Edgewise Therapeutics, Inc. · NASDAQ:EWTX
Edgewise Therapeutics — Investor Day (January 2023)
76 slides from Edgewise Therapeutics's investor day presentation, Jan 3, 2023
Slide 1: EDG-7500: A Novel Sarcomere Modulator for the Treatment of Cardiac Diseases
EDG-7500: A Novel Sarcomere Modulator for the Treatment of Cardiac Diseases with Significant Unmet Need January 3, 2023 1 NASDAQ: EWTX
Slide 2: Disclaimer
Disclaimer This presentation contains forward-looking statements that involve substantial risks and uncertainties of Edgewise Therapeutics, Inc. (“Edgewise” or the “Company”). All statements other than statements of historical facts contained in this presentation, including statements regarding our
Slide 3: Edgewise Therapeutics is a Clinical-Stage Company Focused on Devastating Muscle Disorders
Edgewise Therapeutics is a Clinical-Stage Company Focused on Advancing Innovative Treatments for Devastating Muscle Disorders Experienced management team with deep expertise in muscle physiology/rare diseases Leveraging our discovery and development capabilities to advance innovative programs Develo
Slide 4: Edgewise is Uniquely Positioned to Develop Novel Therapies for Cardiovascular Diseases
Edgewise is Uniquely Positioned to Identify and Develop Novel Therapies Targeting Genetically Defined Cardiovascular Diseases The field of genetically defined cardiovascular diseases, much like oncology, is evolving as an area of significant focus Edgewise is leveraging the knowledge of shared sarco
Slide 5: Our Precision Medicine Platform Generated Two Portfolio Programs
Our Precision Medicine Platform Generated Two Portfolio Programs Across Multiple Indications Currently in Development Program Indications Preclinical Phase 1 Phase 2 Phase 3 EDG-5506 BMD Myosin ATPase Skeletal EDG-5506 DMD Myosin ATPase EDG-5506 LGMD, McArdle Myosin ATPase Cardiovascular EDG-7500 HC
Slide 6: Agenda
Agenda Dr. Martin Maron Kevin Koch Director Hypertrophic Cardiomyopathy Chief Executive Officer Center, Lahey Hospital 1 Hypertrophic Cardiomyopathy: A Clinician’s View Dr. Martin Maron 2 EDG-7500 Introduction & Scientific Overview Marc Evanchik Dr. Marc Semigran Marc Evanchik 3 EDG-7500 Clinical De
Slide 7: Hypertrophic Cardiomyopathy: A Clinician's View
Hypertrophic Cardiomyopathy: A Clinician’s View Martin Maron, M.D. Director Hypertrophic Cardiomyopathy Center, Lahey Hospital 7
Slide 8: Hypertrophic Cardiomyopathy: The Unmet Clinical Needs
Hypertrophic Cardiomyopathy: The Unmet Clinical Needs Martin Maron, MD Director, Hypertrophic Cardiomyopathy Center Lahey Medical Center; Burlington, MA Assistant Professor of Medicine, Tufts School of Medicine Chanin T. Mast Hypertrophic Cardiomyopathy Center Morristown Medical Center, NJ COI: Stee
Slide 9: Hypertrophic Cardiomyopathy (HCM)
Hypertrophic Cardiomyopathy (HCM) “Hypertrophied (increased wall thickness >15 mm) left ventricle in the absence of another cardiac or systemic disease that could produce a similar magnitude of hypertrophy”
Slide 10: Normal Heart vs Hypertrophic Cardiomyopathy
Hypertrophic Normal Heart Cardiomyopathy
Slide 11: Myocardial Substrate In HCM
Myocardial Substrate In HCM
Slide 12: HCM: Significance
HCM: Significance • Most common genetic cardiovascular disease • Most common cause of SCD in the young/ athletes • Important cause of AF and stroke • Important cause of Heart Failure in All Ages
Slide 13: Hypertrophic Cardiomyopathy: Nonobstructive and Obstructive
HYPERTROPHIC CARDIOMYOPATHY NONOBSTRUCTIVE OBSTRUCTIVE (30%) (70%)
Slide 14: Mechanism of Heart Failure in HCM
Mechanism of Heart Failure in HCM Obstructive HCM Nonobstructive HCM LV Outflow Tract Diastolic Obstruction Dysfunction
Slide 15: HCM: Global Burden
HCM: Global Burden 121 Countries involving 90% of world’s population Prevalence 1:200-1:500 Estimated ~15-20 million affected worldwide Clinically Identified ~250,00 in U.S Unidentified ~450,000
