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COYA THERAPEUTICS
Corporate PresentationFall 2021
Certain information set forth in this presentation contains “forward-looking information”, including “future oriented financial information” and “financial outlook”, under applicable
securities laws (collectively referred to herein as forward-looking statements). Except for statements of historical fact, information contained herein constitutes forward looking
statements and includes, but is not limited to, the (i) projected financial performance of the Company along with the achievement of projected milestones; (ii) completion of, and the use
of proceeds from, the sale of the shares being offered Hereunder; (iii) the expected development of the Company’s business, projects and joint ventures; (iv) execution of the
Company’s vision and growth strategy, including with respect to future M&A activity and global growth; (v) sources and availability of third-party financing for the Company’s Projects;
(vi) completion of the Company’s projects that are currently underway, in development, planned or otherwise under consideration; (vi) renewal of the Company’s current supplier and
other material agreements and (vii) future liquidity, working capital, and capital requirements Forward looking statements are provided to allow potential investors the opportunity to
understand management’s beliefs and opinions in respect of the future so that they may use such beliefs and opinions as one factor in evaluating an investment.
These statements are not guarantees of future performance and undue reliance should not be placed on them. Such forward-looking statements necessarily involve known and
unknown risks and uncertainties, which may cause actual performance and financial results in future periods to differ materially from any projections of future performance or result
expressed or implied by such forward looking statements.
Although forward-looking statements contained in this presentation are based upon what management of the Company believes are reasonable assumptions, there can be no
assurance that forward looking statements will prove to be accurate, as actual results and future events could differ materially from those anticipated in such statements. The Company
undertakes no obligation to update forward looking statements if circumstances or management’s estimates or opinions should change except as required by applicable securities laws.
The reader is cautioned not to place undue reliance on forward looking statements.
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Forward Looking Statements
3
Company Highlights
Unique Platform for Broad Indications: Targeting dysfunctional and decreased levels of Regulatory T Cells (Tregs)
that underlie multiple neurodegenerative diseases including Amyotrophic Lateral Sclerosis (ALS), Frontotemporal
Dementia (FTD), Parkinson’s Disease (PD), Alzheimer’s Disease (AD), Multiple Sclerosis (MS), as well as specific
autoimmune conditions.
Production of “Super Tregs”: Coya has pioneered the ability to produce “Super Tregs” from a patient’s own
dysfunctional Tregs. "Super Tregs” confer its properties through reproducible upregulated proteins in the
expanded/post cryopreserved condition (IP Protected). Coya is developing a first-in-class exosome or extracellular
vesicles (EV) derived from the ”Super Tregs” via an autologous and allogeneic approach.
Manufacturing Expertise: Tech transfer to GMP CDMO complete by Q3, 2022, with the ability to manufacture and
cryopreserve up to a 12-month patient’s supply of cells from one manufacturing run overcomes prior limitations and
allowing for maintenance monthly infusions.
Therapeutic Candidates and Catalysts:
• COYA 101: Autologous Treg Cell Therapy, ALS, IND H2, 2022
• COYA 102: Autologous Treg Cell Therapy, FTD, IND H1, 2023
• COYA 201: Autologous Treg Exosomes, ALS, IND H2, 2022
Investment: Seeking Series B to enable completion of 3 clinical studies: Phase 2b (COYA 101) and Phase 1
(COYA102), and Phase 1 (COYA 201), as well as pipeline expansion.
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Leadership Team
Weihua Zhao, M.D., Ph.D.
Head of In Vitro and Translational Research
Michael Mendicino, Ph.D.
CMC and Regulatory
Mary Keville
Quality and Compliance Consultant
Aaron Thome, Ph.D.
Head of Neuroinflammation Platform
David Beers, Ph.D.
Head of Biomarker Program
Howard Berman, Ph.D.
Chief Executive Officer
Adrian Hepner, M.D., Ph.D.
Chief Medical Officer
Stanley Appel, M.D.
Co-Founder
Gene Mack, MBA
Chief Financial Officer
Gregory Machmichael, Ph.D.
