Argenx Se · EURONEXT:ARGX
Argenx — Investor Day (July 2021)
69 slides from Argenx's investor day presentation, Jul 20, 2021
Slide 1: argenx R&D Day, July 20, 2021
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Slide 2: Welcome & Introductions
Welcome & Introductions Beth DelGiacco Vice President, Corporate Communications & Investor Relations
Slide 3: Forward Looking Statements
Forward Looking Statements Safe Harbor: Certain statements contained in this presentation, other than present and changes to the competitive environment. Consequently, actual future results may differ materially historical facts and conditions independently verifiable at the date hereof, may constit
Slide 4: Today's Agenda
Today’s Agenda Advancing Towards argenx 2025 | Tim Van Hauwermeiren, Chief Executive Officer and Co-Founder Efgartigimod: Differentiation of our Anti-FcRn Fc Fragment | Hans de Haard, Chief Scientific Officer and Co-Founder Fifth Efgartigimod Indication: Myositis | Bas van der Woning, Research Fello
Slide 5: Visit the argenx R&D Day Microsite to View Additional Resources
Visit the argenx R&D Day Microsite to View Additional Resources Myositis and Bullous Patient MG Experience Pemphigoid Stories in China Disease Overview Discussion Relevant on FcRn and Albumin Publications 5
Slide 6: Advancing Towards argenx 2025
Advancing Towards argenx 2025 Tim Van Hauwermeiren Co-Founder and CEO
Slide 7: Where critical patient need meets breakthrough science
Where critical patient need meets breakthrough science That is where we redefine immunology
Slide 8: 2021: Reaching Myasthenia Gravis Patients with Efgartigimod
2021: Reaching Myasthenia Gravis Patients with Efgartigimod New modality Only Fc fragment targeting FcRn Defined disease biology Correlation of total IgG and MG ADL Designed ADAPT with patient input Engaging MG community 8
Slide 9: Efgartigimod: A Precision Tool to Revolutionize Autoimmunity
Efgartigimod: A Precision Tool to Revolutionize Autoimmunity Sjogren’s Syndrome ITP GBS Lupus Membranous Nephritis Nephropathy IgG IgG Thyroid Myasthenia Eye Disease Gravis Bullous CIDP Pemphigoid IgG IgG Myositis Neuromyelitis Optica AMR Pemphigus 9
Slide 10: Myositis: IgG-Mediated Biology
Myositis: IgG-Mediated Biology AChR, MuSK, LRP4 Neuromuscular Disease Myasthenia Gravis autoantibodies comprise ~90% of MG patients + ADAPT Data + Chronic Inflammatory 40% anti-myelinated ADHERE Neuromuscular Disease Demyelinating peripheral nerve IgGs GO/NO-GO Polyneuropathy Autoantibodies characte
Slide 11: Bullous Pemphigoid: Expanding the Skin Franchise
Bullous Pemphigoid: Expanding the Skin Franchise Autoimmune Blistering Diseases Pemphigus Pemphigoid Autoantibody Driven DSG1 and DSG3 BP180 and BP230 Convincing Rationale IVIg, PLEX, Immunoadsorption demonstrate role of IgG Unmet Patient Needs Fast-acting, tolerable therapies; ability to taper cort
Slide 12: Our Pipeline Starts with our Immunology Innovation Program
Our Pipeline Starts with our Immunology Innovation Program CLINICAL DEVELOPMENT LEADING TRANSLATIONAL BIOLOGY LABS ANTIBODY ENGINEERING Internal Value Creation External Value Creation Staten AgoMAb First in Class | Unique Design | Multiple Indications ARGX-118 Dualyx (ARGX-116) (ARGX-114) Genor LEO
Slide 13: Neuromuscular Franchise: A Company within a Company
Neuromuscular Franchise: A Company within a Company SMA MMN IIP Programs ALS MG Myositis Congenital MG CIDP ARGX-117 C2 inhibitor MuSK MG ARGX-119 SIMPLE Antibody™ aimed to boost Efgartigimod the neuromuscular junction in disease FcRn antagonist MMN Leveraging infrastructure across multiple Myositis
Slide 14: Building a Leading Immunology Company