Slide 16: Clinical Recognition of HCM
Clinical Recognition of HCM Acute Event (11%) Exertional w SOB Sports/Other Exertional Fatigue Screening (4%) Chest Pain Palpitations Symptom Onset Routine Exam (43%) (33%) Family Screening (13%)
Slide 17: Primary Diagnosis of HCM
Primary Diagnosis of HCM CLINICAL DIAGNOSIS: Non-invasive imaging 2-D echocardiography MRI RAISE SUSPICION of HCM: ECG (Abnormal in 90% but NS) Physical exam: murmur (obstruction only)
Slide 18: (<1%) (7%) (<1%) (15%) (7%) (<1%) (<1%) (15%) (<1%) (<1%)
(<1%) (7%) (<1%) (15%) (7%) (<1%) (<1%) (15%) (<1%) (<1%)
Slide 19: Multiple Variants (Polygenic)
~30% ~70% Sarcomere Sarcomere Positive Negative Multiple Variants (Polygenic) Common HCM Phenotype
Slide 20: Clinical Pathways of Prognosis in HCM
Clinical Pathways of Prognosis in HCM HCM Patients Progressive Progressive AF Sudden HF: HF: & Death Nonobstructive Obstructive Stroke
Slide 21: Clinical Pathways of Prognosis in HCM: Sudden Death
Clinical Pathways of Prognosis in HCM: Sudden Death HCM Patients Progressive Progressive AF Sudden HF: HF: & Death Nonobstructive Obstructive Stroke
Slide 22: HCM: most common causes of SCD in young people and athletes
HCM: most common causes of SCD in young people and athletes
Slide 23: Selection for ICD in Adult HCM Patients
Selection for ICD in Adult HCM Pts : 2020 AHA/ACC Guideline-Based Sudden Death Risk Markers Major Markers (< 60 yrs of age) Family History HCM-SCD Unexplained syncope Increased Risk: Multiple-repetitive NSVT ( ≥ 1 major marker) Reasonable to Massive LVH ≥ 30 mm consider LV apical aneurysm primary pr
Slide 24: Trends in HCM Sudden Cardiac Death Rates
Trends in HCM Sudden Cardiac Death Rates Abdelfattah O et al JACC EP 2022
Slide 25: Sudden Death and Advanced Heart Failure
Sudden Death Advanced t HF
Slide 26: Clinical Pathways of Prognosis in HCM: Heart Failure
Clinical Pathways of Prognosis in HCM: Heart Failure HCM Patients Progressive Progressive AF Sudden HF: HF: & Death Nonobstructive Obstructive Stroke
Slide 27: Obstructive HCM
Obstructive HCM Hypercontractility of the Left Ventricle is a Major Contributor to Mechanism of Outflow Obstruction… Interventions that DECREASE Contractility will Lower or Abolish Outflow Obstruction
Slide 28: Impact of LV Outflow Obstruction on Progression to Advanced Heart Failure and Death
Impact of LV Outflow Obstruction (≥30 mmHg) on Progression to Advanced Heart Failure and Death 100 Freedom From Progression to NYHA Nonobstructive Class III/IV and Death 80 60 P = 0.001 RR = 4.4 Obstructive 40 20 0 0 2 4 6 8 10 Years From First Gradient Measurement Maron MS et al. N Engl J Med. 2003
Slide 29: Contemporary Approach to Management of Symptomatic Obstructive HCM
Contemporary Approach to Management of Symptomatic Obstructive HCM Obstructive HCM With HF Symptoms Beta-Blocker/Verapamil Persistent or Progressive Symptoms Add Stronger Negative Inotropes Surgical Septal Disopyramide Myectomy Mavacamten (or Alcohol Septal Refractory Ablation) Symptoms or Drug Side
Slide 30: Septal Reduction Therapy (SRT)
Septal Reduction Therapy (SRT) Surgical Alcohol Ablation Myectomy (ASA)
Slide 31: Current Unmet Treatment Needs in Obstructive HCM
Current Unmet Treatment Needs in Obstructive HCM Obstructive HCM Avg Age: With HF 50 years old Symptoms Beta-Blocker/Verapamil Very Low Efficacy/Side Effects Persistent or Progressive Symptoms Add Stronger Negative Inotropes Surgical Septal Limited Limited Long- Disopyramide Myectomy Expertise/ Term
Slide 32: Mavacamten
30% NO better or worse in 35% with NO Health Metrics 37% Achieved (KCCQ) Primary Endpoint: Improvement in Symptom/VO2 NYHA class improvement Mavacamten (EXPLORER-HCM; VALOR-HCM) 7% Systolic 43% with Residual Dysfunction/HF LVOT Gradient (≥ 30mmHg)