Chief Technology Officer
5
Board of Directors
Ann Lee, Ph.D.
SVP of Cell Therapy Development and Operations of Bristol Myers Squibb
Dr. Lee is one of the leading cell therapy technical development and supply
chain manufacturing executives. She currently leads teams responsible for
developing new cell therapy processes, designing new facilities, and
building the global supply chain at BMS.
Dov Goldstein, M.D.
CFO and CBO of Indapta Therapeutics
Dr. Goldstein has over 20 years of strategic, financial, and
operational experience within the healthcare sector.
Hideki Garren, M.D., Ph.D.
Chief Medical Officer for Prothena
Dr. Garren has 20 years of experience in the biopharmaceutical industry,
spanning all aspects of novel drug development from discovery, to early-stage
clinical trials, to late-stage clinical trials, to commercialization.
Anabella Villalobos, Ph.D.
Head of Biotherapeutics and Medicinal Sciences of Biogen
Dr. Villalobos is a renowned researcher and respected senior
pharmaceutical executive. She is currently responsible for driving the
advancement of high-quality, differentiated drug candidates through the
clinic at Biogen. Prior to Biogen, she spent 28 years at Pfizer.
Howard Berman, Ph.D.
Chief Executive Officer
Howard has over 18 years of industry experience working at the interplay of
science and business.
6
Scientific Advisory Board
Shimon Sakaguchi, M.D., Ph.D.
University Distinguished Professor at Osaka University.
Renowned for discovery of regulatory T cells (Tregs)
Member- National Academy of Sciences
Lawrence Steinman, M.D.
Prof. of Neurology and Genetics at Stanford University Medical School.
Renowned for discovery of Integrin that led to Development of Tysabri.
Member- National Academy of Sciences and National Academy of
Medicine
Clive Svendsen, Ph.D.
Director of the Cedars-Sinai Regenerative Medicine Institute, Prof. at
UCLA and Consulting Prof. at Stanford. Stem cell biology and
regenerative medicine expert
Malcolm Brenner, M.D., Ph.D.
Founding director of Center for Cell and Gene Therapy
and the Fayez Sarofim Distinguished Service Professor at
Baylor College of Medicine. Renowned for discovery of
anti leukemic effects of IL2 following stem cell
transplantation. Member- National Academy of Medicine
Stanley Appel, M.D.
Stanley H. Appel Department of Neurology Co-Director, Neurological
Institute Houston Methodist. World’s foremost expert in ALS and Treg
dysfunction in neurodegenerative diseases
Joseph Masdeu, M.D., Ph.D.
Chairman of the Neuroimaging Research Group of the World Federation
of Neurology. World renowned expert in Neuroimaging modalities.
Graham Family Distinguished Endowed Chair in Neurological Science
and Director of the Nantz National Alzheimer Center and Neuroimaging
at Houston Methodist
Tregs- The Master Regulatory Cell of the Immune SystemKey discovery by Shimon Sakaguchi MD, PhD, member of Coya’s Scientific Advisory Board:
7Coya Therapeutics, Inc. Non-Confidential Presentation 2020
Tregs are the most versatile
and important immuno-
suppressive cells that regulate
immune response and
establish peripheral tolerance
Tregs are key players in
resolving tissue inflammation
as mediators of tissue healing
Treg Cell Inflammatory Immune Cell
Autoimmunity Healthy Cancer
Reduction and loss of Treg population:
• Loss of homeostasis and peripheral
tolerance
• Loss of immune response
regulation to prevent non-specific
side effects
• Promotes autoimmunity and
autoimmune diseases
Balanced Treg and inflammatory
immune cell populations:
• Promotes homeostasis and
peripheral tolerance
• Regulates immune response to
prevent non-specific side effects
• Permits cancer immuno-
