COYA THERAPEUTICS - PDF document

1 2020 COYA THERAPEUTICS Corporate Present
2020 COYA THERAPEUTICS Corporate Presentation March 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 ;

2 (iv) execution of the Company’s vision
(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 o

3 f future performance and undue reliance
f 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 state

4 ments if circumstances or management’s
ments 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 . 2 Forward Looking Statements 3 The Core of Our Approach Regulatory T - Cell (Treg) Cell Therapy Platform to Slow and Halt the Progression of Neurodegenerative Diseases Mission Offer patients a therapeutic strategy that aims to exponentially improve outcomes over the current standard of care by delaying disease progression and extending the lives of patients Convert millions of patient’s dysfunctional Tregs to billions of functional Tregs – no genetic manipulation required 03 Cryopreservation of Cells: 1 manufacturing run produces a 1 - year patient

5 supply Thaw cryopreserved Tregs with f
supply Thaw cryopreserved Tregs with full functional activity - monthly maintenance infusions of highly suppressive Treg cells to stop progression 02 01 4 Key Investment Highlights 4 Suppressing Neuroinflammation: Tregs Against Inflammation (TAI ™ ) platform is developing disruptive, first in class, autologous Treg and allogeneic exosome therapeutics - leveraging the discovery that dysfunctional Tregs underlie neurodegenerative and autoimmune diseases. Clinical validation achieved in a successful Phase 1. Industrializing Supply Chain Management: Proprietary cryopreservation for Tregs ( Ctreg ™ ) with novel manufacturing steps that overcome prior limitations of Treg cell therapies - single manufacturing round produce cells for a full year’s supply that

6 can be stored, shipped, and administered
can be stored, shipped, and administered at remote outpatient facilities. Value Creation (Upcoming Milestones): (1) Phase 2a topline data in ALS in Q3 2021 (2) Potential manufacturing partnerships (3) IP enhancement (4) FIH trials in other conditions driven by dysfunctional Tregs (Frontotemporal Dementia, Scleroderma) (5) Initiate FIH Treg derived Exosome Phase 1 trial in 2022. Revolutionizing Cell Therapy Manufacturing: Proprietary manufacturing steps that avoid genetic manipulation and instead, ex - vivo isolates and converts millions of dysfunctional Tregs to billions of highly functional Tregs that are neuroprotective and immunosuppressive. Series A financing • Raised $10m in Series A financing in December 2020 with institutional and accredited investors P

7 artnership • Headquartered in Houston,
artnership • Headquartered in Houston, TX with a sponsored research program in conjunction with the laboratory infrastructure of Stanley H. Appel, MD, Co - Director of Houston Methodist Neurological Institute and Chair of the Stanley H. Appel Department of Neurology Leadership • Founded by Treg pioneers, including discoverer of Tregs • Leadership has a successful track record of execution Corporate Snapshot 5 6 Leadership Team 6 Howard Berman, Ph.D. Chief Executive Officer Lou Vaickus , M.D., FACP Acting Chief Medical Officer Mary Keville Quality Control Consultant Aaron Thome , Ph.D. Head of Neuroinflammation Platform Michael Mendicino , Ph.D. CMC and Regulatory Consultant Scientific Advisory Board 7 Shimon Sakaguchi , M.D., Ph.D. University Distinguished

8 Professor at Osaka University Member -
Professor at Osaka University Member - National Academy of Sciences Renowned for discovery of regulatory T cells (Tregs) Lawrence Steinman, M.D. Professor of Neurology and Genetics at Stanford University Medical School Member - National Academy of Sciences and National Academy of Medicine Renowned for discovery of Integrin that led to Development of Tysabri Clive Svendsen, Ph.D. Director of the Cedars - Sinai Regenerative Medicine Institute, Professor at UCLA and Consulting Professor at Stanford University 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 Member - National Academy of Medicine