Slide 33: Mechanism of Heart Failure in HCM
Mechanism of Heart Failure in HCM Obstructive HCM LV Outflow Tract Diastolic Obstruction Dysfunction
Slide 34: Change in NYHA Functional Class Following Surgical Myectomy
Change in NYHA Functional Class Following Surgical Myectomy NYHA Pre- Class operative Follow-up 2 2 247 1 (65%) (0.5%) 5 240 2 7 2 113 (1.8%) (29%) 111 35% 376 25 3/4 (98%) 2 5 (6%)
Slide 35: Clinical Pathways of Prognosis in HCM
Clinical Pathways of Prognosis in HCM HCM Patients Progressive Progressive AF Sudden HF: HF: & Death Nonobstructive Obstructive Stroke
Slide 36: Diastolic Dysfunction in HCM
Diastolic Dysfunction in HCM LV Distensibility: LV Relaxation: • LV Hypertrophy • LV Hypertrophy •Disarray •Myocardial Ischemia •Interstitial Fibrosis • Replacement Scar Altered LV Diastolic Filling/ Low Stroke Vol
Slide 37: Exercise Capacity in HCM Dependent on Diastolic Filling Characteristics
Exercise Capacity in HCM Dependent on Diastolic Filling Characteristics Exercise LV Diastolic Filling HCM: impaired ability to Stroke Volume Increase Stroke Volume Exercise Capacity
Slide 38: Treatment Gaps in Nonobstructive HCM
Treatment Gaps in Nonobstructive HCM Nonobstructive HCM Unmet Tx ~30% Beta-Blocker/ NYHA Calcium Channel Need Blocker Class II Rate of HF Progression: 1.5%/yr ~10% NYHA Heart Transplant Class III/IV
Slide 39: Summary: Unmet Treatment Needs in HCM
Summary: Unmet Treatment Needs in HCM Limiting Long-term, reliable, safe Symptoms: Obstruction Reduction in LVOT Gradient: Preventing HF progression Limiting Symptoms: Therapy to Improve HF Nonobstructive Symptoms/QoL Progression of Nonobstructed Medical Therapy to HCM Prevent HF Progression: to End
Slide 40: EDG-7500: A Novel Sarcomere Modulator for HCM and Diastolic Disease
EDG-7500: A Novel Sarcomere Modulator for HCM and Diastolic Disease Marc Evanchik Edgewise VP of Discovery 40
Slide 41: The Cardiac Cycle: Pressure Volume Loops Inform Cardiac Function
The Cardiac Cycle: Pressure Volume Loops Inform Cardiac Function and Performance Healthy Heart Ventricular Systole Diastole Pressure-Volume (PV) Loop (Pumping) (Filling) End Systole Right Aortic atrium valve Left Tricuspid atrium valve Mitral valve Right ventricle Left ventricle End Diastole Healthy
Slide 42: In oHCM, Hearts Operate With Reduced Forward Blood Flow
In oHCM, Hearts Operate With Reduced Forward Blood Flow and Experience Higher Pressures Ventricular Systole Diastole oHCM Heart PV Loop (Pumping) (Filling) Narrowed LVOT Right Aortic atrium valve Left Tricuspid atrium valve Mitral valve Left Right ventricle Decreased ventricle LV volume Decreased LV
Slide 43: In nHCM, Stroke Volume is Limited by Higher End Diastolic Pressure
In nHCM, No LVOT Obstruction, But Stroke Volume is Limited by Higher End Diastolic Pressure Ventricular Systole Diastole nHCM Heart PV Loop (Pumping) (Filling) Right Aortic atrium valve Left Tricuspid atrium valve Mitral valve Left Decreased Right ventricle ventricle LV volume Decreased LV volume Sy
Slide 44: The Sarcomere is the Molecular Unit Responsible for Heart Contraction and Relaxation
The Sarcomere is the Molecular Unit in Cardiac Muscle Responsible for Heart Contraction and Relaxation Sarcomeric gene mutations cause HCM, and mutations in cardiac myosin binding protein C and β-myosin heavy chain account for 80% of all genetic HCM cases Gene # of mutations to TNNI3 Protein Symbol
Slide 45: HCM Hearts are Hyperdynamic, and Relaxation is Impaired
HCM Hearts are Hyperdynamic, and Relaxation is Impaired HCM is a Disease of the Sarcomere In HCM too many ‘motors’ engaged Healthy sarcomere during systole and diastole Excessive contraction and Normal contraction impaired relaxation Abbreviations: HCM, hypertrophic cardiomyopathy 45
Slide 46: Why Develop a Novel Approach for HCM?