surveillance
Increase of Treg population:
• Loss of cancer immuno-
surveillance
• Promotes suppression of
anti-tumor response
• Promotes cancer
progression
7
8
Treg Dysfunction is a Core Driver of Neurodegeneration Decline
Treg dysfunction is also central to Alzheimer’s Disease,
Parkinson’s Disease, and Frontotemporal Dementia*
SurvivalDisease
Progression
Henkel et al, EMBO Mol Med. 2012 Nov 9
*Faridar et al, Brain Communications, Volume 2, Issue 2, 2020, fcaa112
Discovery that Treg Function Predicts ALS Survival, Disease Progression, and Burden of Disease
Treg Dysfunction Across Neurodegenerative Diseases
*Faridar et al, Brain Communications, Volume 2, Issue 2, 2020, fcaa112 9
The suppressive function of Tregs were comparable between mild cognitive
impairment and healthy controls (Figure B) but a remarkable compromise in
Treg function was documented in Alzheimer patients (Figure C&D)
Treg
dysfunction is
a core driver in
Alzheimer’s
Disease
Treg
dysfunction is a
core driver in
Frontotemporal
Dementia
The suppressive function of Tregs on Tresp proliferation were compromised in
neurodegenerative disorder of FTD
* Formerly known as ALS 001 10
Robust Pipeline
Therapeutic Candidate Indication Product Type Route Status / Expected Milestones
COYA 101*
COYA 102
COYA 201
COYA 202
COYA 301
Amyotrophic Lateral Sclerosis
(ALS)Treg Cell Therapy
Treg Cell Therapy
Treg Exosomes
Treg Exosomes
Novel Biologic
Amyotrophic Lateral Sclerosis
(ALS)
Frontotemporal Dementia
(FTD)
Multiple Neurodegenerative
Diseases
Alzheimer’s Disease
(AD)
Autologous IV
Autologous IV
Autologous IV
Allogeneic IV
New Chemical
Entity Biologic
IND P2b / H2, ‘22
IIT, IND P1 / H1, ‘23
IIT, IND P1 / H2, ‘22
Development
Development
11
Value-Driving Milestones
Q1 Q2 Q3 Q4 Q1
2022
COYA 102 –Treg FTD
COYA 101 - Treg ALS COYA 201 – Exosome ALS
Legend
2023
COYA 101 IND filing
COYA 102 Pre-IND meeting
COYA 102 IND filing
COYA 201 IND Filing COYA 201 Initiate Phase 1
COYA 201 Open label data
COYA 201 Pre- IND meeting
Multiple publications and news flow catalysts for potential IPO and beyond
2024 and beyond
1. COYA 101 Topline Data (completion of P2b)
2. COYA 102 open label data
3. Autologous Treg Exosome IND submission
4. Autologous Treg Exosome trial initiation
5. Allogeneic Treg Exosome IND submission
6. Allogeneic Treg Exosome trial initiation
COYA 101 Initiate P2b
*Market Cap as of 8/30 close12
Coya’s differentiated approach The most clinically advanced Treg cell therapy platform to shift, slow and halt the progression of neurodegenerative diseases
Company Market Cap (Private: $ Raised)
Modality Indication Phase Approach / Mechanism Coya Differentiation
($202M)
Series C: $135M
Small Molecule
Combination
ALS Completed Phase
2
Targets endoplasmic reticulum and mitochondrial
dependent neuronal degeneration pathway
Generic combination targets endoplasmic reticulum stress responses and
neuronal cell death rather than provide Treg neuroprotection
$648M MAB ALS Ongoing Phase 2 C1q inhibitors (targeting C1QA gene) to prevent
synapse loss
Complement Inhibitors await proof-of-concept for efficacy in ALS; Alexion’s trial of
C5 inhibitor halted because of lack of efficacy
$127M Cell Therapy ALS Failed Phase 3 Autologous MSC-NTF cells secrete NTFs,
microRNA, and cytokines activating neuroprotection
and immunomodulation pathways.
Requires bone marrow biopsy and repeated intrathecal administration which can
be limited by frequent painful lumbar punctures
$628M Gene Therapy ALS / FTD Ongoing Phase 1 AAV1 targeting C9orf72 / GRN to increase PGRN
levels
Gene therapy only address those with mutations in the C9orf72, which represent
less than 10% of all ALS patients.
