Immunovant : Corporate Overview

Corporate Overview

January 2020

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,"

"expect," "plan," "anticipate," "believe," "estimate," "intend," "future," "potential," "continue" and other similar expressions

(as well as other words or expressions referencing future events, conditions, or circumstances) are intended to identify forward-looking statements. For example, statements Immunovant makes regarding our business strategy, our plans to develop and commercialize our product candidates, our plans to enter into commercial transactions or strategic partnerships, the safety and efficacy of our product candidates, our expectations regarding timing, the design and results of clinical trials of our product candidates, our plans and expected timing with respect to regulatory filings and approvals, the size and growth potential of the markets for our product candidates, and our ability to serve those markets, and our plans and expected timing with respect to regulatory filings and approvals are forward-looking. Because such statements are subject to risks and uncertainties, actual results may differ materially from those expressed or implied by such forward-looking statements. The product candidates that Immunovant develops may not progress through clinical development or receive required regulatory approvals within expected timelines or at all. In addition, promising interim results or other preliminary analyses do not in any way ensure that later or final results in a clinical trial or in related or similar clinical trials will replicate those interim results. In addition, clinical trials may not confirm any safety, potency or other product characteristics described or assumed in this press release. In addition, such product candidates may not be beneficial to patients, or even if approved by regulatory authorities, successfully commercialized. The failure to meet expectations with respect to any of the foregoing matters may have a negative effect on Immunovant's stock price. All forward-looking statements are based on estimates and assumptions by Immunovant's management that, although Immunovant believes to be reasonable, are inherently uncertain. All forward- looking statements are subject to risks and uncertainties that may cause actual results to differ materially from those that Immunovant expected. Such risks and uncertainties include, among others, the initiation and conduct of preclinical studies and clinical trials; the availability of data from clinical trials; the expectations for regulatory submissions and approvals; the continued development of Immunovant's product candidates and platforms; Immunovant's scientific approach and general development progress; Immunovant's ability to maintain or scale up manufacturing processes and transition such processes; and the availability and commercial potential of Immunovant's product candidates including the size of potentially addressable markets and degree of market acceptance. These statements are also subject to a number of material risks and uncertainties that are described in Immunovant's periodic and other reports filed with the Securities and Exchange Commission (SEC), including the risk factors detailed in Health Sciences Acquisitions Corporation's definitive proxy statement filed with the SEC on November 27, 2019. Any forward-looking statement speaks only as of the date on which it was made. Immunovant undertakes no obligation to publicly update or revise any forward-looking statement, whether as a result of new information, future events or otherwise.

2

Immunovant

Our vision: Normal lives for patients with autoimmune diseases

Our asset: IMVT-1401, a novel, fully human monoclonal antibody inhibiting FcRn-mediated recycling of IgG

Our strategy for IMVT-1401:

• Be best-in-classin target indications where anti-FcRn mechanism has already established clinical proof-of-concept
• Be firstto study FcRn inhibition in target indications with clear biologic rationale and no known in-class competition

Our near-termvalue drivers: Four anticipated data readouts over the next 20 months

4

Immunovant Leadership

Management Team

Pete Salzmann, MD, MBA

Chief Executive Officer

Julia Butchko, PhD

Chief Development and Technology Officer

Brad Middlekauff, JD

General Counsel

Robert Zeldin, MD

Chief Medical Officer

Pamela Connealy, MBA

Chief Financial Officer

Board of Directors

• Douglas Hughes

• Frank Torti, Chairperson

• George Migausky

• Myrtle Potter

• Atul Pande

• Andrew Fromkin

• Pete Salzmann

5

IMVT-1401: Program Highlights

IMVT-1401: A novel, fully human monoclonal antibody inhibiting FcRn

• Early evidence suggests that anti-FcRn agents could transform the treatment of autoimmune diseases mediated by pathogenic IgG antibodies

