NASDAQ: IMVT

In a Phase 1 clinical trial, healthy adults dosed with IMVT-1402 showed deep, dose-dependent IgG reductions. We expect to be able to reach approximately 80% IgG reductions with continued weekly dosing of 600 mg of IMVT-1402, offering deeper IgG reductions than observed with other competitor anti-FcRn programs, therefore representing a potential best-in-class opportunity. In the Phase 1 clinical trial, across all evaluated doses, IMVT-1402 demonstrated no or minimal reductions in albumin and no or minimal increases in LDL cholesterol levels, which are off-target effects observed in some anti-FcRn antibodies, including batoclimab. We believe IMVT-1402’s profile has the potential to offer best-in-class efficacy, in addition to its potentially favorable safety profile and convenient administration with a simple self-administered auto-injector expected at launch.

We are currently progressing a broad set of programs for IMVT-1402 and have ongoing studies in six indications, including potentially registrational trials in GD, difficult-to-treat rheumatoid arthritis (“D2T RA”), MG, CIDP and Sjögren’s disease (“SjD”), and a proof-of-concept trial in cutaneous lupus erythematosus (“CLE”). Our primary focus is to execute these six indications first, with plans to assess new indications for IMVT-1402 in the future. All studies evaluating IMVT-1402 are being conducted using the intended commercial drug formulation and delivery device, the YpsoMate® autoinjector developed by Ypsomed AG, which is utilized for multiple approved products.

IMVT-1402 and batoclimab are fully human monoclonal antibodies that target FcRn. These antibodies are the result of a multi-step, multi-year research program conducted in collaboration with HanAll to design highly potent anti-FcRn antibodies that may be optimized as a simple, subcutaneous injection with dosing that has been shown to deliver better efficacy at the high dose and similar efficacy at the low dose compared to standard FcRn inhibition by competitors.

In April 2026, we announced top-line results from two Phase 3 clinical studies evaluating batoclimab as an investigational treatment for adults with active, moderate-to-severe thyroid eye disease (“TED”), neither of which met the primary endpoint. The safety profile observed in these studies was consistent with prior batoclimab studies, with no new safety signals identified. Following these results, we made a decision to discontinue further development of batoclimab across all indications to focus fully on IMVT-1402. Learnings from the batoclimab program, including clinical data, operational trial experience, and relationships with investigators, have been and continue to be leveraged to inform the development of IMVT-1402.

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Business Strategy

We are pursuing a broad anti-FcRn strategy based on the potential best-in-class profile of IMVT-1402 for the treatment of IgG-mediated autoimmune diseases. To execute our strategy, we plan to:

•Prioritize areas of significant unmet medical need where IMVT-1402 could potentially be first- and best-in-class. We plan to expand the use of FcRn inhibitors in indications that benefit a greater number of patients with several potential first- and best-in-class indications such as GD, D2T RA and CLE with significant unmet medical need. We believe the probability of technical success for IMVT-1402 is strong, given its potential to achieve best-in-class IgG reductions, along with the batoclimab proof-of-concept data we have generated in GD, the IMVT-1402 case study data presented in CLE, and a competitor’s data in RA.

•Maximize the commercial potential of IMVT-1402 with a clear, differentiated and potentially best-in-class profile in established markets. We plan to leverage the potential best-in-class profile of IMVT-1402 in indications where the anti-FcRn mechanism already has established a commercial presence, such as MG and CIDP. Data generated by batoclimab in these indications support our hypothesis that IMVT-1402 could potentially offer best-in-class efficacy at the high dose with the convenience of a well-established self-administered autoinjector and a potentially favorable safety profile.

•Focus on rapid clinical execution as a key priority. We plan to focus on clinical execution to maintain our head start in the indications identified above and to be nearly-first and potentially best-in-class for indications such as SjD where we can launch in close proximity to in-class competition and expect a differentiated clinical profile. Data generated by a competitor in SjD supports our belief that IMVT-1402 could potentially offer best-in-class efficacy at the high dose due to best-in-class IgG reductions with the convenience of a well-established self-administered autoinjector and potentially favorable safety profile.

