Immunovant, Inc. · NASDAQ:IMVT

Immunovant — Investor Day (March 2022)

86 slides from Immunovant's investor day presentation, Mar 30, 2022

  1. Slide 1: Immunovant R&D Day

    Immunovant R&D Day Enabling normal lives for people with autoimmune disease March 30, 2022 Exhibit 99.1

  2. Slide 2: Forward-looking statements

    Forward-looking statements 2 This presentation contains forward-looking statements for the purposes of the safe harbor provisions under The Private Securities Litigation Reform Act of 1995 and other federal securities laws. The use of words such as “may,” “might,” “will,” “would,” “should,” “expect,

  3. Slide 3: Q&A housekeeping

    Q&A housekeeping 3 You may submit questions through the Q&A function at the bottom of the webcast player. Please see the image here for reference. For Investor Audiences Only

  4. Slide 4: Today's agenda

    Today’s agenda 4 Immunovant and batoclimab vision and strategy | Pete Salzmann, MD, CEO Immunovant Thyroid Eye Disease an exciting opportunity | Bill Macias, MD, CMO Immunovant • Andrea Kossler1, MD, FACS, Stanford University School of Medicine • George Kahaly2, MD, PhD, Johannes Gutenberg Universit

  5. Slide 5: Broad development plan enabled by mechanism of action, features and balance sheet

    Broad development plan enabled by an exciting mechanism of action, batoclimab’s features and a strong balance sheet 5 01 02 03 Immunovant remains on track to start three pivotal studies in calendar year 20223, and to announce two new indications by August 2022 1. As of December 31, 2021, per most re

  6. Slide 6: Vision and Strategy

    Pete Salzmann, MD Chief Executive Officer Vision and Strategy

  7. Slide 7: Our vision: Normal lives for people with autoimmune disease

    Our vision: Normal lives for people with autoimmune disease Driven by our core values 7 Love Trailblazing All Voices Bolder, Faster For Investor Audiences Only

  8. Slide 8: Our focus: unmet needs common to many IgG-mediated autoimmune diseases

    Our focus: unmet needs common to many IgG-mediated autoimmune diseases 8 • Improve symptoms and reduce uncertainty • More data to guide a proactive approach Significant improvement in Quality of Life • Variable time to response for existing treatments (e.g., older non-steroidal immunosuppressants) •

  9. Slide 9: IgG antibodies mediate autoimmune disease pathogenesis

    IgG antibodies mediate autoimmune disease pathogenesis • In many autoimmune diseases, IgG antibodies develop that can recognize and bind to normal tissues1 • IgG targets may include cell- surface receptors or circulating proteins • IgG autoantibodies trigger a harmful immune responses resulting in a

  10. Slide 10: FcRn promotes recycling of IgG antibodies

    FcRn promotes recycling of IgG antibodies 10 FcRn Mechanism of Action 1. IgG is taken up into cells in endocytic vesicle 2. FcRn-IgG complexes are sorted from unbound proteins 3. Unbound proteins are trafficked to lysosome for degradation 4. IgG is recycled back into circulation FcRn maintains level

  11. Slide 11: Batoclimab inhibits FcRn, promoting IgG degradation

    Batoclimab inhibits FcRn, promoting IgG degradation 11 Batoclimab Mechanism of Action 1. IgG and batoclimab are taken up into cells in endocytic vesicles 2. Batoclimab binds to FcRn in endosomes 3. FcRn-batoclimab complexes are sorted from unbound proteins 4. Non-receptor bound IgGs are degraded in

  12. Slide 12: Our opportunity: FcRn inhibition has broad therapeutic potential

    Our opportunity: FcRn inhibition has broad therapeutic potential 12 17 indications currently announced or in development across the anti-FcRn class ENDOCRINOLOGY Thyroid eye disease RHEUMATOLOGY Primary Sjogrens Syndrome Systemic lupus erythematosus Rheumatoid arthritis NEUROLOGY Myasthenia Gravis C