In Phase 1, IMVT-1401 generated compelling pharmacodynamic activity

• Clinically meaningful IgG reductions observed (78% IgG reduction at 680 mg dose level)
• No difference observed between intravenous and subcutaneous formulations at equivalent doses

IMVT-1401 has been well-tolerated to date

• No headaches reported in the highest dose multiple dose cohort tested
• No treatment-related serious adverse events (SAEs) or dose limiting toxicities reported
• No confirmed cases of anti-drug antibodies in any subject in multiple dose cohorts

IMVT-1401 was designed from inception for subcutaneous (SC) injection

• Requirement during development process
• Phase 1 data suggests every other week or less frequent dosing achievable for chronic use

6

IMVT-1401: A Pipeline in a Product

T a r g e t I n d i c a t i o n	P r e -	P h a s e	P h a s e	P h a s e	S t a t u s
c l i n i c a l	1	2	3

Myasthenia Gravis	ASCEND-MG	•	Phase 2a open for
(MG)		enrollment
		• Phase 2a open for
Graves'	ASCEND-GO		enrollment
Ophthalmopathy (GO)	• Phase 2b open for
			enrollment
Warm Autoimmune		•	IND cleared for
Hemolytic Anemia	ASCEND-WAIHA
	Phase 2 trial
(WAIHA)			initiation

7

IMVT-1401: Multiple anticipated near-term value inflection points

MG

GO

WAIHA

• Phase 2a open for enrollment

Top-line results of Phase 2a study expected in 1H 2020 Pivotal Phase 3 study initiation expected in 2020

• Phase 2a open for enrollment

Initial results of Phase 2a study in Q1 2020 PPhase 2b proof-of-concept study open for enrollment

Top-line results of Phase 2b study expected in early 2021

• IND submission expected in 2H 2019

Initial results of Phase 2a study expected in Q4 2020

8

IMVT-1401

IgG antibodies implicated in certain

autoimmune diseases

Antibodies in healthy individuals

• Antibodies play an important role in immune defense against pathogens1
• • Clearing bacteria, viruses, and other harmful organisms and substances
  • Eliciting an immune response that leads to inflammation
• IgG antibody subclass accounts for ~75% of antibodies in the plasma of healthy people1

Antibodies in autoimmune disease

• In many autoimmune diseases, IgG antibodies develop that can recognize and bind to normal tissues2
• • Targets may include cell-surface receptors or circulating proteins
  • Result is a harmful immune response that damages critical tissues and organs
• Predisposing factors may include genetic susceptibility, environmental triggers, and factors not yet known3

IgG	IgE	IgD			IgA	IgM

1.	Leusen J.H.W. The Role of IgG in Immune Responses. Molecular and Cellular Mechanisms of Antibody Activity, 2013	10
2.	Isabela S., et al. The role of autoantibodies in health and disease. Romanian Journal of Morphology and Embryology, 2016
3.	Mariani S.M. Genes and autoimmune diseases - a complex inheritance. MedGenMed, 2004

IMVT-1401's mechanism shown to promote IgG

degradation1

FcRn prolongs the	Inhibiting FcRn promotes
half-life of IgG2	IgG degradation2

• FcRn intercepts IgG, which would otherwise be degraded in lysosomes
• The FcRn-IgG complex is then recycled to the cell surface and free IgG is released back into circulation

• IMVT-1401binds to FcRn, thereby preventing it from recycling IgG antibodies back to circulation
• As a result, IgG is increasingly delivered to lysosomes for degradation

Blood (physiological pH)				Blood (physiological pH)
Endocytic					Endocytic
vesicle					vesicle
FcRn binds to					IMVT-1401binds to
	IgG dissociates at			FcRn in acidified	IMVT-1401remains
IgG in acidified		physiological pH			endosome	bound at
endosome						physiological pH
Acidified	Non-receptor bound				Non-receptor bound
proteins are degraded		Acidified	proteins are degraded
endosome	in lysosome		endosome	in lysosome
FcRn-IgG complexes are				FcRn-IMVT-1401 complexes
sorted from unbound					are sorted from unbound
proteins		Lysosome			proteins	Lysosome
Monocyte or endothelial cell					Monocyte or endothelial cell
	Key:	IMVT-1401	IgG	FcRn	Serum protein