Building a Leading Immunology Company Global autoimmune market has surpassed $150B Committed to our Efgartigimod available globally Patients and their Communities Vibrant neuromuscular, hematology and skin franchises Enviable Immunology Efgartigimod in 15 indications (commercial or development) Pipe
Slide 15: Building a Leading Immunology Company
Building a Leading Immunology Company Global autoimmune market has surpassed $150B Committed to our Efgartigimod available globally Patients and their Communities Vibrant neuromuscular, hematology and skin franchises Enviable Immunology argenx Efgartigimod in 15 indications (commercial or developmen
Slide 16: Efgartigimod: Differentiation of our Anti-FcRn Fragment
Efgartigimod: Differentiation of our Anti-FcRn Fragment Hans de Haard Chief Scientific Officer and Co-Founder
Slide 17: FcRn Plays a Key Role in IgG and Albumin Homeostasis
FcRn Plays a Key Role in IgG and Albumin Homeostasis Studies have shown: Endothelial Cell Circulating antibodies are taken up in the cell via pinocytosis. In the 1 endosome, IgG antibodies bind to 3 FcRn1,2 1 IgG Autoantibody Unbound IgGs enter the lysosomal 2 degradation pathway, while FcRn-bound 1
Slide 18: Efgartigimod Fc Fragment Binds to FcRn in Same Way as Endogenous IgGs
Efgartigimod Fc Fragment Binds to FcRn in Same Way as Endogenous IgGs 1 2 3 Endogenous Anti-FcRn mAb FcRn:IgG Interaction Efgartigimod binds to FcRn in the same formation as endogenous IgG Our hypothesis is that different binding properties of FcRn antagonists lead to different subcellular trafficki
Slide 19: Efgartigimod Keeps FcRn in its Recycling Path
Efgartigimod Keeps FcRn in its Recycling Path FcRn over time Normalized Sum Volume (FcRn) Normalized Volume (%) No treatment Efgartigimod Control anti-FcRn mAb Time (Min) 19
Slide 20: Albumin Serves a Crucial Role in Lipid Housekeeping
Albumin Serves a Crucial Role in Lipid Housekeeping Proposed Interactions Between Serum Albumin and CV Outcomes4 Inflammatory process Underlying conditions Low serum albumin levels Small molecule binding Vasodilatory ability ↓ Vascular permeability ↑ Anticoagulation ↓ (toxins & medicines) ↓ Choleste
Slide 21: Efgartigimod Blocks IgG Binding to FcRn Without Reducing Albumin
Efgartigimod Blocks IgG Binding to FcRn Without Reducing Albumin Phase 3 ADAPT Trial of Efgartigimod in Myasthenia Gravis Patients IgG levels – 1st cycle Albumin and LDL Cholesterol levels – 1st & 2nd cycles Albumin (g/L) LDL (mmol/L) Week Week • Potent reduction in IgG levels without decrease in al
Slide 22: Efgartigimod: Data Support Favorable Benefit to Risk Ratio
Efgartigimod: Data Support Favorable Benefit to Risk Ratio 600+ subjects dosed Clinical proof-of-concept in No evidence of dose-limiting 125+ four indications toxicities in healthy volunteers or patients on efgartigimod for (MG, ITP, PV, CIDP) patients across trials over 12 months Opportunity to dos
Slide 23: Fifth Efgartigimod Indication: Myositis
Fifth Efgartigimod Indication: Myositis Bas van der Woning Research Fellow
Slide 24: Idiopathic Inflammatory Myopathy (IIM) or Myositis
Idiopathic Inflammatory Myopathy (IIM) or Myositis Rare, severe autoimmune disorders characterized by chronic muscle inflammation, pain and impaired quality of life; no FDA-approved therapies for myositis MYOSITIS IS MEDIATED BY AUTOANTIBODIES PREVALENCE HALLMARK TREATMENT BURDEN 14 per 100,000 Prox
Slide 25: Many Myositis-Specific Autoantibodies Have Been Identified
Many Myositis-Specific Autoantibodies Have Been Identified PL-7 PL-12 SAE ASyS EJ Myositis classification is Mi-2 based on myositis-specific OJ Jo-1 autoantibodies (IgG) and Polymyositis KS TIF-1γ clinical symptoms IMNM MDA-5 SRP HMGCR PM-Scl MJ DM EULAR/ACR* classification Overlap criteria for adul
Slide 26: IMNM Autoantibodies Trigger Muscle Damage and Impair Muscle Regeneration