9 Renowned for discovery of anti leukemic
Renowned for discovery of anti leukemic effects of IL2 following stem cell transplantation 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 7 Board of Directors 8 Hideki Garren , M.D., Ph.D. Chief Medical Officer for Prothena 8 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. Dov Goldstein, M.D. Chief Financial Officer and Chief Business Officer of Indapta Therapeutics Dr. Goldstein has over 20 years of strategic financial and operation

10 al experience within the healthcare sect
al experience within the healthcare sector. 9 Modality Company Drug Name Target Indication Intrathecal Gene therapy Voyager Therapeutics VY - SOD102 VY - AADC Target SOD1 with AAV ALS, PD Gene Therapy Locana Bio C9orf72 G4C2/C4G2 Repeat Expansion Destruction ALS, PD Gene therapy Passage Bio PBFT02 Target C9orf72 FTD Gene therapy Verge Genomics Preclinical Multiple genes Integrating a unique all - inhuman genomic platform with machine learning ALS, PD Modality Company Drug Name Target Indication Cell therapy Faze Medicine Biomolecular Condensates Identifying proteins that are key components or regulators of disease - causing condensates ALS, TD Intrathecal Cell Therapy Brainstorm Cell Therapeutics NurOwn ® platform (MSC - NTF cells) Engineer, produce

11 , and purify autologous MSC - NTF to ta
, and purify autologous MSC - NTF to target CSF neurotrophic factors ALS Oligomer Antibodies Promis Neurosciences TDP42 SOD1 Bind to toxic oligomers driving ALS (SOD1 and TDP43) and Parkinson’s disease (alpha synuclein ALS, PD w/ Lewy body Antibody Annexon Biosciences ANX005 (IV) C1q inhibition ALS Platform AI/machine learning Insitro Insitro Human (ISH) platform ALS, FTD Coya’s differentiated approach The most clinically advanced Treg cell therapy platform to shift, slow and halt the progression of neurodegenerative diseases Modality Company Drug Name Target Indication Small Molecule Tau Rx Therapeutics TRx0237 Tau aggregation inhibitors, novel chemical form of methylthionine (MT) FTD, AD Yumantiy Therapeutics YTX - 9184 SCD inhibitors. Target

12 s misfolded proteins Dementia w/ Lewy b
s misfolded proteins Dementia w/ Lewy body Inhibikase Therapeutics IKT - 148x Targets c - Abl Dementia w/ Lewy body BioXcel Therapeutics BXCL501 Selective alpha - 2a receptor agonist Agitation in Dementia Lundbeck A/S Memantine Hydrochloride Glutamate antagonist FTD NIAMS Atorvastatin Lowers cholesterol levels by reducing cholesterol production Scleroderma* Athira Pharma ATH - 1017 Targets HGF/MET pathway AD, PD AZ Therapies ALZT - OP1a Cytokine release modifier to address neuroinflammation ALS, AD Biohaven Pharmaceuticals Verdiperstat Neuroinflammation/Oxidative Stress (MPO inhibitor) ALS QurAlis TDP43 Excitotoxicity (TBK1 Inhibition) ALS Iron Horse Therapeutics Preclinical Epha4 Inhibitor ALS Large Molecule Health Partners Institute Novolin - R Insu

13 lin Short acting insulin (rDNA) FTD Al
lin Short acting insulin (rDNA) FTD Alector AL001 Modulates levels of PGRN, a key regulator of microglia function FTD *There has also been a recent increase in academic research and funding in the Scleroderma landscape. George Washington Unive rsi ty, Duke University, Rennes University, Indonesia University, Mayo Clinic, University of Texas Southwestern Medical Center and Cairo U niv ersity are all conducting ongoing clinical trials and exploring alternative therapeutic options. Aging is associated with excessive inflammation and inefficient immune responses as a result of Treg dysfunction 10 Coya Therapeutics, Inc. Non - Confidential Presentation 2020 Age and Treg dysfunction increases risk for numerous autoimmune and neurodegenerative diseases Tregs are critical