•Evaluate potential additional indications. We intend to thoroughly evaluate potential additional indications based on the degree of unmet medical need, the potential benefit offered by anti-FcRn treatment, the target patient population size and the commercial potential.

Our Pipeline and Anticipated Milestones

Our research and development programs are organized and managed by therapeutic area and our clinical trials address specific target indications within these areas. The following is our current development pipeline and anticipated milestones for IMVT-1402:

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The Role of FcRn in Autoimmune Disease

Autoimmune diseases are conditions where an immune response is inappropriately directed against the body’s own healthy cells and tissues. According to the Autoimmune Association, more than 50 million people in the United States (“U.S.”) suffer from one of more than 100 diagnosed autoimmune diseases. Predisposing factors may include genetic susceptibility, environmental triggers and other factors not yet known. Many of these diseases are associated with high levels of pathogenic IgG antibodies. In healthy people, IgG antibodies are the most abundant type of antibody produced by the human immune system, accounting for approximately 75% of antibodies in the plasma, and are important in the defense against pathogens, such as viruses and bacteria. In IgG-mediated autoimmune diseases (an important subset of autoimmune diseases), IgG antibodies inappropriately develop against normal proteins found in the body, directing the immune system to attack specific organs or organ systems.

IgG antibodies are continuously being removed from circulation and internalized in cellular organelles called endosomes. FcRn is the primary protein responsible for preventing the degradation of IgG antibodies. The role of FcRn is to bind to the IgG antibodies under the more acidic conditions of the endosome and transport them to the cell surface, where the neutral pH causes them to be released back into circulation.

Inhibition of FcRn, such as through the use of an anti-FcRn antibody, has been shown to reduce levels of pathogenic IgG antibodies. Anti-FcRn antibodies, including our product candidates, bind to FcRn thereby blocking IgG antibodies from forming complexes with FcRn under the more acidic conditions of the endosome. As a result, unbound IgG antibodies are degraded in the lysosome rather than being transported by FcRn for release back into circulation. This anti-FcRn mechanism of action is depicted in the graphic below.

Limitations of Current Treatment Options in Autoimmune Disease

Treatment for IgG-driven autoimmune diseases varies widely, however many patients are commonly treated using intravenous or subcutaneous immunoglobulins (“IVIg,” “SCIg”), corticosteroids, plasma exchange (“PLEX”) and immunomodulatory therapies. Despite the availability of the therapies, there remains significant unmet medical need. For example, although immunoglobulin therapy (IVIg, SCIg) is effective, it may be associated with significant side effects and complications such as severe headache, thromboembolism and hemolysis. Additionally, IVIg therapy imposes a burden on patients’ time and at-home administration options remain limited. IVIg supply constraints have occurred, and IVIg is also not available in all markets. SCIg therapy often requires frequent administration at multiple infusion sites using an external pump to deliver the requisite volume of therapy, which presents challenges to patients requiring therapy on a continuous basis.

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Corticosteroid therapy, though effective, has well-known serious adverse effects (e.g., weight gain, hypertension, diabetes and osteoporosis), especially with chronic use. PLEX requires central venous access and is not universally available. Immunomodulatory therapies are all associated with significant potential risks, including the possibility of malignancy and infection. For example, these include azathioprine – cytopenia; cyclosporine – hypertension, nephrotoxicity; mycophenolate – blood dyscrasias including neutropenia and red blood cell (“RBC”) aplasia; rituximab – renal toxicity; and cyclophosphamide – cardiac, pulmonary and renal toxicity as well as bone marrow suppression and infertility. The currently available treatments are associated with significant potential risk of adverse effects, generally impose a high burden on patient’s time and effort and may be subject to restricted availability. There remains a high unmet need for safe and effective targeted therapies for patients suffering from autoantibody-driven disease.