IMNM Autoantibodies Trigger Muscle Damage and Impair Muscle Regeneration Macrophage recruitment Necrosis 3 4 and activation IL-1, IL-6, TNF → atrophy Classical complement activation → 2 Myolysis (muscle Blocking myotube enzymes e.g., CK) 5 formation Anti-SRP/-HMGCR autoantibodies bind 1 muscle fiber
Slide 27: DM and ASyS Autoantibodies Activate Complement and Type 1 Interferon
DM and ASyS Autoantibodies Activate Complement and Type 1 Interferon Complement 1 Myolysis 2 Necrosis Activation complement Complement Disruption of capillaries 1 2 Hypoperfusion Activation Atrophy Autoantibodies Dendritic cells produce Increased Type 1 interferon from 1 2 autoantibody Interferon im
Slide 28: Autoantibodies are Central Mediators of Myositis Pathophysiologies
Autoantibodies are Central Mediators of Myositis Pathophysiologies Summary of Mode of Action of Autoantibodies complement Complement activation of muscle lysis Complement activation of endothelial cell lysis autoantibody myotube Interferon production alpha/beta induce atrophy Inhibition of myotube f
Slide 29: Efgartigimod Designed to Clear IgG Autoantibodies Regardless of Target Antigen
Efgartigimod Designed to Clear IgG Autoantibodies Regardless of Target Antigen IMNM (70% MSA+) ASyS (100% MSA+) DM (75% MSA+) anti-SRP anti-Jo-1 anti-PL-7 anti-Mi-2 anti-TIF-1y Anti-HMGCR anti-PL-12 other anti-synthetases anti-NXP-2 anti-SAE MAA or Abs against unidentified targets anti-MDA5 MAA or A
Slide 30: Biology Rationale is at the Core of our Indication Selection
Biology Rationale is at the Core of our Indication Selection Preclinical Evidence Clinical Evidence Passive transfer model of IMNM autoantibodies No approved targeted therapies for myositis but from patient serum induce muscle weakness and common immune therapies* show correlation of loss of grip st
Slide 31: Autoantibody Levels Correlate to Indicators of Myositis
Autoantibody Levels Correlate to Indicators of Myositis: CK Levels and Muscle Strength Patients were treated with standard of care immunosuppressants • Similarly, anti-HMGCR, -Jo-1 and -Mi-2 titers correlate with CK levels and muscle strength • Anti-MDA5, -Jo-1 and -Mi-2 titers correlate with extram
Slide 32: ASyS and DM: Anti-Jo-1 and Anti-Mi-2 Patients Respond to Rituximab
ASyS and DM: Anti-Jo-1 and Anti-Mi-2 Patients Respond to Rituximab Shorter time to improvement in patients positive for anti-Jo-1 and anti-Mi-2 autoantibodies Anti-Jo-1 and anti-Mi-2 levels decreased after B-cell depletion Correlation of anti-Jo-1 and anti-Mi-2 titers with disease activity measures
Slide 33: DM Patients Respond to IVIg
DM Patients Respond to IVIg ProDERM study: % of patients with increase of ≥20 points on Total Improvement Score (TIS) at week 16 IVIg Placebo TIS≥20 78.7% 43.8% TIS≥40 68.1% 22.9% 2g/kg IVIg/Placebo Aggarwal et al., Arthritis Rheumatol. 2020 33
Slide 34: IMNM Autoantibodies from Patient Serum Induce Muscle Weakness
IMNM Autoantibodies from Patient Serum Induce Muscle Weakness and Loss of Grip Strength IgG purified from plasma from anti-SRP and anti-HMGCR IMNM Necrosis and complement deposition are observed similarly in patients causes loss of grip strength and muscle weakness in recipient mice as in IMNM patie
Slide 35: Significant Market Opportunity Across Myositis Subsets
Significant Market Opportunity Across Myositis Subsets DM: REACHING PATIENTS 3 21K pts U.S. ASyS: 33K 2 8K pts U.S. Estimated 1 IMNM: eligible myositis 4K pts U.S. patients in U.S. DEFINING NEW BIOLOGY Role of autoantibody is Basket trial approach to best-characterized in IMNM include ASyS and DM as
Slide 36: Adaptive Phase 2/3 Enrichment Design