  13. Slide 13: Potential for anti-FcRn technology to help a broad range of people

    Potential for anti-FcRn technology to help a broad range of people impacted by autoimmune disease 13 2.3M+* PEOPLE Additional, potentially IgG- mediated autoimmune diseases EXPANDED OPPORTUNITY in US and EU INITIAL OPPORTUNITY in US and EU 364K* PEOPLE MG TED wAIHA Estimated number of people with au

  14. Slide 14: Batoclimab has a potentially unique combination of attributes

    Batoclimab has a potentially unique combination of attributes within the anti-FcRn class to address unmet patient needs 14 Novel, fully human, monoclonal antibody inhibiting FcRn-mediated recycling of IgG Batoclimab Tailored dosing to address varying symptom severity across indications and stage of

  15. Slide 15: Pioneering anti-FcRn technology to advance quality of care

    Pioneering anti-FcRn technology to meaningfully advance the quality of care for people living with autoimmune diseases 15 Novel, fully human, monoclonal antibody inhibiting FcRn-mediated recycling of IgG Batoclimab + + + + + + Intentionally designed to deliver potent IgG reductions via a standard su

  16. Slide 16: Pursuing a broad development program with batoclimab

    Pursuing a broad development program with batoclimab 16 Target Indication Phase 1 Phase 2 Phase 3 Anticipated Milestones Myasthenia Gravis (MG) Phase 3 initiation planned in first half of 2022; top line results expected in 2024 Thyroid Eye Disease (TED) Two of these four indications will be initiate

  17. Slide 17: Thyroid Eye Disease: An exciting opportunity

    Pete Salzmann, MD Chief Executive Officer Thyroid Eye Disease An exciting opportunity Pre-Record

  18. Slide 18: Fireside chat on Thyroid Eye Disease

    Fireside chat on Thyroid Eye Disease Andrea Kossler, MD, FACS Director, Oculoplastic Surgery & Orbital Oncology Assistant Professor of Ophthalmology Byers Eye Institute @ Stanford University Bill Macias, MD Chief Medical Officer, Immunovant 4 immunovant

  19. Slide 19: Opportunities in Thyroid Eye Disease

    Opportunities in Thyroid Eye Disease LIVE

  20. Slide 20: Thyroid eye disease presents with a variety of clinical symptoms

    Thyroid eye disease presents with a variety of clinical symptoms UNDERSTANDING TED: • Also referred to as Graves’ Ophthalmopathy or Graves’ Orbitopathy (GO) due to close temporal relationship with Graves’ Disease • Progressive disease marked by inflammation that can lead to fibrosis • Clinical featu

  21. Slide 21: Patients with active TED report substantial impact on lifestyle and work-life

    Patients with active TED report a substantial impact on their lifestyle and work-life 21 Source: TED Patient Quantitative Survey (n=50) by Immunovant, 2022 Moderate lifestyle modifications 46% None of the respondents stated that they make “no lifestyle modifications” around their TED Major lifestyle

  22. Slide 22: People with TED prioritize different treatment goals

    Not surprisingly for a heterogeneous disease, people with TED prioritize different treatment goals 22Source: TED Patient Quantitative Survey (n=50) by Immunovant, 2022 Improves physical appearance, 2% Potential to address the multiple symptoms associated with my TED, 10% Improves visual ability, 42%

  23. Slide 23: Thyroid Eye Disease Mechanism of Action

    Thyroid Eye Disease Mechanism of Action George J. Kahaly, MD, PhD Professor of Medicine and Endocrinology/Metabolism Johannes Gutenberg University GU) Medical Center Department of Medicine | ORPHAN Disease Center for Graves’ Orbitopathy and Autoimmune Polyendocrinopathy 4 immunovant

  24. Slide 24: Understanding Thyroid Eye Disease

    Understanding Thyroid Eye Disease

  25. Slide 25: Anti-TSHR autoantibodies drive pathogenesis of Graves' Disease and TED

    25 TSHR IGF-1R Anti-TSHR autoantibodies TED clinical presentationOcular orbitThyroid Thyroid follicle Orbital fibroblast Proliferation, differentiation IgG, immunoglobulin g; MOA, mechanism of action; TED, thyroid eye disease; TSHR, thyroid stimulating hormone receptor; IGF-1R insulin grow th factor