Product Candidate - IMVT-1402

IMVT-1402 is a fully human monoclonal antibody that inhibits FcRn with a potentially best-in-class profile, offering potentially best-in-class efficacy, a favorable route of administration and a potentially favorable safety profile.

IMVT-1402 has been assigned the nonproprietary name imeroprubart on the World Health Organization’s Recommended International Nonproprietary Names List 93, which has also been approved by the U.S. Adopted Names Council.

In September and November of 2023, we announced results from a Phase 1 clinical trial in healthy adults in New Zealand. In the study’s 300 mg multiple-ascending dose (“MAD”) cohort, a statistically significant reduction of 63% from baseline in mean total IgG levels was observed after four weekly 300 mg subcutaneous doses of IMVT-1402. In the 600 mg MAD cohort, we observed a statistically significant reduction of 74% from baseline in mean total IgG levels after four weekly 600 mg subcutaneous doses of IMVT-1402. No or minimal reductions in albumin and no or minimal increases in LDL cholesterol levels were observed in healthy adults administered IMVT-1402 in either dose cohort; the changes in albumin and LDL cholesterol were similar to those observed with placebo administration. Across all doses evaluated, treatment with IMVT-1402 was generally well tolerated, with only mild or moderate treatment-emergent adverse events observed.

Based on trial results announced to date across the anti-FcRn class and the strength of its potential best-in-class profile, we are pursuing development of IMVT-1402 in endocrinology, neurology, rheumatology, dermatology and possibly other therapeutic areas, with a focus on indications representing first-in-class opportunities, or opportunities where we can leverage our own batoclimab or existing in-class clinical data to build confidence in a best-in-class profile. We are currently progressing a broad set of programs for IMVT-1402 and have ongoing studies in six indications, including potentially registrational trials in GD, D2T RA, MG, CIDP and SjD, and a proof-of-concept trial in CLE.

Our Therapeutic Areas

Endocrine Diseases

Graves’ Disease

GD Overview

GD is an autoimmune disease that affects the thyroid gland. Patients with GD develop IgG autoantibodies that bind to the thyroid-stimulating hormone receptor (“TSHR”) present on the thyroid gland, which induces increased and uncontrolled secretion of thyroid hormones, resulting in hyperthyroidism. GD is the most common cause of hyperthyroidism and occurs at all ages but especially in adults aged between 20 and 50 years and can impact women of reproductive age. Because thyroid hormones play an important role in controlling functions of many organs such as heart, central and peripheral nervous system, muscle, bone, and skin, the presence of excessive thyroid hormones is associated with a variety of signs and symptoms including enlarged thyroid gland (goiter), palpitations, arrhythmia, anxiety, weight loss, insomnia, osteoporosis, and pretibial myxedema.

The treatment of GD has seen minimal innovation in therapeutic options over the past 70-plus years. Antithyroid drugs (“ATDs”), as the only existing pharmacological therapy, do not address the underlying disease pathology characterized by high levels of stimulating TSHR antibodies (“TRAb”). A conservative analysis of Inovalon claims data estimates that the prevalence of Graves’ patients is approximately 880,000 in the U.S., and further analysis suggests that there are approximately 330,000 patients who have relapsed on ATDs and who have opted not to pursue ablation. Other market-sizing analyses by various methods suggest that 25-30% of Graves’ patients are relapsed, uncontrolled on or intolerant to ATDs, representing a potentially significant unmet medical need.

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Current Treatment Paradigm

The main treatment goal of GD is to reduce thyroid hormone levels. There are 3 options currently available: surgery, radioiodine (“RAI”), and ATDs. The most commonly prescribed ATDs in the U.S. are the thionamides, methimazole and propylthiouracil. An internal chart review of over 1,000 patient records from over 140 endocrinologists and a patient survey of 100 patients indicate that approximately 25-30% of GD patients remain uncontrolled on ATDs. A recent study showed that Graves’ patients with persistent stimulating TRAb levels had a 6-fold increased risk for relapse after ATD withdrawal. Collectively, these data suggest that a treatment for GD targeting the reduction or elimination of circulating stimulating TRAb would address the underlying autoimmune pathogenesis of the disease and would restore normal thyroid function.