Adaptive Phase 2/3 Enrichment Design 180 patients Total Duration: 26 weeks Proposed Endpoints 1000mg efgartigimod SC (+ SOC) Independent Primary adjudication committee IMNM Response based on Placebo SC (+ SOC) Total Improvement Score (TIS) Stratified for ACR/EULAR endorsed • IMNM 1000mg efgartigimod
Slide 37: Conclusions
Conclusions >30,000 IMNM, ASyS and DM patients in the U.S. Diverse panel of IgG autoantibodies emerge as key driver of muscle inflammation Clinical evidence links IgG levels to disease activity Efgartigimod is designed to reduce all IgGs regardless of target antigen and can further elucidate myositi
Slide 38: Sixth Efgartigimod Indication: Bullous Pemphigoid
Sixth Efgartigimod Indication: Bullous Pemphigoid Peter Verheesen Research Fellow
Slide 39: Bullous Pemphigoid: Most Common Autoimmune Blistering Disease
Bullous Pemphigoid: Most Common Autoimmune Blistering Disease Severe, rare, chronic and recurrent autoimmune disorder characterized by fluid-filled blisters, itching and skin redness BULLOUS PEMPHIGOID IS MEDIATED BY AUTOANTIBODIES PREVALENCE BURDEN TREATMENT UNMET NEED 12 per 100,0001 Severe bliste
Slide 40: Bullous Pemphigoid Autoantibodies are Origin of Blister Formation
Bullous Pemphigoid Autoantibodies are Origin of Blister Formation • BP180 and BP230: key pathogenic hemidesmosomal antigens driving blistering between epidermis and dermis • Autoantibody actions: • Mechanical disruption of keratinocyte adhesion • IgG autoantibody deposition triggers complement activ
Slide 41: Passive Transfer Model Highlights Toxicity of Bullous Pemphigoid Autoantibodies
Passive Transfer Model Highlights Toxicity of Bullous Pemphigoid Autoantibodies Mice injected with BP180 Ab HDIG lowers BP180 Ab levels and improves disease scores Pathogenic autoantibodies induce typical skin lesions in murine passive transfer model of bullous pemphigoid Mice injected with BP180 Ab
Slide 42: Bullous Pemphigoid Disease Activity Improves with Increasingly Selective IgG Therapies
Bullous Pemphigoid Disease Activity Improves with Increasingly Selective IgG Therapies Selectivity for IgG Trial Response • Phase 3 double-blind randomized trial • Clear therapeutic benefit • 56 patients • Stronger response in severe disease IVIg • High dose IVIg (5 days) + oral • Fast improvement c
Slide 43: IgG-Targeted Therapies Drive Fast Remissions
IgG-Targeted Therapies Drive Fast Remissions IVIg1 Protein A Immunoadsorption3 Change in erosions/blisters Disease activity BP180 NC16A ELISA (U/ml)1 Plasma Exchange (PLEX) 2 (1) Amagai et al., J. Dermatol. Sci. 2017 (2) Mazzi, Transfusion and Apheresis Science. 2013 (3) Kasperkiewicz et al., J Am A
Slide 44: Pemphigus Serves as Proof of Concept for Autoimmune Blistering Diseases
Pemphigus Serves as Proof of Concept for Autoimmune Blistering Diseases SKIN BLISTERING DISEASES – AUTOANTIBODY DRIVEN PEMPHIGUS BULLOUS PEMPHIGOID Proof of Concept in Initial Indication… …Before Expansion into Adjacent Indications Fast onset of action Autoantibodies initiate disease • 90% disease c
Slide 45: Registrational Study of Bullous Pemphigoid to Start in 2021
Registrational Study of Bullous Pemphigoid to Start in 2021 Study Population Total Duration: 36 weeks Endpoints Bullous Pemphigoid Proposed primary endpoint Randomization (1:1) • proportion of participants in Moderate-to-severe complete or partial remission while off OCS disease (BPDAI activity scor
Slide 46: Conclusions
Conclusions ~41K bullous pemphigoid patients in U.S. Preclinical and clinical evidence links IgG autoantibody level to disease activity IgG autoantibodies against BP180/BP230 Robust Phase 2 PoC data for efgartigimod in pemphigus are hallmark of bullous pemphigoid lead to bullous pemphigoid Phase 3 t
Slide 47: KOL Panel: Myositis and Bullous Pemphigoid
KOL Panel: Myositis and Bullous Pemphigoid