  26. Slide 26: Anti-TSHR autoantibody-mediated activation of orbital fibroblasts drives TED pathology

    26 Anti-TSHR autoantibody-mediated activation of orbital fibroblasts drives TED pathology and clinical manifestations GAG, edema Diplopia, lid edema, optic nerve compression Differentiation Adipocyte Orbital fibroblast T S H R -D R IV E N P A T H W A Y (IG F -1 R IN D E P E N D E N T ) Cytokines, hy

  27. Slide 27: Anti-TSHR autoantibodies activate fibroblasts via TSHR and IGF-1R crosstalk

    27 Within the orbit, anti-TSHR autoantibodies bind and activate fibroblasts via crosstalk between TSHR and IGF-1R Orbital fibroblast IgG TSHR IGF-1R β-arrestin 1 Hyaluronan TSHR- and IGF-1R-mediated pathways combine through crosstalk to induce synergistic hyaluronan secretion. While blocking TSHR in

  28. Slide 28: Batoclimab's mechanism of action inhibits FcRn

    Batoclimab's mechanism of action is designed to inhibit FcRn, potentially fostering the degradation of circulating pathogenic autoantibodies 28 Anti-TSHR autoantibodies are transported to the lysosome for degradation decreasing their levels in the circulation With batoclimab, FcRn is blocked from bi

  29. Slide 29: Batoclimab reduces pathogenic anti-TSHR autoantibodies

    29 Batoclimab has been observed to reduce pathogenic anti-TSHR autoantibodies that drive Thyroid Eye Disease Ocular orbit Thyroid Orbital fibroblast X X Batoclimab MOA ↓ IgG autoantibodies IgG, immunoglobulin g; MOA, mechanism of action; TED, thyroid eye disease; TSHR, thyroid stimulating hormone re

  30. Slide 30: Opportunities in Thyroid Eye Disease

    Opportunities in Thyroid Eye Disease LIVE

  31. Slide 31: Batoclimab in Thyroid Eye Disease

    Batoclimab in Thyroid Eye Disease Exploratory analyses used to inform further development because trial voluntarily halted with inconclusive primary endpoint

  32. Slide 32: Observed reductions in total IgG with 12 weeks of batoclimab

    CONFIDENTIAL 32 0 1 2 3 4 5 6 7 8 9 10 11 12 13 15 19 13 13 13 13 13 13 12 13 13 12 12 12 12 12 6 6 6 6 6 6 4 6 6 6 5 6 6 6 14 13 14 14 13 12 12 12 12 13 12 12 13 12 12 12 12 12 12 11 9 11 11 12 10 11 10 10 ULN LLN 0 2 4 6 8 10 12 14 16 C o n c e n tr a ti o n ( g /L ), m e a n ± S D Weeks post-base

  33. Slide 33: Observed reductions in stimulatory anti-TSHR antibodies

    CONFIDENTIAL 33 Source: Data on File, Immunovant, Inc. 1SRR is the “Sample to Reference Ratio”. This cell-based assay readout is the ratio of the sample signal to that of a reference control; avalue less than 140 is considered negative for stimulatory antibody; a value greater than or equal, positiv

  34. Slide 34: Post-hoc analysis of proptosis response at week 6

    CONFIDENTIAL 1 Proptosis response defined as proptosis reduction ≥2 mm in study eye, without ≥2 mm increase in non-study eye at same visit. Week 6 data selected as it represents the latest time point at which the largest amount of patient data is available prior to the volunta ry pause Source: Data

  35. Slide 35: Total muscle volume at 12 weeks post-baseline

    CONFIDENTIAL CT: computed tomography. Represents all patients who had a baseline and week 12 CT scan, a subset of all study participants Source: Data on File, Immunovant, Inc. The efficacy of batoclimab and clinical outcomes were deemed inconclusive, in part, because the study was terminated early.

