
• Further assays to be added potentially incorporating ProMIS’ proprietary peptide antigens & tests for additional neurodegenerative diseases
• ProMIS’ ultimate mission with its partner, BCNI, is to build a portfolio of assays that enables early detection and monitoring of disease progression before symptoms arise
• Discussions for screening projects have started – goal revenue in 2021, possibly Q4 2020
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ProMIS therapeutic vaccine for Alzheimer’s disease
• Large patient population with symptomatic AD in need of effective treatment (n≥5M, USA) –> Therapeutic vaccination
• Ever greater number of individuals in the pre-symptomatic phase of the disease (potentially 40% of the population over 65, ~50M) –> Prophylactic preventative vaccine
• Vaccine approach will benefit from recent progress in the development of blood-based biomarkers of neurodegeneration to diagnoseAD and identify individuals at risk of developing disease
• ProMIS discovery platform being applied to devise a safe and effective vaccine to induce a specific immune response against toxic Ab oligomers • Identified a set of 6 conformational peptide epitopes selectively exposed on toxic Ab oligomers • All 6 peptide epitopes shown to be capable of inducing selective and protective antibodies against toxic Ab oligomers • Successful proof of concept vaccination study conducted with one of the peptides (cSNK) in a mouse model of AD (APP/PS1
mice): Neuronal protection and improvement in cognitive deficits2• Concept: multivalent vaccine with some or all 6 Ab peptides. Tau peptides recently identified could also be included.
• Immediate aims: Construct and test multivalent Ab vaccine for ability to induce a protective antibody response
281Marciani DJ, 2019, AAAS Research, https://doi.org/10.34133/2019/5341375; 2Silverman, JM et al, 2018, ACS Chem Neurosci
Benefit of vaccination with ProMIS Ab oligomer (AbO) epitope
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Mice vaccinated with conformational Ab oligomer epitope (cSNK) coupled to KLH
PMN301,3
02,30
3,304
,305
PMN301-N
MS(1:5)
PMN302-N
MS(1:5)
PMN303-N
MS(1:5)
PMN304-N
MS(1:5)
PMN305-N
MS(1:5)
NMS-100
0
20
40
60
80
Bin
ding
Res
pons
e (R
U)
AbM(HFIP) AbM(untreated) AbO(SynAging)
Robust, sustained antibody response (SPR)
Improvement in behavioral deficits of APP/PS1 mice
Protection against synaptic damage
Biological support for multivalent vaccine approach:Greater binding with mixture of sera from mice
immunized with different AbO epitopes vs immune serum against individual peptides
Silverman et al. 2018. ACS ChemNeurosci 9: 1591-1606
AbO
SPR
HFIP Abmonomers
Untreated Abmonomers
(normal mouse serum)
ProMIS: current portfolio of antibodies selectively targeting toxic mis-folded proteins
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Scientific Literature:mis-folded protein role
in disease pathogenesis;
role of other forms (molecular species)
Predict conformational
epitopes on target molecular species
Immunize and screen antibody candidates
for selectivity
Assess functional benefit in vitro and in vivo; assess binding strength to enriched patient biomaterial
IND enabling development
Biomarker readouts of pharmacologic
effect in Ph1
Predict Produce Prioritize Lead program early POC
Amyloid beta PMN310, ready for final IND enabling work
Alpha SynucleinSeveral leads, active
partnering discussions
TDP43 Several leads, active partnering discussions
tau Early leads, immunization ongoing , active partnering discussions
Many ongoing discovery: RACK1, DISC1, FUS, SOD1, Amylin, PrP, other
ProMIS Summary Investment Thesis
• Unique technology platform – rapid, cost-effective, differentiated
• Rapid response to COVID-19; goal to create differentiated immunity serology assay, potential near term revenue if successful
• Strategic portfolio in Alzheimer’s based on unique platform – Detect – Treat – Prevent
• PMN310 scientifically superior to likely “first in class” therapy Biogen’s aducanumab, PMN310 selective for toxic oligomers, stronger binding
• Biogen filed for regulatory approval, potential launch mid 2021, will be strong catalysts for the field, especially improved amyloid targeted therapies like PMN310
• ProMIS broad portfolio, programs targeting mis-folded versions of TDP43, alpha synuclein, tau, ongoing partnering discussions (timing affected by industry priority shift to COVID, lab closures, etc.)
• Aducanumab launch will also likely lead to dramatic growth in demand for screening and diagnosis of dementia
• ProMIS JV with BCNI will enable capitalizing on that growing demand with both established and proprietary assays
• ProMIS technology enables potential Alzheimer’s vaccine – building on early POC
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Name
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
25+
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
James Kupiec Chief Medical Officer 25+
§ Former VP, Global Clinical Leader for Parkinson’s disease, and Clinical Head of the Neuroscience Research Unit for Pfizer, Inc
§ Clinical focus on development of therapies for neurodegenerative disorders§ Held positions at Sanofi-Synthelabo and Ciba-Geigy Pharmaceuticals
Name
Anthony Giovinazzo
Richard Gregory
Bill Wyman
Johannes Roth
Pat Kirwin
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Independent board of directors
31
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
Scientific Advisory Board
32
Prior ExperienceYears of Experience
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
20+
25+
20+
Sharon Cohen, MD 20+ Medical Director & Principal Investigator of Toronto Memory ProgramFRCPC in neurology from Royal College of Physicians of Canada and a fellowship in Behavioural Neurology from the University of Toronto
Rudy Tanzi, PhD 20+ Professor of Neurology at Harvard University, Vice Chair of Neurology, Director of Genetics & Aging Research Unit, Co-Director McCance Center for Brain Health at Mass General Hospital
C. Warren Olanow, MD 25+ Previous Henry P & Georgette Goldschmidt Professor & Chairman, Department of Neurology at Mount Sinai School of Medicine, presently Professor Emeritus Department of Neurology & Department of Neuroscience, CEO of CLINTREX
Affiliations
Andre Strydom, MD, PhD Professor Institute of Psychiatry, Psychology and Neuroscience at King’s College London Honorary Consultant psychiatrist, South London and the Maudsley NHS Foundation Trust
25+
José Molinuevo, MD, PhD 20+ Scientific Director, Alzheimer Prevention Program at Barcelonaβeta Brain Research Center, Barcelona SpainAssociate Professor, Pompeu Fabra University, Barcelona, Spain
Hans Frykman, MD, PhD 20+ Clinical assistant professor of medicine at the University of British ColumbiaCEO and Medical Director of BC Neuroimmunology Lab (BCNI)
Thank You
Eugene Williams, Executive [email protected]+1 (617) 460-0978
Website: www.promisneurosciences.comTwitter: https://twitter.com/ProMISincLinkedIn:https://www.linkedin.com/company/promis-neurosciences
Please feel free to contact us with any additional questions.
Elliot Goldstein, MD, [email protected]+1 (415) 341-5783
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