Slide 48: Russell P. Hall III, MD and Rohit Aggarwal, MD, MS
Russell P. Hall III, MD J. Lamar Callaway Professor, Department of Dermatology, Duke University Medical Center Rohit Aggarwal, MD, MS Rheumatology, Professor of Medicine, Medical Director, Arthritis and Autoimmunity Center, Co-Director UPMC Myositis Center, Division of Rheumatology and Clinical Immu
Slide 49: ARGX-117 Phase 1 Data | New Biology Insights for Multifocal Motor Neuropathy
ARGX-117 Phase 1 Data | New Biology Insights for Multifocal Motor Neuropathy Olivier Van de Steen, Medical Director Inge Van de Walle, Principal Scientist
Slide 50: ARGX-117 is First in Class Targeting C2
ARGX-117 is First in Class Targeting C2 (Auto)antibodies Microorganisms Classical Lectin Alternative IgG IgM Mannose sugar Foreign surface C1 MBL C3 qrs C4 MASPs C2 CFB CFD C3 convertase C3b C3 C3a C3a-R Clearance by macrophages C5 convertase C5 C5a C5a-R Inflammation C5b-C9 Membrane damage MAC Subl
Slide 51: C2 is Ideal Point of Intervention within Complement Cascade
C2 is Ideal Point of Intervention within Complement Cascade (Auto)antibodies Microorganisms Classical Lectin Alternative IgG IgM Mannose sugar Foreign surface C1 MBL C3 2 qrs Intact alternative pathway to reduce 3 C4 C2 MASPs CFB CFD infection risk Crossroad of classical & lectin pathways Manageable
Slide 52: C2 is Ideal Point of Intervention within Complement Cascade
C2 is Ideal Point of Intervention within Complement Cascade (Auto)antibodies Microorganisms Classical Lectin Alternative IgG IgM Mannose sugar Foreign surface C1 MBL C3 2 qrs Intact alternative pathway to reduce 3 C4 C2 MASPs CFB CFD infection risk Crossroad classical & lectin pathway Manageable C2
Slide 53: C2 is Ideal Point of Intervention within Complement Cascade
C2 is Ideal Point of Intervention within Complement Cascade (Auto)antibodies Microorganisms Classical Lectin Alternative IgG IgM Mannose sugar Foreign surface C1 MBL C3 2 qrs Intact alternative pathway to reduce 3 C4 C2 MASPs CFB CFD infection risk Crossroad classical & lectin pathway Manageable C2
Slide 54: C2 is Ideal Point of Intervention within Complement Cascade
C2 is Ideal Point of Intervention within Complement Cascade (Auto)antibodies Microorganisms Classical Lectin Alternative IgG IgM Mannose sugar Foreign surface C1 MBL C3 2 qrs Intact alternative pathway to reduce 3 C4 C2 MASPs CFB CFD infection risk Crossroad Crossroadofclassical classical&&lectin le
Slide 55: ARGX-117 Blocks and Actively Removes C2 from Circulation
ARGX-117 Blocks and Actively Removes C2 from Circulation Features of ARGX-117 Sweeping Antibody 1 Bind & block C2 pH and Ca2+ switch 2 4 Uptake & drop off C2 Recycling of ARGX-117 Optimal No effector recycling function 3 Degradation of C2 55
Slide 56: Ongoing Robust Phase 1 First-in-Human Study
Ongoing Robust Phase 1 First-in-Human Study 0.1 mg/kg 0.5 mg/kg 2.5 mg/kg 10 mg/kg 30 mg/kg 60 mg/kg 60 mg/kg 80 mg/kg 15 mg/kg IV IV IV IV IV IV SC IV SC N=8 N=8 N=8 N=7 N=7 N=8 N=8 N=8 N=8 Single Ascending Dose (SAD): IV and SC 10-10-10-10* 60-10-10# 10-50-20# 15-15-15-15* mg/kg mg/kg mg/kg mg/kg
Slide 57: Phase 1 Safety Results Support Proof of Concept Studies in Patients
Phase 1 Safety Results Support Proof of Concept Studies in Patients Treatment-Emergent Adverse Events (TEAE) 0.1 0.5 2.5 10 30 60 60 80 15 10-10-10-10 60-10-10 10-50-20 15-15-15-15 mg/kg mg/kg mg/kg mg/kg mg/kg mg/kg mg/kg mg/kg mg/kg mg/kg mg/kg mg/kg mg/kg SC SC SC N (%) Any 6 (75.0) 5 (62.5) 5 (6
Slide 58: ARGX-117 SAD: Long Half-life and Sustained PD Profile
ARGX-117 SAD: Long Half-life and Sustained PD Profile Pharmacokinetics Free C2 levels 95% reduction 99% reduction Days Days • Estimated half-life ~ 65-70 days Conclusions • Dose proportional increase of Cmax • Sustained reduction in free C2 levels by 95% for > 100 days as of 30 mg/kg dose 58