1.	Collins J. and Jones L., et al. IMVT-1401(RVT-1401), A Novel Anti-FcRn Monoclonal Antibody, Was Well Tolerated in Healthy Subjects	11
	and Reduced Serum IgG Following Subcutaneous or Intravenous Administration. Presented at American Academy of Neurology
	Annual Conference, 2019. Program # P5.2-079
2.	Derry C., et al. FcRn: the neonatal Fc receptor comes of age. Nature Reviews Immunology, 2007

Broad range of potential applications for anti-FcRn mechanism

IgG-mediated autoimmune diseases where FcRn mechanism may be relevant:

Myasthenia Gravis	Graves'	Warm Autoimmune
Ophthalmopathy	Hemolytic Anemia

Chronic Inflammatory		Idiopathic
Demyelinating	Neuromyelitis Optica	Thrombocytopenic
Polyneuropathy		Purpura

Guillain-Barré	PLA2R+ Membranous	Pemphigus Vulgaris
Syndrome	Nephropathy

Additional IgG-mediated autoimmune diseases

Note: List of diseases is illustrative only and does not necessarily represent our targeted indications

12

Phase 1 SAD/MAD study design

Single Ascending Dose SC		Single Ascending Dose IV		Multiple Ascending Dose SC

Fixed 765 mg	N = 6:2
Fixed 1530 mg	N = 6:2

	N = 6:2	Fixed 765 mg	N = 6:2
Fixed 500 mg

Fixed 340 mg	N = 6:2	Fixed 340 mg	N = 6:2

5.0 mg/kg	N = 6:2	Fixed 100 mg	N = 6:2

	1.5 mg/kg		N = 6:2	0.1 mg/kg	N = 4:0
	0.5 mg/kg	N = 3:0

Numbers presented as [subjects receiving IMVT-1401] : [subjects receiving placebo]

Fixed weekly

680 mg dose N = 8:2 x 4

Fixed weekly

340 mg dose N = 8:2 x 4

Key

Canada

Australia

13

IMVT-1401 produced clinically meaningful IgG reductions in Phase 1 study

Preliminary results from Phase 1 SAD/MAD cohorts

Single-dose administration produced	Repeat dosing at 680 mg SC resulted in
a 78% IgG reduction
dose-dependent IgG reductions
without the need for IV induction

Mean total IgG reduction after single dose in healthy

volunteers
	20%
from Baseline	0%
-20%
IgG Reduction
-40%
Serum	-60%
			Placebo			340 mg SC
			0.5 mg/kg SC		500 mg SC
Percent	-80%
		1.5 mg/kg SC		765 mg SC
			5.0 mg/kg SC
	-100%
	0	7	14	21	28	35	42	49	56
			Nominal Day After First Dose

Mean total IgG reduction after 4 weekly doses in healthy volunteers

20%
0%
-20%
-40%
-60%
							Placebo
-80%							340 mg SC
							680 mg SC
-100%
0	7	14	21	28	35	42	49	56

Nominal Day After First Dose

14

IMVT-1401 reduced levels of all four IgG subtypes

Preliminary results from Phase 1 MAD cohorts

					IgG1
Serum IgG Reduction		20%
	0%
from Baseline	-20%
-40%
-60%
-80%
-100%
Percent
	0	7	14	21	28	35	42	49	56
			Nominal Day After First Dose
					IgG3

Serum IgG Reduction		20%
	0%
from Baseline	-20%
-40%
-60%
-80%
-100%
Percent		0	7	14	21	28	35	42	49	56
			Nominal Day After First Dose

			IgG2
20%
0%
-20%
-40%
-60%
-80%
-100%
0	7	14	21	28	35	42	49	56
		Nominal Day After First Dose