$115M MAB ALS Ongoing Phase 2 Humanized IgG1 antibody blocking CD40 Ligand
(CD154)
Does not address the dysfunction of Tregs in ALS. Blocks co-stimulatory factor
CD40L to impair the immune synapse.
$375M Exosomes Oncology/
Neurology
Ongoing Phase 1 Engineered exosomes displays IL-12 on PTGFRN
on T and NK-cells & ASO surface loaded exosomes
targeting NLRP3
Engineering required for direct tropism, currently focused on oncology with neuro
in discovery phase.
($59M)
Series A: $59M
Tregs Oncology/
Inflammation
Preclinical Platform maps Treg behavior to disease pathology
for discovery of targets
Still preclinical with initial targets yet to be revealed. Coya in clinic with high
potency Treg with >85% suppressive function.
($335M)
Series B: $265M
Tregs RA, IBD Preclinical CAR-Treg platform targets tissue with high specificity
and a Teff conditioning biologic program
Preclinical stage company, currently outside of neuro and assumes driver antigen
identification for CAR-Treg cell development.
($95M)
Series A: $95M
Tregs MS Preclinical Autologous TCR-engineered Tregs slows immune-
mediated destruction, restores homeostasis
Treg cell therapy armed with a TCR that selectively recognizes degraded myelin,
with applications only in MS at this time.
($20M)
Series A: $20M
Small Molecule Oncology Ongoing Phase
1/1b
Lead candidate, MPT-0118 inhibits the MALT1
enzyme as to sustain Tregs neg immunosuppressive
role
Oral therapy looking for synergy with anti-PD-1 via Induction of interferon
gamma-producing Tregs in tumors
($10.5M)
Series A/A-2: $10.5M
Exosomes Dermatology Ongoing Phase
1/2a
MSC derived exosomes isolated preserving structure
/ function
Isolation of extracellular vesicles from allogenic bone marrow derived MSC-not as
potent as Coya’s exosome platform.
Autologous Tregs Therapies
14
Coya Addresses Limitations of other Treg Cell Therapy Approaches
Coya’s Treg Cell Therapy CAR Treg Cell Therapy Engineered Treg Cell Therapy
ManufacturingStandardized in an automated bioreactor with vein-to-vein
times of 21 days. Readily scalableUnknown (Preclinical) Unknown (Preclinical)
Genetic
Engineering
Not required: Polyclonal Tregs are best suited approach for
efficacy given lack of known disease-driving antigens in ALS.
CAR Treg approaches are not viable.
Required: Assumes identification of driver
antigens for a disease state. Genetic
manipulation complicates manufacturing
Required: Viral Vector Technology
manipulates Effector T Cell Function which
complicates manufacturing
Final Product
Identity
Patented reproducible compositions of matter (proteins) in
expanded Tregs resulting in more functional Treg cell
products prior to release
Unknown (Preclinical) Unknown (Preclinical)
PotencyFinal Treg product highly potent with >85% Suppressive
functionUnknown (Preclinical) Unknown (Preclinical)
AdministrationMonthly outpatient IV therapy via 5–10-minute infusion using
thawed cellsUnknown (Preclinical) Unknown (Preclinical)
Storage
Cryopreservation patent permits ability to freeze Tregs
(Tregs are highly unstable)- one manufacturing run produces
enough cells for patient’s serial infusions.