Surgery, which involves partial or entire removal of the thyroid gland (thyroidectomy) is an option, especially for patients with large goiters, women planning pregnancy and, in some cases, patients who have failed to respond to ATDs. Although any such surgical procedure may lead to an immediate resolution of the hyperthyroidism, it is associated with potential complications including parathyroid gland injury, which may lead to hypocalcemia, and damage of the laryngeal nerve. Treatment with RAI destroys the thyroid using ionizing radiation. It is considered an alternative to medical management in several countries, especially if ATDs are contraindicated or among patients who do not respond to this drug class. Since RAI can worsen TED, it is not recommended in patients with TED or in smokers who are at higher risk of developing TED, and in women who are pregnant or lactating. Finally, recent data suggest an association between RAI and increased risk for several types of cancer. In addition, RAI is associated with sustained increases in TRAb titers, risk for de novo TED and worsening of pre-existing TED. Both thyroidectomy and RAI may result in hypothyroidism, requiring lifelong treatment with thyroid hormone replacement. Given these risks, the treatment paradigm for GD continues to shift away from RAI and thyroidectomy, resulting in an increasing number of patients who are not controlled on ATDs but who are choosing not to undergo ablation. Rates of surgery and RAI have declined significantly in the U.S. in recent years, to about 11% of patients in 2021, according to an analysis of claims data, from more than half of patients in 2005.

Proof-of-Concept Trial with Batoclimab

We initially tested the potential of FcRn inhibition for the treatment of GD in a Phase 2 proof-of-concept trial (NCT05907668) evaluating our first-generation FcRn inhibitor, batoclimab.

The study included a 24-week batoclimab treatment period with a dose step-down midway through the treatment period (Weeks 0-12 at 680 mg weekly (“QW”) subcutaneously (“SC”) and Weeks 13-24 at 340 mg QW SC), followed by a 24-week off-treatment follow-up period. The study enrolled participants with active GD as documented by presence of elevated TRAb and who were hyperthyroid despite current treatment with standard of care ATD therapy. The primary endpoint of the study measured response as the proportion of participants who at Week 24 achieved normalization of free triiodothyronine (“T3”) and free thyroxine (“T4”), or have T3/T4 below the lower limit of normal (“LLN”), without an increase in ATD dose from baseline. A total of 25 subjects were enrolled in the treatment period, and 21 subjects entered the 24-week off-treatment follow-up period and could be assessed for maintenance of response. In data previously disclosed in September 2024 that was reanalyzed to include an additional patient who discontinued prior to Week 12 but remained in off-drug follow-up, at the end of the first 12 weeks, a mean IgG reduction of 77% and an 80% response rate (defined as T3 and T4 falling below the upper limit of normal (“ULN”) without increasing the ATD dose) were observed. 60% of subjects treated with higher dose batoclimab were observed to have an ATD-Free Response (defined as T3 and T4 falling below the ULN and the patient simultaneously tapering completely off their ATD) at the end of the first 12 weeks. During weeks 13 to 24, patients receiving lower dose batoclimab were observed to have mean IgG reduction of 65% with a correspondingly lower responder rate of 72% and a lower ATD-Free Response rate of 40% at the end of the second 12 weeks. Patients who were observed to have at least a 70% IgG reduction at the end of the evaluation period had nearly a threefold higher ATD-Free Response rate than those who did not (64% vs. 23%).

Six-month off-treatment data was presented at the American Thyroid Association Annual Meeting in September 2025. At completion of the follow-up period at Week 48 (i.e., subjects off-treatment for 24 weeks), approximately 80% (17/21) of those subjects maintained T3/T4 values ≤ ULN, suggestive of strong durability of the response observed at Week 24 as evaluated at approximately six months off treatment at Week 48. Of these 17 subjects, approximately 50% (8/17) were ATD-free and an additional approximately 30% (5/17) were on ATD doses of 2.5 mg/day at six months off batoclimab treatment. Total IgG and TRAb levels declined through Week 24, consistent with previous observations, and while total IgG rebounded after treatment ended, pathogenic TRAb levels remained suppressed at Week 48. Safety and tolerability were observed to be consistent with prior batoclimab studies.