			IgG4
20%
0%
-20%
-40%
-60%
-80%
-100%
0	7	14	21	28	35	42	49	56
		Nominal Day After First Dose

15

Generally well-tolerated in Phase 1 study

Preliminary results from Phase 1 SAD/MAD cohorts

• 99 subjects dosed to date through SAD and MAD portions of Phase 1
• • IMVT-1401:77 subjects
  • Placebo: 22 subjects
• Most common AEs were mild erythema and swelling at injection site
• • Injection site reactions were not dose or frequency related
  • Occurred at similar incidence for drug and placebo treated subjects
• No headaches observed in 680 mg SC MAD cohort
• Albumin changes:
• • Dose-dependent,reversible, and asymptomatic albumin reductions observed
  • At day 28, mean albumin levels were 37.5 g/L in the 340 mg cohort, and 32.4 g/L in 680 mg cohort (normal range 36-51 g/L)
• 2 SAEs observed in two separate SAD cohorts, both ruled unrelated to treatment by study investigator (cancer, appendicitis)
• Treatment-emergentADA confirmed in 8% of IMVT-1401-treated subjects and 6% of placebo-treated subjects
• • No subject in MAD cohorts has developed a confirmed ADA response to IMVT-1401

16

Adverse events reported in Phase 1

Preliminary results from Phase 1 SAD/MAD cohorts

						Single-Ascending Dose						Multiple-Ascending
												Dose
			Intravenous Infusion				Subcutaneous Injection			Subcutaneous Injection
	0.1	100	340	765	1530	Placebo	0.5	1.5	5	340	500	765	Placebo	340	680	Placebo
	mg/kg	mg	mg	mg	mg		mg/kg	mg/kg	mg/kg	mg	mg	mg		mg	mg
	n=4	n=6	n=6	n=6	n=6	n=8	n=3	n=6	n=6	n=6	n=6	n=6	n=10	n=8	n=8	n=4
MedDRA Preferred Term
Abdominal pain									1					1
Abdominal pain upper													2	1
Abnormal sensation in eye					1					1
Back pain						2					1		1	1
Constipation						1								1
Cough											1		2
Diarrhea														2
Dizziness						1							1			1
Dry skin													1		1
Erythema							1								1
Fatigue	1			1	1	1	1			1			1
Headache	1	1	1	1	1			1	1	4	1		1	2
Injection site erythema									5	1	5	6	7	8	7	4
Injection site pain											1			2		1
Injection site swelling									3		2	4	3	7	6	2
Insomnia									1					4
Myalgia														1	1
Nasal congestion									1		1		1	1
Nausea									1	1			1		1	1
Ocular hyperaemia															2
Oropharyngeal pain	1			1	2				1		1		1	2
Pain in extremity						1							1
Procedural complication								1		1
Procedural dizziness					2						1
Pyrexia			1	1					1
Rash					2				2				2		1
Rhinorrhea									1				2
Sinusitis			1										1
Somnolence		1							1
Upper respiratory tract
infection	1	1	1				3		1	1				1
Vision blurred					1					1

17

IMVT-1401 has been given as a SC injection

Subcutaneous Injection

Subcutaneous Infusion

Intravenous Infusion

<10 seconds

30-60 minutes

Potentially Hours

18

IMVT-1401 designed from inception to be a potentially class-leading SC injection

• Fully human monoclonal antibody

• Generated from Ligand/OMT's OmniAb transgenic rat platform

• • >400 antibody campaigns ongoing that use OmniAb technology1
  • 12 clinical-stage antibodies in development1
• IgG1 backbone Fc-engineered to reduce effector function
• Optimized for SC delivery
• • Current clinic formulation is 170 mg/mL
  • Delivered by 27-gauge needle