  36. Slide 36: Individual muscle volume at 12 weeks post-baseline

    CONFIDENTIAL CT: computed tomography. Analysis conducted in the intent to treat population Represents all patients who had a baseline and week 12 CT scan, a subset of all study participants Source: Data on File, Immunovant, Inc. The efficacy of batoclimab and clinical outcomes were deemed inconclusi

  37. Slide 37: Thyroid Eye Disease: An exciting opportunity

    Thyroid Eye Disease An exciting opportunity

  38. Slide 38: Many patients with TED may benefit from a new therapy

    7K – 18K total Many patients with Thyroid Eye Disease may benefit from a new therapy 38 Addressable Population (US) Moderate-to-severe Incidence (15K-20K) Residual symptoms after teprotumumab (1K-5K) Controlled on teprotumumab Symptoms recur after teprotumumab (1K-6K) Initiate tepro More moderate sy

  39. Slide 39: Thyroid Eye Disease key take-aways

    Thyroid Eye Disease key take-aways 39 TED is a multi-faceted condition – presenting with a range of clinical manifestations and substantial impact on patient functioning and quality of life Data from batoclimab’s clinical program are encouraging for continued development in TED Batoclimabrepresents

  40. Slide 40: Myasthenia gravis: A multifaceted disease

    Pete Salzmann, MD Chief Executive Officer Myasthenia gravis A multifaceted disease Pre-Record

  41. Slide 41: Fireside chat on Myasthenia Gravis

    Fireside chat on Myasthenia Gravis Pete Salzmann, MD Katherine Ruzhansky, MD, MS Chief Executive Officer, Clinical Neurologist, Associate Professor of Immunovent Neurology and Director of the EMG lab at the Medical University of South Carolina Af immunovant Nicholas Silvestri, MD, FAAN Clinical Neur

  42. Slide 42: A Beautiful Life: An Unpredictable Journey with Myasthenia Gravis

    A Beautiful Life An Unpredictable Journey with Myasthenia Gravis (MG) + Jonni ¢ ctory Le + \f iMMuNovant

  43. Slide 43: Myasthenia Gravis — a multifaceted disease

    Myasthenia Gravis — a multifaceted disease Pete Salzmann, MD Chief Executive Officer, Immunovant Af immunovant

  44. Slide 44: Phase 3 trial in MG designed to address unmet patient needs

    Phase 3 trial in MG is designed to address unmet patient needs and differentiate batoclimab 44 Flexible dosing to match disease fluctuations: Myasthenia gravis waxes and wanes over time; clinicians and patients desire a data-driven approach to optimize care over time Peace of mind over time: Chronic

  45. Slide 45: Flexible Phase 3 design, a first for an MG trial

    Flexible Phase 3 design that is common in immunology trials but a first for an MG trial 45 Gain control INDUCTION PHASE Keep control MAINTENANCE PHASE Optimize control LONG-TERM EXTENSION (LTE) For Investor Audiences Only

  46. Slide 46: MG Phase 3 trial design

    MG Phase 3 trial design (N ~ 200) 46 QW = weekly; Q2W = bi-weekly; SC = subcutaneous injection; AChR Ab+ = acetylcholine receptor antibody-positive; MG-ADL = Myasthenia Gravis Activities of Daily Living scale Placebo-controlled, two dose regimens: Period 1: Induction (12 weeks) Maximize efficacy thr

  47. Slide 47: Warm autoimmune hemolytic anemia

    Pete Salzmann, MD Chief Executive Officer Warm autoimmune hemolytic anemia Pre-Record

  48. Slide 48: Disease state of Warm Autoimmune Hemolytic Anemia

    Disease state of Warm Autoimmune Hemolytic Anemia David Tucker, MB ChB, BSc, MD MRCP, FRCPath Consultant Haematologist Blood Transfusion and Patient Blood Management Lead NIHR CRN Regional Subspecialty Lead for Malignant and Non-Malignant Haematology Royal Cornwall NHS Trust fv immunovant

  49. Slide 49: An Overview of Warm Autoimmune Haemolytic Anaemia (wAIHA)

    An Overview of Warm Autoimmune Haemolytic Anaemia (wAIHA) Dr David Tucker MD MRCP FRCPath Consultant Haematologist and Research Lead for Haematology Royal Cornwall Hospital NHS Trust, Cornwall, United Kingdom