This study is now completed, with its data suggesting the potential of FcRn inhibition for the treatment of GD by modifying the underlying disease pathology, which is driven by TRAb. As such, GD is a key strategic priority for our development of IMVT-1402.

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IMVT-1402 Development Program in GD

In December 2024, we initiated a potentially registrational trial evaluating IMVT-1402 in adults with GD. This study (NCT06727604) is a randomized, placebo-controlled, 52-week trial in Graves’ patients who are hyperthyroid despite treatment with an ATD for 12 or more weeks prior to beginning the study. The study is expected to enroll approximately 240 participants randomized (1:1:1) to one of two blinded treatment groups each receiving IMVT-1402, 600 mg weekly SC, or a matched placebo group. Participants will be evaluated over two consecutive 26-week blinded treatment periods. Over the course of the treatment periods, background ATD treatment will be titrated to the lowest effective dose, including elimination of ATD treatment, to maintain normal thyroid lab values. Following the initial 26-week period, participants in the IMVT-1402 treatment group 2 will be assigned to either continued treatment with IMVT-1402 at the same dose or matching placebo for the second 26-week study period based on the participant’s TRAb value and euthyroid status determined at week 26. The study’s primary endpoint is the proportion of participants who are euthyroid and off ATD at study week 26. A key secondary endpoint will measure the proportion of participants who become euthyroid and stop ATD treatment at week 52. We expect to report top-line results from this trial in calendar year 2027.

More details on the trial design are described in the figure below:

In June 2025, we initiated a second potentially registrational trial evaluating IMVT-1402 in adults with GD. This study (NCT07018323) is a randomized, placebo-controlled, 26-week trial in Graves’ patients who are hyperthyroid despite treatment with an ATD for 12 or more weeks prior to beginning the study. The study is expected to enroll approximately 210 participants randomized (1:1:1) to one of three blinded treatment groups receiving IMVT-1402 600 mg weekly SC, IMVT-1402 300 mg weekly SC, or matched placebo group. Over the course of the treatment periods, background ATD treatment will be titrated to the lowest effective dose, including elimination of ATD treatment, to maintain normal thyroid lab values. The study’s primary endpoint is the proportion of participants in the 600 mg weekly SC dose group who are euthyroid and are off ATD versus placebo at study week 26. A key secondary endpoint will measure the proportion of participants in the 600 mg weekly SC dose group who have T3 (Total T3 or FT3) and FT4 ≤ULN and are off ATD versus placebo. We expect to report top-line results from this trial in calendar year 2027.

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More details on the trial design are described in the figure below:

Rheumatology Diseases

Rheumatoid Arthritis

RA Overview

RA is a chronic progressive autoimmune disease that causes inflammation in the joints and surrounding tissues. Inadequate control of the joint inflammation associated with RA may result in irreversible joint erosions. The estimated prevalence of patients treated with biologic or targeted synthetic disease modifying anti-rheumatic drugs (“DMARDs”) in the U.S. is approximately 820,000, approximately 15% of which had an inadequate response to two or more such prior advanced DMARD mechanisms. The RA described in this subset of patients is sometimes referred to as difficult-to-treat (“D2T”), refractory, or multi-advanced mechanism failure RA. Of those, approximately 70% are autoantibody positive, representing approximately 85,000 patients with significant unmet medical need in the U.S. Several autoantibodies have been identified in RA, including rheumatoid factor (“RF”) and anti-citrullinated protein antibodies (“ACPA”). These RA-specific autoantibodies are found in 70-80% of RA patients and exacerbate inflammation via immune complex formation. Positivity for RF and ACPA seems to have an amplifying effect on disease, resulting in an aggressive phenotype with more severe disease manifestations. Seropositive RA is also associated with poor outcomes on currently available therapies.