IMVT-1401

1. Ligand 2019 Analyst Day presentation, presented March 12, 2019

19

IMVT-1401 has the potential to deliver a class-leading profile

IMVT-1401 attribute

Clinically meaningful

IgG reductions

SC injection

Simple dosing

schedule

Fully human antibody

Fc-engineered to reduce

effector function

Potential patient benefit

• 680 mg SC weekly: 78% reduction after four doses
• 340 mg SC weekly: 63% reduction after four doses
• Fast and minimally invasive
• No requirement for IV induction doses or lengthy SC infusions
• Provides option for at-home administration
• Fixed dosing, vs. weight-based, reduces potential for dose miscalculations
• Low risk of immunogenicity
• Low potential for unintended immune responses

20

IMVT-1401 and competitors' programs with

subcutaneous (SC) injection or infusion

Company

Anti-FcRn candidate

SC administration regimen

IV induction dosing

SC dose

Mean IgG reduction observed

IMVT-1401

SC injection

N/A

340 mg SC weekly

680 mg SC weekly

63-78% after 4

doses

Efgartigimod

(ARGX-113)

IV induction,

followed by SC

injection1

20 mg/kg IV x 2

doses1

300 mg SC

weekly1

"Approximately" 50% after two IV induction doses followed by

8 SC doses2

Rozanolixizumab

(UCB7665)

SC infusion

given over

30-60 minutes3,4

N/A

7mg/kg SC

weekly5

56% after 3

doses5

68% after 6

doses5

ABY-039M281 ALXN1830 (SYNT001)

SC injection

N/A
	Not in clinic	Not in clinic
	with SC	with SC
200 mg SC	formulation	formulation
single dose6

~45%

Note: data as of 9/24/2019 and is not based on head-to-head comparison studies

1.	argenx, corporate presentation, August 2018	4.	UCB, ASH presentation, December 2017	21
2.	argenx, press release, issued June 14, 2018. Phase 1 data	5.	UCB, press release, issued October 18, 2018. Phase 2 data
3.	Kiessling P., et al. The FcRn inhibitor rozanolixizumab reduces	6.	Affibody, PEGS conference presentation, April 2019
	human serum IgG concentration: A randomized phase 1 study.
	Science Translational Medicine, 2017

IMVT-1401 for Myasthenia Gravis

Myasthenia Gravis overview

• Rare autoimmune disorder affecting an estimated 65,000 people in the US1
• Characterized by weakness of voluntary muscles including ocular, facial, oropharyngeal, limb, and respiratory muscles1
• 15-20%of MG patients will experience at least one myasthenic crisis over their lifetimes, a potentially life-threatening acute complication2
• Disease caused by autoantibodies targeting the neuromuscular junction1
• ~93% of patients have an identified autoantibody1
• • Anti-acetylcholinereceptor (AChR) antibodies (~85%)
  • Anti-muscle-specifictyrosine kinase (MuSK) antibodies (~8%)

Normal Neuromuscular

Neuromuscular Junction

Junction

in Myasthenia Gravis

Receptors

Acetylcholine

Blocked by

Nerve

Neuron

Antibodies

ACh

Receptor

Muscle

Reduced Transmission

Normal Muscle Contraction

Impaired Muscle Contraction

1. Meriggioli M.N. and Sanders D.B. Muscle autoantibodies in myasthenia gravis: beyond diagnosis? Expert Review	23
Clinical Immunology, 2012

2. Sudulagunta S.R., et al. Refractory myasthenia gravis - clinical profile, comorbidities and response to rituximab. German Medical Science, 2016

Unmet need persists despite availability of treatment options

Current treatment paradigm1

	1st Line			2nd Line			3rd Line		4th Line
•	Acetylcholinesterase		•	Immunosuppressive		•	IVIg		• Eculizumab
	inhibitors			agents		•	Plasma exchange
•	Corticosteroids		•	Thymectomy		•	Immunoadsorption
						•	Rituximab1

Unmet need

• ~10% of MG patients refractory to current treatments, while 80% fail to achieve complete stable remission1
• Existing therapies associated with significant side effects
• • Early line agents can lead to disease exacerbation and do not always prevent disease progression
  • Treatment for more advanced disease often requires invasive and burdensome infusions
• Patients with anti-MuSK antibodies more likely to become refractory2
• • ~50% of the refractory MG population, despite comprising <10% of the overall MG population
  • Newest treatment option, eculizumab, only indicated for anti-AChR positive patients