14 for suppressing inflammation but Treg
for suppressing inflammation but Treg dysfunction increases with age Degree of Treg dysfunction correlates to the rate of clinical decline in ALS, Alzheimer’s, and other neurodegenerative diseases Benedetto et al, Neuroscience and Biobehavioral Reviews 75 (2017) 114 – 128 10 Tregs - The Master Regulatory Cell of the Immune System Key discovery by Shimon Sakaguchi MD, PhD, member of Coya’s Scientific Advisory Board: 11 Coya Therapeutics, Inc. Non - Confidential Presentation 2020 Tregs are the most versatile and important immunosuppressive cells that regulate immune response and establish peripheral tolerance Tregs not only maintain immune response but are key players in resolving tissue inflammation as mediators of tissue healing Treg Cell Inflammatory I

15 mmune Cell Autoimmunity Healthy Cancer R
mmune 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 2019 IQ Biosciences 11 Discovery that Treg Dysfunction is a Core Driver of Neurodegeneration Decline Treg Function Predicts ALS Survival, Disea

16 se Progression, and Burden of Disease Tr
se Progression, and Burden of Disease Treg dysfunction is also central to Alzheimer’s Disease, Parkinson’s Disease, and Frontotemporal Dementia* Survival Survival to 100 AALS Points Henkel et al, EMBO Mol Med. 2012 Nov 9 * Faridar et al, Brain Communications , Volume 2, Issue 2, 2020, fcaa112 12 Treg Dysfunction Across Neurodegenerative Diseases 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 Faridar A, et al, Brain communication, 2020 13 The suppressive function of Tregs o

17 n Tresp proliferation were compromised
n Tresp proliferation were compromised in neurodegenerative disorder of FTD Molecular Neurodegeneration volume 15, Article number: 32 (2020) 14 Scientific Rationale for Treg Intervention in Neurodegeneration: Unlocking New Treatment Options Coya Therapeutics, Inc. Non - Confidential Presentation 2020 Neuroinflammation underlies neurodegeneration, which is driven by an imbalanced ratio of pro - inflammatory effector T cells and Tregs Impacted by high degree of dysfunctional Tregs Treg driven inflammation drives numerous diseases: • Alzheimer’s Disease • Amyotrophic Lateral Sclerosis (ALS) • Frontotemporal Dementia (FTD) • Parkinson’s Disease • Autoimmune conditions 15 Proprietary Platform Technology and Scalable Manufacturing Process Overcomes Supply

18 Chain Management Barriers Coya’s CTre
Chain Management Barriers Coya’s CTreg TM 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 Cryopreserve Tregs for 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 & Administer TAI ™ (Tregs Against Inflammation) platform offers potential therapeutic approaches to address the unmet and significant medical needs of patients with ALS, Parkinson’s, Alzheimer’s,

19 FTD and other neurodegenerative and auto
FTD and other neurodegenerative and autoimmune diseases ❷ Convert & Expand Current Manufacturing Capabilities* 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 • Yields billions of highly functional Tregs • Short expansion time through ex - vivo process that avoids genetic manipulation Controlled manufacturing platform geared towards commercialization • Cryopreserved under cGMP conditions • Sustainable over longer periods of time - single manufacturing round produces cells for a full year’s supply, and is conveniently stored, shipped and administered IP protection for manufacturing including effective

20 cryopreservation of autologous Tregs â€
cryopreservation of autologous Tregs • Extended treatment times with successive doses • Functionally superior Treg products • Cost effective and sustainable *Additional details related to manufacturing available under NDA 16 17 Robust and Reproducible Supply Chain Solution: Manufacturing and Cryopreservation Non - confidential – Scientific – October 2020 Data on file for 12+ months stability, purity, and suppressive function post thaw Robust and Consistent Treg Expansion Consistent Treg Purity with Highly Suppressive Treg Function Pre and Post Thaw 18 Our Treatment Pipeline Targets Billion Dollar Markets Coya Therapeutics targets the critical progenitor of the inflammatory pathway – namely Treg dysfunction, regardless of individua l downstream pathways