Single infusion- Unlikely to work secondary
to Treg dysfunction to inflammatory conditions
in vivo
Single infusion- Unlikely to work secondary
to Treg dysfunction to inflammatory conditions
in vivo
Stage of
DevelopmentClinical: Phase 1 and 2a Complete- Phase 2b/3 under
development (No safety signals and compelling efficacy)Preclinical Preclinical
15
Proprietary Platform Technology and Scalable Manufacturing Produces
”Super Tregs” and Overcomes Supply Chain Management Barriers
Manufacturing process converts dysfunctional Tregs to “Super Tregs”, that have been extensively phenotyped to
identify reproducible upregulated proteins that confer the super suppressive function
Coya’s CTregTM platform (cryopreservation for Tregs) is the first in
the industry to convert dysfunctional Tregs to functional Tregs
and expand to the billions of cells
No genetic manipulation required
“Super Treg” produced characterized by upregulated proteins that
are reproduced from batch to batch, including but not limited to,
FOXP3, CTLA4, and CD25
Cryopreserve Tregs for up
to one year of monthly
maintenance infusions
Ship cells to outpatient infusion
center
Thaw cells and provide monthly
recurring infusions to patient
allowing for an ‘off the shelf’ Treg
cell therapy that has not been
feasible to date
❶ Collect
Draw one-time sample from
patient
❸ Cryopreserve ❹ Ship, Thaw & Administer❷ Convert & Expand
1.M. Obermann & M. Lyon (2015) Financial cost of amyotrophic lateral sclerosis: A case study, Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration, 16:1-2, 54-57, DOI:
10.3109/21678421.2014.951946
2. https://alsworldwide.org/research-and-trials/article/rilutek-riluzole & https://www.drugs.com/price-guide/rilutek/
3. https://www.accessdata.fda.gov/drugsatfda_docs/label/2016/020599s017lbl.pdf
4. https://www.accessdata.fda.gov/drugsatfda_docs/label/2017/209176lbl.pdf
16
Treg Pharmacoeconomics for ALS
Annual ALS healthcare costs range from $16,000 to $200,000 annually depending on the stage of the illness
Lifetime cost of ALS ~ $1,433,992
Efficacy Data……
• Marketed for 23 years
• Generics available
• Annual cost ~$40,000 (branded) and ~$2,200 (generic) for 50mg tablets taken 2x daily
• FDA Approved May 2017, first to be approved for ALS in > 20 years
• Due to high cost, policies generally restrict use on early-stage patients and who can
• remain independent, retain functionality for daily activities, and normal respiratory function.
• $1,100 / infusion (2 x 30mg/100mL)
• ~$146,000 / year excluding associated healthcare costs
1
Coya Therapeutics plans to price similarly to other immunotherapies COGS: Currently $150,000 annually / patient
Projected $75,000 at scale ….
(riluzole)2
Did not hit stat sig in
survival curves for time to
death or tracheotomy
(Logrank test p=.12)
Treatment differential
between edaravone and
placebo was 2.4 points on
ALSFRS-R scale
(p=.0013)
3
4
Nov 2019 BY LESLIE SANDS - ALS Overview
*Simpson, E.P.; Yen, A.A.; Appel, S.H. Oxidative stress: A common denominator in the pathogenesis of amyotrophic lateral sclerosis. Curr. Opin. Rheumatol. 2003, 15, 730–736. 17
Amyotrophic lateral sclerosis (ALS) Overview
17Coya Therapeutics, Inc. Non-Confidential Presentation 2020
5,000people are diagnosed per year and the
average life expectancy is 2-5 years
10% of cases are inherited through a mutated gene
90% of cases occur without family history
Up to $200,000 is the estimated out-of-pocket cost, per year, for
caring for a person with ALS
Despite 160 years of recorded research history in ALS and more than 200 clinical trials, there has been no cure developed
for ALS, and only two modestly effective disease-modifying treatments that slow its progression are available.*
ALSFRS-R: The Standard Outcome Measure
Employed Across ALS Trials
18
The ALS Functional Rating Scale-Revised
(ALSFRS-R) stratifies severity of patients
with ALS that has been validated and
employed in both clinical trials and practice.
In clinical trials, ALSFRS is gauged on a 24-
week.
ALSFRS-R is based on 12 areas of patient
functionality grouped into 4 domains:
bulbar, fine motor, gross motor, and
respiratory. When a patients ALSFRS-R
score decreases, it is correlated with a
reduction in capability of carrying out
activities essential to daily life.