  50. Slide 50: Conflicts of Interest

    Conflicts of Interest • Advisory Board – Roche, Abbvie, Novartis • Conference attendance: Amgen, Takeda Warm Auto-Immune Haemolytic Anaemia (wAIHA) 50

  51. Slide 51: wAIHA represents a complex and fascinating challenge

    wAIHA represents a complex and fascinating challenge… • An unpredictable and potentially life-threatening auto-immune disease caused by antibody-mediated red cell destruction. • A rare disease with few large data-sets to guide management. • Corticosteroids are usually effective but with significant

  52. Slide 52: Normal Red Cell Physiology

    Normal Red Cell Physiology 100 – 120 day lifespan Travels 250km 3 layered elastic membrane allows erythron to “tank-tread” Warm Auto-Immune Haemolytic Anaemia (wAIHA) 52 Normal red blood cell Red cell spherocyte For Investor Audiences Only

  53. Slide 53: Warm Auto-Immune Haemolytic Anaemia

    29/03/2022 Warm Auto-Immune Haemolytic Anaemia (wAIHA) 53 Warm Auto-Immune Haemolytic Anaemia For Investor Audiences Only

  54. Slide 54: wAIHA – Who is Affected?

    wAIHA – Who is Affected? Causes • Primary (Idiopathic) wAIHA • (40-60% of cases) (Hill et al. Roumier et al.) • Secondary wAIHA • (50% of cases) (Hill et al. Roumier et al.): • Auto-immune diseases e.g. SLE, ITP, Rheumatoid arthritis • Lymphoproliferative diseases e.g. CLL, Lymphoma (NHL and HL) • I

  55. Slide 55: wAIHA – The Patient Experience

    wAIHA – The Patient Experience • Mild / Onset (Hb >10g/dL): often gradual with mild fatigue, breathlessness and mild icterus (jaundice) • Moderate (Hb 8.0 – 10g/dL): breathlessness and fatigue on moderate exertion (climbing stairs), ankle swelling, palpatations, more obvious jaundice, dark urine. •

  56. Slide 56: How do we manage wAIHA?

    How do we manage wAIHA? • Because wAIHA is a rare disease there are few large data sets to guide management which is mainly empirical and based on expert opinion. • The cornerstone of management is immunosuppression with corticosteroids. • Historically, the treatment-related mortality rate is 8 to 1

  57. Slide 57: wAIHA Management – 1st line treatment

    wAIHA Management – 1st line treatment Corticosteroids • 80% of patients respond (Allgood et al. ; Zupanska et al.) • Only 20% remain in remission when steroids are discontinued (Allgood et al. Roumier et al.) • 40% can maintain control on long-term steroids but side effects are significant (Roumier

  58. Slide 58: wAIHA Management – beyond 1st line

    wAIHA Management – beyond 1st line Rituximab (Monoclonal Antibody) (Maung et al. 2013; Michel et al. 2017; Birgens et al.) • 70% of patients respond (about half of these respond completely); • Median time to response 3 – 6 weeks; • Relapses occur in 40-50% of cases after 30 months • More than half o

  59. Slide 59: wAIHA Management – beyond 2nd line

    wAIHA Management – beyond 2nd line Splenectomy • 70% response rates (but response unpredictable) (Barcellini et al.) • Irreversible and not definitively curative • Risk of severe infection after splenectomy (3 – 5%) which is life-threatening in 50% of cases (Roumier et al.) • Venous thrombosis risk:

  60. Slide 60: Evidence for a need for new therapeutic options

    wAIHA – Evidence for a need for new therapeutic options In studies of patients with wAIHA over 3 – 4 years: • Less than half (47%) of patients remain in remission off treatment • 25% of patients remain on low dose steroids • 28% have ongoing disease and require higher dose steroids or other immunosu