21 that may be abnormal. We plan to a ggres
that may be abnormal. We plan to a ggressively expand trial and regulatory approval for neurodegenerative as well as autoimmune/inflammatory diseases driven by Treg dysfunction after initial commercialization for Treg ALS treatment . Partner for all Studies DEVELOPMENT PROGRAM PRODUCT CANDIDATE INDICATION DELIVERY ROUTE PRECLINICAL PHASE 1 PHASE 2 PHASE 3 Treg Cell Therapy ALS001 Amyotrophic Lateral Sclerosis Intravenous FTD080 Frontotemporal Dementia Intravenous AID912 Scleroderma Intravenous Treg Exosome Therapy EX001 Amyotrophic Lateral Sclerosis Undisclosed EX050 Frontotemporal Dementia Undisclosed EX098 Scleroderma Undisclosed Tregs as a durable solution for the treatment of ALS, Neurodegenerative, and Autoimmune Diseases Nov 2019 BY LESLIE SANDS - ALS Overvie

22 w *Simpson, E.P.; Yen, A.A.; Appel, S.H.
w *Simpson, E.P.; Yen, A.A.; Appel, S.H. Oxidative stress: A common denominator in the pathogenesis of amyotrophic lateral scle ros is. Curr . Opin . Rheumatol . 2003, 15 , 730 – 736. 20 Amyotrophic lateral sclerosis (ALS) Overview 20 Coya Therapeutics, Inc. Non - Confidential Presentation 2020 5,000 people 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 $250,000 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

23 its progression are available.* ALS pro
its progression are available.* ALS progression is driven by a hyper immune response: byproduct of dysfunctional Tregs 19 ALS progression is driven by excessive inflammation at the site of motor neurons as a byproduct of dysfunctional Tregs Beland et al., Brain Communications , Volume 2, Issue 2, 2020, fcaa124 *David Beers, Stanley Appel; Lancet Neurol 2019; 18: 211 – 20 Discovery: Tregs for Delaying Progression of ALS Dysfunctional and decreased levels of Tregs underlie neurodegeneration and ALS progression 22 • 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: * •

24 Proinflammatory monocytes & central ner
Proinflammatory monocytes & central nervous system (CNS) microglia are increased in ALS • Neuroprotective Tregs are decreased and dysfunctional in ALS patients 22 Autologous Tregs for Treatment of ALS Our Lead Program (ALS001): an autologous, expanded Regulatory T cell therapy for ALS that is infused to patients. ALS001 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 (1 × 106 cells/kg) were administered IV at earlier stages (4 doses over 2 months) and later stages (4 doses over 4 months) of disease • Concomitant interleukin - 2 (2 × 105 IU/m2/injection) was administered subcutan

25 eously 3 times weekly over the entire st
eously 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 23 RESULTS * Thonhoff J, et.al . Expanded autologous regulatory T - lymphocyte infusions in ALS. Neurol Neuroimmunol Neuroinflamm 2018 May ALS001: Phase 1 Study Results (n=3)* • Treg percentage and suppressive function increased during infusions • Enhanced Treg suppressive function correlated with slowing of functional decline • MIPs (Respiratory Function) stabilized during infusions INFUSIONS WERE FOUND TO BE SAFE ONGOING PHASE 2A TRIAL • No infusion - related adverse events were observed • No cl

26 inically significant changes in laborato
inically significant changes in laboratory findings • No electrocardiogram findings were observed • All patients noted increases in the frequency, intensity, and distribution of fasciculations during each round of infusions • Data release scheduled for summer 2021 • Leverage monthly maintenance infusion of Tregs • Determine the optimal dose and schedule of Treg infusion to increase the durability of response in patients with ALS 24 Non - confidential – Scientific – October 2020 ALS001: Phase 1 Results Disease progression slowed during each round of Treg infusions as measured by standard clinical ALS scales, and correlated with increased Treg suppressive function 25 Expanded autologous Treg - lymphocyte infusions in ALS Expanded autologous regulato