Current Treatment Paradigm

Therapeutic approaches for RA are intended to help control joint inflammation, damage and other associated disease manifestations. Currently available treatments include a variety of conventional oral, targeted synthetic and biologic DMARD treatments. These therapies primarily function by modulating the immune response and limiting the activity of pro-inflammatory cytokines such as tumor necrosis factor-alpha (“TNF-α”), interleukin-6 (“IL-6”), and others impacting the pathogenesis of RA. While many patients experience symptom relief and disease control with these agents, D2T RA patients continue to experience active disease despite undergoing multiple lines of therapy with different mechanisms of action. For these patients, therapeutic options remain very limited while the risk of irreversible joint damage persists, highlighting a critical unmet medical need. The European Alliance of Associations for Rheumatology (EULAR) has defined this RA subset in the clinical setting as D2T RA and provided points to consider in its management. Nevertheless, innovative strategies and novel therapeutic targets are needed to improve outcomes and quality of life for this patient population.

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Anti-FcRn as a Potential Treatment for D2T RA

Because of the role of FcRn in preventing the degradation of IgG autoantibodies, such as ACPAs, FcRn inhibition is an attractive mechanism as a potential treatment for ACPA-positive RA. Recent industry experience with anti‑FcRn therapies has informed our approach to evaluating RA. Johnson & Johnson’s IRIS-RA Phase 2a placebo-controlled, proof-of-concept trial evaluating nipocalimab in patients with RA and inadequate response or intolerance to anti-TNF therapy demonstrated that deeper ACPA IgG reduction correlated with improved rates of clinical response. We are focused on the subset of RA patients with ACPA-positive D2T RA, who have failed two or more prior advanced mechanism therapies, inclusive of biologics (TNFα inhibitors, IL-6R inhibitors, CD80/86 inhibitors, CD20 inhibitors) and targeted synthetic DMARDs (e.g., Janus kinase (“JAK”) inhibitors). For patients failing two or more prior advanced mechanisms in addition to conventional DMARDs, IMVT-1402 would be the fourth line or later line of therapy.

IMVT-1402 as a Potential Treatment for D2T RA

In December 2024, we initiated a potentially registrational trial evaluating IMVT-1402 in ACPA-positive D2T RA. This trial (NCT06754462) is fully enrolled, and all participants have completed an initial 16-week open-label, active treatment period (Period 1). To ensure the enrollment of patients with active D2T RA, the trial inclusion criteria require elevated ACPA levels, on stable conventional DMARD treatment, and prior inadequate response to at least two (but not more than four) classes of advanced mechanisms (biologics or targeted synthetic DMARDs). The study will evaluate IMVT-1402 600 mg weekly SC during the open-label induction phase of the trial with the intent of maximizing reduction in ACPA levels. Participants achieving a response at weeks 14 and 16 in Period 1 per the American College of Rheumatology response criteria 20 (“ACR20”) will be randomized in a 1:1:1 ratio to receive blinded treatment in Period 2 with either IMVT-1402 600 mg, IMVT-1402 300 mg or placebo, weekly SC for 12 weeks. The primary endpoint will assess the proportion of such participants who maintain the ACR20 response at week 28. Eligible participants who complete week 28 will have the option to receive IMVT-1402 for an additional period of 48 weeks as part of a long-term extension period.

More details on the study design are described in the figure below:

The trial is currently ongoing and has enrolled a total of 170 participants in Period 1. At the completion of Period 1, 165 of the 170 enrolled patients were evaluable for ACR20 response to determine eligibility to continue to Period 2 and the primary efficacy analysis for the study. The enrollment inclusion criteria described above resulted in a heavily pretreated population: 86.7% (143/165) had failed two prior mechanisms of advanced therapies (i.e., biologic or targeted synthetic DMARDs), and the mean time from disease diagnosis was 12.8 years. Baseline disease activity was high, with a mean of 24.2 tender joints, 16.7 swollen joints, and DAS28-CRP score of 6.1.