  61. Slide 61: wAIHA In Summary

    wAIHA In Summary • This is a rare disease with few large data-sets to guide management • There is an unmet need because a large proportion of patients remain on immunosuppressive therapy long-term • There is a significant side-effect burden for patients from long- term immunosuppression • There is a

  62. Slide 62: References

    References • Allgood JW, Chaplin J. Idiopathic acquired autoimmune hemolyticanemia. A review of forty-seven cases treated from 1955 through 1965., Am J Med, 1967, vol. 43 2(pg. 254-273) • Balague C, Targarona EM, Cerdan G, et al. Long-term outcome after laparoscopic splenectomy related to hematologi

  63. Slide 63: Thank you for listening

    Thank you for listening Dr David Tucker Warm Auto-Immune Haemolytic Anaemia (wAIHA)

  64. Slide 64: Cholesterol management

    Bill Macias, MD Chief Medical Officer Cholesterol management Pre-Record

  65. Slide 65: Relationship between CVD and Hypercholesterolemia

    Relationship between CVD and Hypercholesterolemia • The causes of cardiovascular disease (CVD) are multifactorial – Modifiable risk factors: lifestyle (especially an unhealthy diet) tobacco use and sedentary habits, high blood pressure, diabetes and dyslipidemias – Nonmodifiable risk factors: age, g

  66. Slide 66: Theory of Circulating LDL and Causation of Atherosclerosis

    14 Reduce LDL 20 The Theory of Circulating Low Density Lipoproteins (LDL) and Causation of Atherosclerosis Healing lesion less likely to rupture or cause thrombosis - (fewer endpoints). 66For Investor Audiences Only

  67. Slide 67: Elevated LDL-c over time associated with atherosclerosis development

    Elevated LDL-c over time associated with atherosclerosis development 67For Investor Audiences Only

  68. Slide 68: Support for LDL Causality in ASCVD

    Support for LDL Causality in ASCVD • Observational data • Interventional data • Genetic studies • Experimental 68For Investor Audiences Only

  69. Slide 69: Statins Reduce CVD Events—Trials in the 1990s

    Evidence: Statins Reduce CVD Events—Trials in the 1990s WOSCOPS = The West of Scotland Coronary Prevention Study; CARE = Cholesterol and Recurring Events (trial); LIPID = Long-term Intervention with Pravastatin in Ischemic Disease; AFCAPS/TexCAPS = Air Force/Texas Coronary Atherosclerosis Prevention

  70. Slide 70: Reduction in Incidence of Major CVD Events and Absolute LDL-C

    Boekholdt SM et al. J Am Coll Cardiol. 2014;64:485-494. Relation Between Reduction in Incidence of Major CVD Events and Mean Absolute LDL-C *Meta-analysis of 14 statin trials (CTT collaborators) Reduction in LDL-C level (mg/dL) P ro p o rt io n a l R e d u ct io n in C H D E ve n t R a te n= >90,000

  71. Slide 71: It Does Not Matter How You Lower LDL-C

    We Have Observed That it Does Not Matter How You Lower LDL-C (Evidence from Mendelian Randomization Studies) ABCG5/G8 = ATP binding cassette subfamily G member 5/8; APOB = apolipoprotein B; CHD = coronary heart disease; CI = confidence interval; HMGCR = 3-hydroxy-3-methylglutaryl-CoA reductase; LDL-

  72. Slide 72: Benefit Related to Absolute Reductions in LDL-C and Duration

    We Have Observed That Benefit is Related to Absolute Reductions in LDL-C and the Duration of That Absolute Reduction CI = confidence interval; LDL = low-density lipoprotein. Ference BA, et al. Eur Heart J. 2017; doi: 10.1093/eurheartj/ehx450. 4S HPS WOSCOPS 80604020 40% 20% 30% 10% 0% CARE P ro p o

  73. Slide 73: Match Intensity of LDL-C Reduction to Level of Risk

    <5% ≥10% to 20% ≥30 0 10 20 30 40 50 1.0 1.5 2.0 2.5 1.2 1.7 2.2 2.7 4 5 7 8 8 11 14 17 11 16 21 2520 30 38 46 GUIDELINES Match the Intensity of the LDL-C Reduction to the Level of Risk in the Individual The Basis for Each Individual Consult in Every Clinic! • Global guidelines identify four groups