1.	Rituximab is not approved for myasthenia gravis but is used in clinical practice	24
2.	Mantegazza R. and Antozzi C. When myasthenia gravis is deemed refractory: clinical signposts and treatment

strategies. Therapeutic Advances in Neurological Disorders, 2018

ASCEND-MG: Phase 2a study design

Screening

Key Inclusion Criteria:

• MGFA Class II-IVa
• QMG score ≥ 12 at screening
• Anti-AChRantibody positive

Up to 3 weeks

Treatment

IMVT-1401 680 mg

N = 7

IMVT-1401 340 mg

N = 7

Placebo

N = 7

6 weeks

Open label	Follow-up
extension
340 mg every
other week

6 weeks

6 weeks

Primary Endpoints:	Secondary Endpoints:	Exploratory Endpoints:
•	Safety & tolerability	•	IMVT-1401 pharmacokinetics	• Biomarkers (gene expression,
•	Change from baseline levels	•	Change from baseline in	serum pro-inflammatory
	of anti-AChR antibodies, total		QMG, MG-ADL, quality of life	markers, receptor occupancy)
	IgG, and IgG by subclass		measures

25

IMVT-1401 for

Graves' Ophthalmopathy

Graves' Ophthalmopathy overview

• Also called Graves' orbitopathy or thyroid eye disease (TED)
• 15,000-20,000patients with active GO in the United States per year
• Clinical features1:
• • Proptosis
  • Eye pain
  • Double vision
  • Light sensitivity
• Can be sight-threatening2
• Caused by autoantibodies that activate cell types present in tissues surrounding the eye2
• Close temporal and pathobiologic relationship with Graves' disease

Bahn, 2010

Figure 1. Patients with Graves' Ophthalmopathy

Panel A shows a 59-year-old woman with excess proptosis, moderate eyelid edema, and erythema with moderate eyelid retraction affecting all four eyelids. Conjunctival chemosis (edema) and erythema with bilateral edema of the caruncles, with prolapse of the right caruncle, are evident. Panel B shows a 40-year old woman with excess proptosis, minimal bilateral injection, and chemosis with slight erythema of the eyelids. She also had evidence, on slit-lamp examination, of moderate superior limbic keratoconjunctivitis.

1.	Davies T. and Burch H.B. Clinical features and diagnosis of Graves' orbitopathy (ophthalmopathy), UpToDate, 2018	27
2.	McAlinden C. An overview of thyroid eye disease. Eye and Vision, 2014

Anti-TSHR autoantibodies drive progression of

GO and Graves' disease

Graves' ophthalmopathy			Graves' disease
Orbital fibroblast	TSHR	Anti-TSHR		Thyrocyte	TSHR	Anti-TSHR
antibody		antibody
or adipocyte

Inflammation and	Thyroid hormone
production
proliferation
• Thyroid-stimulating hormone receptor (TSHR)	• TSHR highly expressed on thyrocytes (cells
highly expressed on ocular fibroblasts and	that make up the thyroid gland)3
adipocytes1	• Activation leads to increased production of
• Activation leads to inflammation and proliferation	thyroid hormone3
• Autoantibodies against insulin-like growth factor-
1 receptor (IGF-1R) also identified2

IMVT-1401 could address GO and Graves' disease caused by

any IgG autoantibody, whether against TSHR or IGF-1R

1. Smith T.J., et al. Role of IGF-1 pathway in the pathogenesis of Graves' orbitopathy. Best Practice & Research: Clinical Endocrinology & Metabolism,	28
2013

1. Liaboe C.A., et al. An Introductory Tutorial and Overview of Disease - Thyroid Eye Disease (TED), 2016
2. Varewijck A.J., et al. Circulating IgGs may modulate IGF-I receptor stimulating activity in a subset of patients with Graves' ophthalmopathy. Journal of Clinical Endocrinology & Metabolism, 2013