*David Beers, Stanley Appel; Lancet Neurol 2019; 18: 211–20
Discovery: Tregs for Delaying Progression of ALSDysfunctional and decreased levels of Tregs underlie neurodegeneration and ALS progression
19
• Dysfunctional Tregs regain suppressive function with
ex-vivo expansion
• In ALS mouse models, infusion of Tregs and
upregulation of endogenous Tregs slow disease
progression and prolong survival
Our Basic Science/Translational Discoveries: *
• Proinflammatory monocytes & central nervous system
(CNS) microglia are increased in ALS
• Neuroprotective Tregs are decreased and dysfunctional
in ALS patients
19
Autologous Tregs for Treatment of ALSOur Lead Program (COYA 101): an autologous, expanded Regulatory T cell
therapy for ALS that is infused to patients. COYA 101 is cryopreserved and
can be readministered for up to 1 year after processing.
Phase 1 Study Schema: N= 3 patients with ALS
• Patients underwent leukapheresis, and Tregs were subsequently isolated
and expanded ex vivo
• Tregs (1x106 cells/kg/infusion) were administered IV at earlier stages (4
doses over 2 months) and later stages (4 doses over 4 months) of disease
• Concomitant interleukin-2 (2x105 IU/m2/injection ) was administered
subcutaneously 3 times weekly over the entire study period
• Patients were closely monitored for adverse effects and changes in disease
progression rates
• Treg numbers and suppressive function were assayed during and
following each round of Treg infusions
20
Treg infusions halt disease progression in 3 ALS patientsCOYA 101 Phase 1 Proof of Concept Study in ALS (n=3)
ALSFRS-R Scores over Two Tregs Infusion Schedules Multiple Months Apart
Bi-Weekly Tregs InfusionsMonthly Tregs Infusions
InfusionsBegin
InfusionsEnd
InfusionsBegin
InfusionsEnd
InfusionsBegin
InfusionsEnd
InfusionsBegin
InfusionsEnd
21
*Thonhoff J, et.al. Expanded autologous regulatory T-lymphocyte infusions in ALS. Neurol Neuroimmunol Neuroinflamm 2018 May
Highlights of Topline Phase 1 Results (n=3)*
22
► Treg percentage and suppressive function increased
during infusions
► Enhanced Treg suppressive function correlated with
slowing of functional decline
► MIPs (Respiratory Function) stabilized during
infusions
► All patients noted increases in the frequency,
intensity, and distribution of fasciculations during each
round of infusions
Infusions found to be safe and well
tolerated
• No infusion-related adverse events observed
• No clinically significant changes in laboratory
findings
• No electrocardiogram findings observed
COYA 101: Completed Phase 2a Trial Schema (N=8)A Randomized, Placebo-Controlled Phase 2a Trial to Evaluate the Biological Activity, Safety, and Tolerability of
Autologous Regulatory T Lymphocytes (Tregs) Expanded Ex-Vivo and Returned Intravenously in Combination
with Low-Dose IL-2 in People with ALS
• Age ≥ 18 years
• ALS meeting EI Escorial criteria for
possible, probable, lab-supported
probable, or definite ALS
• Forced vital capacity (FVC) ≥ 65%
of predicted capacity for age,
height, and gender at screening
• Patient able and willing to undergo
leukapheresis
N=8*
* 2 patients will enter the OLE directly and not participate in RDB
Primary endpoint: Change in Treg suppressive function in blood from baseline to
week 24 during Months 1 – 6 and from start to finish of each dosage level during Open
Label Extension
Secondary endpoint: Change in Treg numbers, Safety, Tolerability
Exploratory endpoint: Change in AALS Score, ALSFRS-R, FVC, Tracheostomy
Free Survival, Post 1 ye. Function and Survival
Treg Placebo: Placebo consisting of normal saline infusions containing
5% human serum albumin /0.2% DMSO and subcutaneous injections of
normal saline per the same schedule above: n=3
Autologous Treg: 1x106 cells/kg/infusion
Concomitant subcutaneous administration of IL-2(2x105 IU/m2/injection
three times weekly): n=3
Months 1 - 6
Randomized, Double Blind (RDB)
Months 6 - 12
Open Label Extension (OLE)
Autologous Treg: n=8
(6 from RDB and 2
entered directly OLE)
Dose Escalation
Infusions #1 and #2 = 1x dose
Infusions #3 and #4 = 2x dose
Infusions #5 and #6 = 3x dose
23
24
Highlights of Topline Phase 2a Results*
*More data available under NDA
► Clinically Meaningful Responses: With monthly infusions of COYA 101, clinically meaningful responses
(ALSFRS-R) observed in majority of patients over a 24-week treatment period in open label portion of trial.