27 ry T - lymphocyte infusions in ALS, A ph
ry T - lymphocyte infusions in ALS, A phase I, first - in - human study Jason R. Thonhoff , MD, PhD,* David R. Beers, PhD,* Weihua Zhao, MD, PhD, Milvia Pleitez , MD, Ericka P. Simpson, MD, James D. Berry, MD, Merit E. Cudkowicz , MD, and Stanley H. Appel, MD Neurol Neuroimmunol Neuroinflamm 2018;5:e465. 25 Non - confidential – Scientific – October 2020 ALS001: Phase 1 Increased Treg Function in All Patients Treg percentage and suppressive function increased during each round of Treg infusions 26 Coya Therapeutics, Inc. Non - Confidential Presentation 2020 26 Non - confidential – Scientific – October 2020 ALS001: P1 Demonstrated Stabilized Inspiratory Pressure Maximal inspiratory pressures stabilized during Treg infusions 27 Coya Therapeutics, Inc

28 . Non - Confidential Presentation 2020 2
. Non - Confidential Presentation 2020 27 ALS001: Ongoing Phase 2a Trial (N=8) A Randomized, Placebo - Controlled Phase 2a Trial to Evaluate the Biological Activity, Safety, and Tolerability of Autologous Regu latory T Lymphocytes (Tregs) Expanded Ex - Vivo and Returned Intravenously in Combination with Low - Dose IL - 2 in People with ALS 28 Phase 2a Study design: Inclusion criteria, treatment regimen and endpoints Double Blind Randomized Control Trial with Open Label Extension • 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 pa

29 tients will enter the OLE directly and n
tients will enter the OLE directly and not participate in RCT 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 Autologous Treg: 1x10 6 cells/kg/infusion Concomitant subcutaneous administration of IL - 2(2x10 5 IU/m2/injection three times weekly) Months 1 - 6 Randomized,

30 Double Blind Months 6 - 12 Open Label E
Double Blind Months 6 - 12 Open Label Extension Autologous Treg: Dose Escalation Infusions #1 and #2 = 1x dose Infusions #3 and #4 = 2x dose Infusions #5 and #6 = 3x dose 28 Novel Autologous & Allogeneic Exosome Technology Platform Further information and data available under NDA iscEXOTM Science and Technology Overview 30 The iscEXO TM Platform: Coya has developed a first - in - class exosome or extracellular vesicle (EV) product • Highly suppressive ex vivo expanded i mmuno s uppressive c ells (the iscEXO TM Platform) Most Potent Anti - inflammatory Exosome Platform: derived from two of the most prominent anti - inflammatory and neuroprotective cell types - Tregs and M2 Macrophages • Leverage mesenchymal stem cell (MSc) derived EVs • EVs are not cells an

31 d avoid potential cell - based issues su
d avoid potential cell - based issues such as immune rejection and polarization to a pro - inflammatory cell type Compared to MSc Derived Exosomes, iscEXO TM is significantly more immunosuppressive Unique and differentiated approach: 30 • EVs are membrane - derived small vesicles that originate from endocytosis and are rich in proteins and RNAs. With small diameters they can be delivered into plasma and impact target cells • Release of exosomes from parent cells (such as Treg or M2 cell types) accounts for the immunosuppressive effects to neighboring cells and tissues • Treg cells deliver the most potent immunosuppressive exosome products by several mechanisms, which can be distinguished as contact dependent or independent Rojas C, Campos - Mora M et al.