GO characterized by an active phase, followed by a static phase

Rundle's Curve describes natural history of disease1

Intensity

Inflammation

Severity

Desired outcome with early intervention in active phase

	0-2 years (active phase)		2+ years (static phase)
•	Orbital tissue actively		• Inflammatory tissue replaced by fibrotic tissue
	inflamed		• Steroids and immunosuppression no longer
•	Steroids and other		effective
	immunosuppressive		• Patients to be evaluated for surgery
	treatments can be effective
	1. Adapted from Hiromatsu Y., et al. Graves' ophthalmopathy: epidemiology and natural history. Internal Medicine, 2014	29

Limited treatment options for GO

Current treatment paradigm1

1st Line			2nd Line			3rd Line		Inactive disease
• Corticosteroids		•	Orbital radiotherapy		•	Rituximab2		• Orbital surgery
		•	Immunosuppressive
			agents

Unmet need

• Currently no FDA-approved therapies for GO
• Corticosteroids are not effective in all patients, and approximately one-third of patients will relapse
• Sight-threateningdisease may occur in 3-5% of patients with Graves' disease3
• • Medical emergency requiring immediate hospitalization and evaluation for surgery3
• Up to 20% of GO patients require surgical invervention3

1. Bothun E.D., et al. Update on thyroid eye disease and management. Clinical Ophthalmology, 2009

30

1. Rituximab is not approved for Graves' ophthalmopathy but is used in clinical practice
2. Bartalena L., et al. Management of Graves' Ophthalmopathy: Reality and Perspectives. Endocrine Reviews, 2000

ASCEND-GO Phase 2 clinical program

ASCEND-GO1

• Phase 2a
• • Trial ongoing in Canada
  • Single arm, open label
  • N=8
  • 6 weeks of dosing
  • • 680 mg weekly x 2 doses
    • 340 mg weekly x 4 doses

ASCEND-GO2

• Phase 2b
• • Trial ongoing in USA and Europe
  • Double masked, placebo controlled, randomized
  • N=77
  • 3 drug arms vs placebo
  • 12 weeks of dosing

31

ASCEND-GO 1: Phase 2a study design

Screening

Treatment

Follow-up

Key Inclusion Criteria:

• Moderate-to-severe

active GO

IMVT-1401 680 mg/

•

Clinical activity score

340 mg SC

(CAS) ≥4

N = 8

• Anti-TSHR antibody

positive

3-6 weeks

6 weeks

12 weeks

Primary Endpoints:

Secondary Endpoints:

Exploratory Endpoints:

•

Safety & tolerability

•

Change in proptosis

•

Biomarkers (gene expression,

• Change from baseline levels

•

PK/PD

serum pro-inflammatory

of anti-TSHR antibodies, total

•

Anti-drug antibody levels

markers, receptor occupancy)

IgG, and IgG by subclasses

•

CT scans

32

ASCEND-GO 2: Phase 2b study design

Screening

TreatmentFollow-up

Key Inclusion Criteria:

• Moderate-to-severeactive GO
• Clinical activity score
  (CAS) ≥4
• Anti-TSHRantibody positive

3-6 weeks

Primary Endpoints:

• Proptosis responder rate
• Safety & tolerability

IMVT-1401 680 mg SC

N = 22

IMVT-1401 340 mg SC

N = 22

IMVT-1401 255 mg SC

N = 11

Placebo

N = 22

12 weeks

Secondary Endpoints:

• CAS responder rate
• Change from baseline levels of anti-TSHR antibodies, total IgG, and IgG by subclasses

8 weeks

Exploratory Endpoints:

• Biomarkers (gene expression, serum pro-inflammatory markers, receptor occupancy)
• CT scans