► Sustained and Stable Breathing Function: The favorable clinical responses over the 24-week period
corresponded with sustained and stable breathing function, measured by Maximal Inspiratory Pressure (MIP)
► Durability of Response: In patients infused with COYA 101 over 48 weeks, clinically meaningful responses
were sustained and durable over this period.
► Serum biomarkers Indicative of Oxidative Stress/Inflammation: Lack of responsiveness associated with
elevated levels at baseline and throughout the 12-month treatment period.
► Safe and Well tolerated Treatment: Good safety profile in Phase 2a consistent with safety in Phase 1 study.
► Double-Blind 24-week treatment period curtailed by COVID-19: Only 3 pts received COYA 101 and 3 pts
received placebo, thus limiting statistical analysis of double-blind portion.
Manufacturing
Autologous Treg Cell Therapy
Manufacturing Capabilities to Produce ”Super Treg” Cell Therapy
Proprietary manufacturing process has been established to produce a highly pure, stable,
and consistent Treg product covering: GMP infrastructure, automation and quality control
Optimized Treg expansion to produce a ”Super Treg” in automated bioreactor
• Yields billions of highly functional and neuroprotective Tregs
• Short expansion time through automated process that avoids genetic manipulation
• Phenotypic Characterization of Expanded Tregs Cells (Reproducible for each lot)
Controlled manufacturing platform geared towards commercialization
• Cryopreserved under cGMP conditions
• Sustainable over longer periods of time - single manufacturing round produces cells
for up to a full year’s supply, and is conveniently stored, shipped and administered
IP protection for manufacturing including effective cryopreservation of autologous Tregs
• Extended treatment times with successive doses
• Superior Treg products- “Super Tregs” defined by unique compositions of matter
• Cost effective and sustainable
26
27
Treg Purity and Suppressive Function Maintained in the Bioreactor
Robust, Consistent, and Quick Treg
Expansion Within 7-14 Days
Data on file for 12+ months for stability, purity, and suppressive function post thaw
Consistent Treg Purity with Highly Suppressive
Treg Function Pre and Post Thaw
Bioreactor Runs
0
20
40
60
80
100
CD4+CD25+ Cells
% C
D4+
CD
25+
Ce
lls
(of
CD
4+
Cell
s)
Baseline
Pre-Freeze
Post-Thaw
Bioreactor Runs
0
20
40
60
80
100
Treg Suppressive Function
% S
up
pre
ss
ion
(of
Tre
sp
Pro
life
rati
on
)
Baseline
Pre-Freeze
Post-Thaw
Exosome Technology Platform
Autologous and Allogeneic
iscEXO: Science and Technology Overview
29
The iscEXO Platform: Coya has developed a first-in-class exosome or
extracellular vesicle (EV) product derived from Tregs
• Highly suppressive ex vivo expanded immunosuppressive cells (the
iscEXO Platform)
Most Potent Anti-inflammatory Exosome Platform: derived from
Tregs and M2 Macrophages, two of the most prominent anti-
inflammatory and neuroprotective cell types
Leverage mesenchymal stem cell (MSC) derived EVs
• EVs are not cells and avoid potential cell-based issues such as
immune rejection and polarization to a pro-inflammatory cell type
Compared to MSC Derived Exosomes, iscEXOTM is significantly more immunosuppressive
Unique and differentiated approach:
1 0 5 1 0 6 1 0 7
0
1 0
2 0
3 0
4 0
5 0
6 0
7 0
8 0
9 0
1 0 0
E x p a n d e d T r e g E x o
T r e s p p r o life ra t io n
E x o so m e d o se
(p a r t ic le s )
Tre
sp
Su
pp
re
ss
ion
M S C E xo
T re g E xo