Why Develop a Novel Approach for HCM? 1 • Direct inhibition of the myosin motor (CMIs) reduces cross-bridges during the entire cardiac cycle − Inhibitors limit cardiac function during both systole and diastole with a steep dose response requiring careful echo-guided dose titration − Inhibition of ca
Slide 47: Edgewise's Approach – Develop an Indirect Myosin Modulator
Edgewise’s Approach – Develop an Indirect Myosin Modulator • EDG-7500 regulates myosin by targeting the complex sarcomere protein- protein interactions that control contraction and relaxation processes • Reduce the excessive residual actin-myosin cross-bridges during diastole, facilitating relaxatio
Slide 48: EDG-7500 Improved HCM Clinical Manifestations in Translatable Models
EDG-7500 has Demonstrated Improvement in a Variety of HCM Clinical Manifestations in Translatable Models of Both oHCM and nHCM Key Result Preclinical Model ✓ Preserves myosin head motor function In vitro: Myofibril systems Novel target ✓ Slows contraction, increases compliance In vivo: Pressure Volu
Slide 49: EDG-7500 was Designed to Work Independently of Myosin Motor Activity
EDG-7500 was Designed to Work Independently of Myosin Motor Activity EDG-7500 ATPase Activity 150 Normalized ATPase Activity (%) 100 EDG-7500 was designed specifically to preserve full motor activity in isolated myosin 50 (‘S1’) systems demonstrating a novel mechanism of action 0 0.001 0.01 0.1 1 10
Slide 50: EDG-7500 Slows Contraction and Improves Compliance in Healthy Canines
EDG-7500 Slows Contraction and Improves Compliance/ Dispensability in Healthy Canines EDG-7500 Slows EDG-7500 Increases Compliance Contraction End diastolic volume increased; end diastolic pressure maintained 10 25 ns 12 ✱ ✱✱ End Diastolic Pressure (mmHg) Pre Ejection Period (% cycle) End Diastolc V
Slide 51: Reduction in Systolic Contraction is Self-Limiting in Healthy Canines
Moreover, the Reduction in Systolic Contraction is Self-Limiting in Healthy Canines Treated with EDG-7500 ✱✱ 2,100 20 12.4x 1,800 dP/dtmax (mmHg/s) 0 dP/dtmax (%) 1,500 -15% -20 -8% 1,200 -40 900 PRE POST 0.3 mg/kg 0 200 400 600 800 LV Pressure Development EDG-7500 Free Fraction (ng/mL) SD shown; Fo
Slide 52: Hypertrophic Cardiomyopathy with Left Ventricular Outflow Tract Obstruction (oHCM)
Hypertrophic Cardiomyopathy with Left Ventricular Outflow Tract Obstruction (oHCM) 52
Slide 53: MYBPC3 A31P Feline Model Exhibits HCM Phenotype with LVOT Obstruction
MYBPC3 A31P Feline Model Exhibits HCM Phenotype with Left Ventricular Outflow Tract (LVOT) Obstruction MYBPC3 A31P Feline Model of oHCM Gradient = 13.4 mmHg • Purpose bred felines with naturally occurring homozygous MYBPC3 A31P mutation • MYBPC3 A31P felines exhibit left ventricular hypertrophy and
Slide 54: MYBPC3 A31P Feline Model LVOT Gradient Alleviated with EDG-7500
MYBPC3 A31P Feline Model LVOT Gradient Alleviated with EDG-7500 MYBPC3 A31P felines exhibit left ventricular EDG-7500 treated MYBPC A31P feline shows hypertrophy and outflow tract obstruction LVOT gradient relief consistent with oHCM d d Gradient = 13.4 mmHg Gradient = 2.5 mmHg Pressure gradient is
Slide 55: EDG-7500 Improves Contractility and Alleviates LVOT Gradient in Feline Model
EDG-7500 Improves Contractility and Alleviates LVOT Gradient in an Established Feline Model of oHCM Hypercontractility Improved to within LVOT Gradient Removed Normal Range 100 100 20 20 Left Ventricular Fractional Shortening (%) Left Ventricular Fractional Shortening (%) ✱ ✱✱ 80 80 LVOT Gradient (m