33

IMVT-1401 for Warm Autoimmune Hemolytic Anemia

Warm Autoimmune Hemolytic Anemia overview

Anti-red blood cell	Red blood	Anti-RBC autoantibodies	Antibody-coated RBCs undergo
autoantibody	cells (RBCs)	bind to RBCs	extravascular hemolysis

• Blood disorder marked by red blood cell destruction
• Estimated prevalence of 42,000 patients in US and 66,000 patients in EU1
• Presentation typically non-specific and occurs over several weeks to months
• • Fatigue, weakness, skin pallor, shortness of breath
• Severe cases can be fatal2

1. Park S.H. Diagnosis and treatment of autoimmune hemolytic anemia: classic approach and recent advances.	35
Blood Research, 2016

2. Roumier M., et al. Characteristics and outcome of warm autoimmune hemolytic anemia in adults: new insights based on a single-center experience with 60 patients. American Journal of Hematology, 2014

Limited options for treating WAIHA

Current treatment paradigm1,2

	1st Line		2nd Line		3rd Line		4th Line
•	Corticosteroids		• Immunosuppressive		• Rituximab3		• Splenectomy
•	RBC transfusion		agents

Unmet need

• Currently no FDA-approved therapies for WAIHA
• Only one-third of all patients maintain sustained disease control once steroids are discontinued
• • Majority of patients will require either long-term steroid treatment or additional therapies1
• No clear guidelines on choice of treatment in patients failing treatment with corticosteroids
• RBC transfusions are indicated in patients who require immediate stabilization, despite the fact that autoantibodies present in WAIHA patients may react against RBCs in the transfusion product1,2

1. Salama A. Treatment Options for Primary Autoimmune Hemolytic Anemia: A Short Comprehensive Review.	36
Transfusion Medicine and Hemotherapy, 2015

1. Park S.H. Diagnosis and treatment of autoimmune hemolytic anemia: classic approach and recent advances. Blood Research, 2016
2. Rituximab is not approved for warm autoimmune hemolytic anemia but is used in clinical practice

ASCEND-WAIHA: Phase 2 study design

Screening

Key Inclusion Criteria:

• Primary or secondary
  WAIHA
• Direct Antiglobulin Test (DAT) positive
• Failed or intolerant to at least 1 prior treatment
• Stable on any current therapies

4 weeks

TreatmentFollow-up

IMVT-1401 680 mg

N = 8

IMVT-1401 340 mg

N = 8

12 weeks

8 weeks

Primary Endpoints:	Secondary Endpoints:	Exploratory Endpoints:
•	Hemoglobin response rate*	•	Change in hemoglobin, LDH,	• Biomarkers (gene
•	Safety & tolerability		bilirubin, & haptoglobin	expression, serum pro-
		•	Time to response	inflammatory markers,
		•	QOL measures	receptor occupancy)
		•	PK/PD
		• Anti-drug antibody levels

* Defined as hemoglobin level ≥10 g/dL with at least a ≥2 g/dL increase from baseline	37

Immunovant Recap

Our vision: Normal lives for patients with autoimmune diseases

Our asset: IMVT-1401, a novel, fully human monoclonal antibody inhibiting FcRn-mediated recycling of IgG

Our strategy for IMVT-1401:

• Be best-in-classin target indications where anti-FcRn mechanism has already established clinical proof-of-concept
• Be firstto study FcRn inhibition in target indications with clear biologic rationale and no known in-class competition

Our near-termvalue drivers: Four anticipated data readouts over the next 20 months

39

IMVT-1401: Multiple anticipated near-term value inflection points

MG

GO

WAIHA

• Phase 2a open for enrollment

Top-line results of Phase 2a study expected in 1H 2020 Pivotal Phase 3 study initiation expected in 2020

• Phase 2a open for enrollment

Initial results of Phase 2a study in Q1 2020 PPhase 2b proof-of-concept study open for enrollment

Top-line results of Phase 2b study expected in early 2021

• IND submission expected in 2H 2019

Initial results of Phase 2a study expected in Q4 2020

40