  74. Slide 74: ACC/AHA Guidelines Define Four Statin Benefit Groups

    Risk Stratification: ACC/AHA Guidelines Define Four Statin Benefit Groups Category Recommendation Clinical ASCVD Secondary prevention •High-intensity statin if age ≤ 75 years •Moderate intensity statin if age > 75 years or not a candidate for high-intensity statin •Combination therapy if 50% LDL-C l

  75. Slide 75: Low Absolute Risk: Number Who Benefit is Modest

    In Patients with Low Absolute Risk the Number Who Benefit with LDL-C Reduction is Modest 8 mmol/L total cholesterol is about 320 mg/dl in these units 75For Investor Audiences Only

  76. Slide 76: High Absolute Risk: Number Who Benefit is More Pronounced

    In Patients with High Absolute Risk the Number Who Benefit with LDL-C Reduction is More Pronounced 76For Investor Audiences Only

  77. Slide 77: Secondary Prevention: Patients with Clinical ASCVD

    © 2018 PRIME® Education, LLC. Al l Rights Reserved. 77 Secondary Prevention: Patients with Clinical ASCVD Clinical ASCVD Healthy Lifestyle ASCVD not at very high risk* Very high-risk* ASCVD Age ≤75 y Age >75 y High-intensity or maximal statin (Class I) High-intensity statin (Goal: ↓ LDL-C ≥50%) (Cla

  78. Slide 78: Conclusions

    Conclusions • LDL-C is causal for atherosclerotic cardiovascular disease • The risk is determined by the absolute levels of LDL-C and the duration of the elevation measured in years (i.e cholesterol-years) • National guidelines have been developed to match the intensity of therapy to the absolute ri

  79. Slide 79: Cholesterol management: Healthy Volunteer study preliminary data

    Cholesterol management Healthy Volunteer study preliminary data

  80. Slide 80: Healthy volunteer study to measure LDL impact of concomitant statin therapy

    Healthy volunteer study initiated to measure LDL impact of concomitant statin therapy with batoclimab 680mg batoclimab dose with and without 40mg atorvastatin: Treatment Period 1 6 weeks *40mg atorvastatin dosing initiated 14 days prior to initiation of 680mg batoclimab dosing 680mg batoclimab QW SC

  81. Slide 81: Healthy volunteer study preliminary data

    0 50 100 150 200 250 -4 -3 -2 -1 0 1 2 3 4 5 6 7 M e a n L D L c h o le s te ro l (m g /d L ) ± S D LDL cholesterol vs. time 680mg batoclimab + 40mg Atorvastatin 680mg batoclimab + placebo Exclusion criteria for LDL in MG study* Healthy volunteer study preliminary data 81 Mean LDL cholesterol for fi

  82. Slide 82: Key take-aways on the impact of batoclimab on LDL cholesterol

    Key take-aways on the impact of batoclimab on LDL cholesterol 82 Mechanism is not unique to batoclimab Cholesterol changes are reversible Cholesterol changes expected to be manageable 1 2 3 LDL changes correlated with on target changes in albumin Dose dependent changes in LDL returned to normal with

  83. Slide 83: Closing and Q&A

    Closing and Q&A Normal lives for people with autoimmune disease fv immunovant

  84. Slide 84: Path forward for Immunovant

    Path forward for Immunovant Pete Salzmann, MD Chief Executive Officer What comes next

  85. Slide 85: Broad development plan enabled by mechanism of action, features and balance sheet

    Broad development plan enabled by an exciting mechanism of action, batoclimab’s features and a strong balance sheet 85 01 02 03 Immunovant remains on track to start three pivotal studies in calendar year 20223, and to announce two new indications by August 2022 1. As of December 31, 2021, per most r

  86. Slide 86: Investor Q&A

    Pete Salzmann, MD Chief Executive Officer Renee Barnett Chief Financial Officer Bill Macias Chief Medical Officer Investor Q&A

Immunovant — Investor Day (March 2022) on 6ix