Slide 56: EDG-7500 Markedly Reduces LVOT Gradient at Plasma Concentrations With Modest Contractility Changes
EDG-7500 Markedly Reduces LVOT Gradient at Plasma Concentrations Associated with Modest Changes in Contractility MYBPC3 A31C Feline Model of oHCM IC50 IC75 IC50 IC75 20 100 Fractional Shortening (% vs. PRE) 15 LVOT Gradient (mmHg) 10 50 G G 5 0 0 0 100 200 300 400 500 0 100 200 300 400 500 EDG-7500,
Slide 57: Non-Obstructive Hypertrophic Cardiomyopathy (nHCM)
Non-Obstructive Hypertrophic Cardiomyopathy (nHCM) 57
Slide 58: Myosin Heavy Chain R403Q Porcine Model of nHCM
Myosin Heavy Chain R403Q Porcine Model of nHCM Presents with Characteristic Non-Obstructive HCM Phenotype Observed in Humans Left ventricular (LV) hypertrophy, small cavity, and increased filling pressure leads to increased left atrial (LA) size Wild Type Non-Obstructive HCM • Genetically engineered
Slide 59: Rapid Normalization of HCM Cardiac Structure and Function in Porcine Model
Rapid Normalization of HCM Cardiac Structure and Function in the MYH7 R403Q Porcine with a Single Dose of EDG-7500 Hypercontraction EDG-7500 Drives Improvement in LV Filling and Reduction in LA Size Retuned to WT Levels Consistent with Reduced Filling Pressure ✱✱ 80 15 8 30 ✱ ✱ Left Ventricular Ejec
Slide 60: EDG-7500: First-in-Class Sarcomere Modulator for HCM
EDG-7500: First-in-Class Sarcomere Modulator Intended to Address the Molecular Underpinning of HCM • EDG-7500 is an oral, selective cardiac sarcomere modulator • EDG-7500 normalizes excess systolic and diastolic cross-bridges, the underlying pathology of both obstructive and non-obstructive HCM, wit
Slide 61: HCM Clinical Development Program
HCM Clinical Development Program Marc Semigran, M.D. Edgewise Chief Development Officer 61
Slide 62: HCM Represents a Patient Population with Significant Unmet Need
HCM Represents a Patient Population with Significant Unmet Need and Ample Opportunity for a Novel Therapy Such as EDG-7500 Perceived Limitations of Approved and In Development Cardiac Myosin Inhibitors: •1 Complex pharmacology and variable metabolism based largely on genetics, resulting in potential
Slide 63: Limited Efficacy of Current Therapeutic Approaches in oHCM
The Limited Efficacy of Current Therapeutic Approaches is One of the Unmet Needs in the Management of oHCM Patients Residual LV Outflow Tract Gradients After Treatment % of Patients with No Improvement in NYHA Functional Class Following Treatment 100% 40% 90% 88% 35% 35% 35% % of patients with LV ou
Slide 64: Algorithm for Reaching a Safe Dose of Camzyos (1/3)
Algorithm for Reaching a Safe and Efficacious Dose of Camzyos® Requires Multiple Clinic Visits; Lack of Adherence Can Result in HF (1/3) STEP 1: Initiation Phase Week 4* Week 8* Week 12* Valsalva LVOT Valsalva gradient 1. Restart on 2.5 mg if LVEF ≥50% and LVOT gradient Withhold drug recheck clinica
Slide 65: Algorithm for Reaching a Safe Dose of Camzyos (2/3)
Algorithm for Reaching a Safe and Efficacious Dose of Camzyos® Requires Multiple Clinic Visits; Lack of Adherence Can Result in HF (2/3) STEP 2: Continued Dose Adjustments to Achieve Maintenance Dose Week 12 + every 12 weeks LVEF <50% Interrupt treatment. See STEP 3 LVEF 50-59%, regardless of Valsal
Slide 66: Algorithm for Reaching a Safe Dose of Camzyos (3/3)