29
COYA 201 & 202: First-in-Class Treg-Derived Exosome Platform
Coya is planning on an autologous phase 1 first-in-human (FIH) trial in 2022, with allogeneic
approach in 2023
30
• Most companies leverage mesenchymal stem cell (MSC) derived exosomes, not Treg derived exosomes
• Treg derived exosomes have an order of magnitude higher suppressive capacity and anti-inflammatory
function than MSC derived exosomes required for neuroinflammatory suppression (data on file)
• The Coya team has:
• developed the only manufacturing platform to isolate highly neuroprotective Treg derived exosomes
(not feasible without Coya’s primary proprietary Treg expansion process)
• optimized cryopreservation and full functional stability of Treg exosomes 12+ months post thaw
allowing for chronic off the shelf administration
• Coya’s proprietary platform allows it to isolate, normalize and expand cells with concurrent extraction of the
cellular EV contents and provides an unprecedented opportunity to shift the paradigm of EV based
treatments
What makes
our exosome
platform
different? …
Tregs maintain tolerance to self and limit other immune responses—they achieve this through different
mechanisms including the release of exosomes
30
• Cryopreservation, Shipping, and Rethawing
Methods
• Characterization of Suppressive Exosome
Phenotype (Compositions of Matter)
• Isolation and Manufacturing Methods
• Therapeutic Modality in Multiple Disease
States
• Autologous and Allogeneic Approaches
• Scalability and automation with bioreactors
• Conversion of Dysfunctional to Functional Tregs
• Characterization of ”Super Treg” Phenotype
• Manufacturing and Expansion Methods
• Cryopreservation, Shipping, and Rethawing
Methods and Composition of Matter
• Therapeutic Modality in Multiple Disease States
• Biomarkers of responsiveness
• Automation and Scalability with Bioreactors
31
Strong IP PortfolioProtection on Treg Manufacturing; Cryopreservation, Storage, and Thawing; and Composition of Matter
Exosome Platform Treg Platform
32
Company Highlights
Unique Platform for Broad Indications: Targeting dysfunctional and decreased levels of Regulatory T Cells (Tregs)
that underlie multiple neurodegenerative diseases including Amyotrophic Lateral Sclerosis (ALS), Frontotemporal
Dementia (FTD), Parkinson’s Disease (PD), Alzheimer’s Disease (AD), Multiple Sclerosis (MS), as well as specific
autoimmune conditions.
Production of “Super Tregs”: Coya has pioneered the ability to produce “Super Tregs” from a patient’s own
dysfunctional Tregs. "Super Tregs” confer its properties through reproducible upregulated proteins in the
expanded/post cryopreserved condition (IP Protected). Coya is developing a first-in-class exosome or extracellular
vesicles (EV) derived from the ”Super Tregs” via an autologous and allogeneic approach.
Manufacturing Expertise: Tech transfer to GMP CDMO complete by Q3, 2022, with the ability to manufacture and
cryopreserve up to a 12-month patient’s supply of cells from one manufacturing run overcomes prior limitations and
allowing for maintenance monthly infusions.
Therapeutic Candidates and Catalysts:
• COYA 101: Autologous Treg Cell Therapy, ALS, IND H2, 2022
• COYA 102: Autologous Treg Cell Therapy, FTD, IND H1, 2023
• COYA 201: Autologous Treg Exosomes, ALS, IND H2, 2022
Investment: Seeking Series B to enable completion of 3 clinical studies: Phase 2b (COYA 101) and Phase 1
(COYA102), and Phase 1 (COYA 201), as well as pipeline expansion.