Slide 59: ARGX-117 MAD: Consistent Activity
ARGX-117 MAD: Consistent Activity Pharmacokinetics Free C2 levels 95% reduction 99% reduction Days Days • Induction dose followed by maintenance dosing concept established Conclusions • Resulting robust PK/PD model informing dosing strategy for Phase 2 studies 59
Slide 60: Model Predicts Potential for Infrequent Dosing
Model Predicts Potential for Infrequent Dosing Free C2 levels Model assumes full complement blockage as of free C2 levels < 0.2 µg/mL or >99% reduction of free C2 levels 60
Slide 61: Phase 1 Data Support Path Forward and Potential for Individualized Dosing
Phase 1 Data Support Path Forward and Potential for Individualized Dosing Schedule in Patients Favorable safety & tolerability profile supports advancing to Phase 2 patient trials Consistent PK/PD profile across IV and SC dosing that may enable infrequent dosing Phase 2 trial in multifocal motor neu
Slide 62: Multifocal Motor Neuropathy: A Serious, Debilitating Autoimmune Disease
Multifocal Motor Neuropathy: A Serious, Debilitating Autoimmune Disease Need for new therapies that slow progression of disease and reduce reliance on IVIg PREVALENCE HALLMARK DIAGNOSIS UNMET NEED ~13,000 patients in the U.S. – Slowly progressive muscle Often misdiagnosed as ALS Steroids ineffective
Slide 63: Anti-GM1 Antibodies Activate Classical Complement Pathway
Anti-GM1 Antibodies Activate Classical Complement Pathway 1 2 IgM autoantibodies IgM autoantibodies are potent activators bind to GM1 located on of the complement cascade motor neurons and Schwann cells IgM titer is correlated with classical pathway complement deposition 3 4 Complement activity SoC
Slide 64: ARGX-117 Inhibits Complement Deposition on Motor Neurons and Schwann Cells
ARGX-117 Inhibits Complement Deposition on Motor Neurons and Schwann Cells Serum MMN Patient Motor neurons IVIg Isotype control C2 depleted serum C2 depleted serum + 100% C2 ARGX-117 C3 DEPOSITION Complement active serum Schwann cells C3 DEPOSITION 64
Slide 65: ARGX-117 Blocks C3 Deposition in Dose-Dependent Manner
ARGX-117 Blocks C3 Deposition in Dose-Dependent Manner Motor neurons Isotype control ARGX-117 (200 µg/mL – 3,1 µg/mL) C3 DEPOSITION Complement active serum Schwann cells C2 depleted serum Reconstitution with hC2 (1,97 µg/mL - 30 µg/mL) C3 DEPOSITION Complement active serum 65
Slide 66: ARGX-117 Protects Axon Integrity While Blocking C3 Deposition
Isotype control ARGX-117 ARGX-117 Protects Axon C3 deposition Integrity While Blocking C3 Deposition in ex vivo Model ARGX-117 prevents loss of neurofilament Neurofilament staining at the nerve terminal and thereby preserves the integrity of the axon by blocking C3 deposition and downstream compleme
Slide 67: Phase 2 Multifocal Motor Neuropathy Trial Design
Phase 2 Multifocal Motor Neuropathy Trial Design Patient Population 4-10 weeks Total Duration: 16 weeks Key Outcome Measures Trial to enroll Safety and tolerability approximately 45 MMN ARGX-117 Dose Randomization (1:1:1) patients Regimen 1 (N=15) Time to IVIg re-treatment • Probable or definite MMN
Slide 68: ARGX-117: Pipeline-in-a-Product
IgAN Indications IRI LN ARGX-117: Kidney C4GN MN Pipeline-in-a- Therapeutic Franchises BP Skin Product HS Opportunity CAD Heme fitting our ITP franchises Classical Pathway Lectin Pathway MGUS anti-MAG Neuro GBS MMN MG ALS 68
Slide 69: Q&A
Q&A Tim Van Hauwermeiren Peter Verheesen, PhD Chief Executive Officer and Co-Founder, argenx Research Fellow, argenx Hans de Haard, PhD Rohit Aggarwal, MD, MS Chief Scientific Officer and Co-Founder, argenx University of Pittsburgh Wim Parys, MD Russell P. Hall III, MD Chief Medical Officer, argenx