Algorithm for Reaching a Safe and Efficacious Dose of Camzyos® Requires Multiple Clinic Visits; Lack of Adherence Can Result in HF (3/3) STEP 3: Treatment interruption at any clinic visit if LVEF <50% 1. Interrupt treatment 2. Recheck ECHO parameters every LVEF ≥50% 4 weeks until LVEF ≥50% 1. Restar
Slide 67: EDG-7500 Has a Modest Effect on Cardiac Contractility at Plasma Levels Eliminating LVOT Obstruction
EDG-7500 has a Modest Effect on Cardiac Contractility at Plasma Levels that Eliminate LVOT Obstruction IC50 IC75 100 60 Treatment with EDG-7500 is associated with a LV FS (%) Healthy feline range† 50 modest effect on contractility with free drug levels of ~55 to 140 ng/mL achieving IC50 to IC75 grad
Slide 68: Phase 1 Study of EDG-7500 in Healthy Volunteers and HCM Patients to Start in 2023
Phase 1 Study of EDG-7500 in Healthy Volunteers and HCM Patients to Start in 2023 GOAL: To evaluate safety and tolerability of EDG-7500 and establish POM and POC in HCM patients Healthy Volunteers Key Outcome Measures Safety and tolerability PK and Cardiovascular PD - Echocardiogram SAD/MAD Study de
Slide 69: Summary
Summary • EDG-7500’s unique MOA targets both abnormal systolic and diastolic function in HCM patients, suggesting the ability to drive a broad efficacy response at a low risk of decreasing LVEF below normal • EDG-7500’s excellent selectivity, bioavailability, and favorable half-life should potential
Slide 70: Future Direction and Closing Remarks
Future Direction and Closing Remarks Kevin Koch Edgewise Chief Executive Officer 70
Slide 71: HCM Represents a Patient Population with Significant Unmet Need
HCM Represents a Patient Population with Significant Unmet Need and Ample Opportunity for a Novel Therapy Such as EDG-7500 HCM patients rely on polypharmacy and Healthy Heart Hypertrophic Cardiomyopathy SRT, an invasive surgical option Optimal care and patient outcomes require highly specialized HCM
Slide 72: EDG-7500 has Attractive First-in-Class Drug Attributes
EDG-7500 has Attractive First-in-Class Drug Attributes EDG-7500 Preclinical Drug Attributes Target Non-myosin motor, sarcomeric protein • Oral, once daily therapy LVFS Limited reduction Human t1/2 (projected) 1-2 days CYP450 induction EC50 >30 μM • Rapid onset of action CYP450 inhibition IC50 >30 μM
Slide 73: Highly Innovative Cardiac Clinical Candidate Progressing into IND-Enabling Studies
Highly Innovative and Differentiated Cardiac Clinical Candidate for HCM Progressing into IND-Enabling Studies with IND Projected 3Q/23 Our goal is to reverse the causal pathophysiology of HCM without the limitations observed with cardiac myosin inhibitors Non-Myosin Motor Targeted Sarcomere Modulato
Slide 74: Strong Execution in 2022 Allowed Edgewise to Achieve Multiple Key Milestones
Strong Execution in 2022 Allowed Edgewise to Achieve Multiple Key Milestones CANYON Becker Phase 2/3 Study Start ✓ LYNX Duchenne Phase 2 Dose-Ranging Study Start ✓ ARCH BMD OL Study Data 6 Month Readout ✓ Phase 2 Exercise Challenge Start in LGMD2i and McArdle ✓ Selection of a Novel Cardiac Candidate
Slide 75: Well-Capitalized to Execute Important Value-Driving Milestones
Well-Capitalized to Execute Important Value-Driving Milestones Across EDG-5506, EDG-7500 and Other Pipeline Programs (1) (1) $365M 63.2M Cash, Cash Equivalents and Common Shares Outstanding Marketable Securities No Debt NASDAQ: EWTX (1) As of September 30, 2022 75
Slide 76: Thank You and Questions
Thank You and Questions Donec sit amet cursus ante. Nullam elementum sem a vestibulum interdum. 76 NASDAQ: EWTX