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At Week 16, the ACR20, ACR50, and ACR70 response rates observed were 72.7%, 54.5%, and 35.8%, respectively; participants who discontinued prior to Week 16 were imputed as non-responders. Among the subset of participants who had failed at least a JAK inhibitor and an anti-TNF inhibitor (N=107), the ACR20, ACR50, and ACR70 response rates observed at Week 16 were 72.0%, 53.3%, and 37.4%, respectively. ACR20 response is defined as a ≥ 20% improvement from baseline in tender joint count and swollen joint count and a ≥ 20% improvement from baseline in at least 3 of 5 additional clinical parameters. Similarly, ACR50 and ACR70 responses are a calculation of 50% or 70% improvement, respectively, in the number of swollen and tender joints and 3 of 5 assessment parameters.

Period 1 was conducted in an open-label setting, with joint assessments performed by independent assessors blinded to treatment status to control for the potential for assessor bias in the response measures. IMVT-1402 was observed to be safe and well-tolerated in Period 1, and no new drug-related safety signals were identified. Study participants meeting the criteria for an ACR20 response at Week 16 are eligible to advance to Period 2 of the trial, where the primary endpoint will be assessed at Week 28. Further updates on this program are expected in the second half of calendar year 2026.

Sjögren’s Disease

SjD Overview

Sjögren’s disease, formerly referred to as Sjögren’s syndrome, is a chronic autoimmune disease characterized by lymphocytic infiltration of the salivary and lacrimal glands. It is classically associated with severe dryness of the eyes and mouth; the latter frequently associated with difficulty swallowing or speaking, tooth decay, gum disease and impaired quality of life. Up to 50% of affected individuals also develop extra-glandular manifestations that can impact a variety of organ systems such as the joints, skin, lungs, gastrointestinal tract, nervous system, or kidneys.

SjD may occur in isolation (primary SjD) or in association with another systemic autoimmune disease such as rheumatoid arthritis (secondary SjD). It can be challenging to diagnose SjD based on symptoms alone due to the heterogeneity at presentation. However, serological testing including autoantibodies can help inform diagnosis. Autoantibodies including anti-Ro/SSA and anti-La/SSB have been detected in approximately 50-70% of patients with primary SjD and play crucial roles in both the diagnosis and prognosis of the disease.

The estimated prevalence of primary SjD is approximately 290,000 in the U.S. It is estimated that up to 30% of primary SjD patients have moderate-to-severe disease with anti-Ro/SSA antibodies, representing approximately 90,000 SjD patients with significant unmet medical need in the U.S.

Current Treatment Paradigm

No therapies have been approved specifically for the treatment of SjD. Therapeutic approaches for SjD disease include local agents such as pilocarpine hydrochloride and cevimeline hydrochloride for oral and ocular dryness as well as systemic treatments such as hydroxychloroquine, methotrexate, mycophenolate sodium, azathioprine, and cyclosporine to address organ manifestations. This results in frequent visits with healthcare professionals and a high burden of treatment for Sjögren’s patients, suggesting a need for the development of novel treatments that target the underlying pathophysiological mechanism of this disease.

Anti-FcRn as a Potential Treatment for SjD

Recent in-class data from a Phase 2 placebo-controlled, multicenter trial evaluating nipocalimab in patients with SjD provides support for anti-FcRn proof of mechanism. The study met its primary endpoint, with statistically significant improvement in Clinical European League Against Rheumatism Sjögren’s Syndrome Disease Activity Index (“ClinESSDAI”) score, a key SjD activity index, in the high dose nipocalimab group compared to placebo. A clear dose response in ClinESSDAI observed in the trial supports the potential correlation between degree of IgG suppression and improved clinical outcomes.