32 (2020) T regulatory cells - derived extr
(2020) T regulatory cells - derived extracellular vesicles and their contribution to the generation of immune tolerance. J Leukoc Biol What are EVs? Allows Tregs to modulate immunosuppressive activity on surrounding cells and tissues 31 Exosome Method of Suppression: Secretion of EVs by Treg cells is a critical cell - contact independent manner Our EVs are remarkably stable and solve supply chain management limitations 31 First in Class Treg Derived Exosomes Platform Summary Coya is planning on an autologous phase 1 first in human (FIH) trial in 2022, with allogeneic approaches to follow 32 • Most companies leverage mesenchymal stem cell (MSC) derived exosomes, not Treg derived exosomes • Treg derived exosomes have an order of magnitude higher suppressive capacit

33 y and anti - inflammatory function than
y and anti - inflammatory function than MSC derived exosomes required for neuroinflammatory suppression (data on file) • Coya has developed the only manufacturing platform to isolate highly neuroprotective Treg derived exosomes ( not feasible without Coya’s primary proprietary Treg expansion process ) • Coya has 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 an

34 d limit other immune responses — they
d limit other immune responses — they achieve this through different mechanisms including the release of exosomes 32 In Vivo Treg Subcutaneous Injection Technology Platform In Vivo Treg Subcutaneous Injection Platform 34 34 While ALS likely requires ex - vivo administered Tregs/Treg exosomes, in - vivo modulation of Tregs via a biologic combination maybe efficacious in numerous orphan diseases Our laboratory has identified a combination therapeutic strategy of two immunomodulatory agents that enables potent in vivo modification of Treg function Preclinical data of the therapeutic combination is compelling in Alzheimer’s Disease and supports our 2020 publication on the importance of Treg dysfunction in this disease* Recent clinical data in our laboratory (not publ

35 ished) of one of these agents has illus
ished) of one of these agents has illustrated a significant clinical benefit in a cohort of mild/moderate Alzheimer’s Disease We believe that the combination approach (delivered by subcutaneous injection) will prove to be synergistic and additive in providing long term and durable responses in various orphan disease conditions 01 02 03 04 Next Steps and Milestones: Intellectual Property Filings and Enhancement (2020 - 2021); Manufacturing formulation (2021) Intellectual Property Treg Platform • Conversion of Dysfunctional to Functional Tregs • Manufacturing and Expansion Methods • Cryopreservation, Shipping, and Rethawing Methods • Composition of Matter • Therapeutic Modality in Multiple Disease States 36 Strong IP Portfolio Exosome Platform • Isolati

36 on and Manufacturing Methods • Cryopre
on and Manufacturing Methods • Cryopreservation, Shipping, and Rethawing Methods • Composition of Matter • Therapeutic Modality in Multiple Disease States • Autologous and Allogeneic Approaches Protection on Treg Manufacturing; Cryopreservation, Storage, and Thawing; and Composition of Matter 37 Key Investment Highlights 37 Suppressing Neuroinflammation: Tregs Against Inflammation (TAI ™ ) platform is developing disruptive, first in class, autologous Treg and allogeneic exosome therapeutics - leveraging the discovery that dysfunctional Tregs underlie neurodegenerative and autoimmune diseases. Clinical validation achieved in a successful Phase 1. Industrializing Supply Chain Management: Proprietary cryopreservation for Tregs ( Ctreg ™ ) with novel manufac

37 turing steps that overcome prior limitat
turing steps that overcome prior limitations of Treg cell therapies - single manufacturing round produce cells for a full year’s supply that can be stored, shipped, and administered at remote outpatient facilities. Value Creation (Upcoming Milestones): (1) Phase 2a topline data in ALS in Q3 2021 (2) Potential manufacturing partnerships (3) IP enhancement (4) FIH trials in other conditions driven by dysfunctional Tregs (Frontotemporal Dementia, Scleroderma) (5) Initiate FIH Treg derived Exosome Phase 1 trial in 2022. Revolutionizing Cell Therapy Manufacturing: Proprietary manufacturing steps that avoid genetic manipulation and instead, ex - vivo isolates and converts millions of dysfunctional Tregs to billions of highly functional Tregs that are neuroprotective