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IMVT-1402 as a Potential Treatment for SjD

In June 2025, we initiated a potentially registrational trial evaluating IMVT-1402 in SjD. This trial (NCT06979531) is a randomized, double-blind, placebo controlled, parallel-group study to assess the efficacy, safety, and tolerability of IMVT-1402 in adult participants with moderate to severe systemic primary SjD. The trial is anticipated to enroll approximately 180 participants randomized in a 1:1:1 ratio to receive IMVT-1402 600 mg, IMVT-1402 300 mg or placebo weekly SC for two 24-week blinded treatment periods. The primary endpoint will assess the efficacy of IMVT-1402 compared to placebo as assessed by ClinESSDAI score at week 24. Participants assessed as responders at week 24, defined as participants that show an improvement of ≥ 4 points from baseline ClinESSDAI score, will continue on treatment for a second 24-week period. A key secondary endpoint will assess change from baseline in ClinESSDAI score at week 48. We expect to report top-line results from this trial in calendar year 2028.

More details on the trial design are described in the figure below:

Dermatology Diseases

Cutaneous Lupus Erythematosus

CLE Overview

CLE is a rare, chronic skin disease characterized by skin-specific disease activity, inflammation and eventually damage. Triggered by sun exposure, CLE manifests as a recognizable rash and painful skin lesions, often with related symptoms such as itching, burning and alopecia. Subacute Cutaneous LE (“SCLE”) and Chronic Cutaneous LE (“CCLE”) are subtypes of CLE with distinct skin presentation and clinical course and high unmet medical need. The estimated prevalence of SCLE and CCLE is approximately 153,000 in the U.S. Approximately 50% of these SCLE and CCLE patients do not adequately respond to first-line therapies representing approximately 75,000 patients with potential significant unmet medical need in the U.S. IgG autoantibodies and immune complexes are observed to play a critical role in CLE disease pathophysiology.

Current Treatment Paradigm

First-line therapies are photoprotection, topical steroids and broad-spectrum therapies (i.e. DMARDs, antimalarials and corticosteroids) followed by IVIg or off-label biologics. It is estimated that approximately 50% of patients are not optimally managed with or without topical steroids due to insufficient response, relapse, or risk of retinopathy following first-line antimalarials.

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IMVT-1402 as a Potential Treatment for CLE

There is growing biologic and translational evidence supporting the role of IgG autoantibodies and immune complexes in the pathogenesis of CLE. Furthermore, published case studies using IVIg offer strong mechanistic evidence for the role of IgG autoantibodies in driving disease. Blocking FcRn may disrupt CLE pathology by providing upstream inhibition of the inflammatory cascade triggered in cells by pathogenic antibodies and immune complexes.

In addition, in April 2025, we presented observations from a proof-of-principle case study evaluating IMVT-1402 in a SCLE patient over a period of 12 weeks. The participant in the case study, a 57-year-old female, had alopecia and skin manifestations in multiple locations with a baseline Cutaneous Lupus Erythematosus Disease area and Severity Index activity (“CLASI-A”) score at screening of 36, which falls into the severe range on the clinical scale. The participant received open-label weekly treatment with 600 mg of IMVT-1402 for 12 weeks and saw significant clinical improvement in both skin lesions and alopecia. By week 12, the participant had a greater than 60% reduction in CLASI-A score to 13. A 5-point reduction in CLASI-A is considered clinically meaningful and this participant improved by 23 points by week 12. The participant also achieved approximately 78% total IgG reduction from baseline by week 12. A second patient dosed in this study also showed significant clinical improvement, with a CLASI-A score of 18 at screening reduced to 8 by week 12 of QW dosing, a > 50% improvement. We believe the initial data from this case study may provide important support for the mechanism and for the potential of IMVT-1402 as a first- and best-in-class anti-FcRn therapy in CLE.

IMVT-1402 Proof-of-Concept Trial in CLE

In February 2025, we initiated a proof-of-concept trial of IMVT-1402 in CLE. This Phase 2b trial (NCT06980805) is a randomized, double-blind, placebo-controlled trial to assess the safety, tolerability and efficacy of IMVT-1402 in participants with active SCLE and/or CCLE with or without systemic manifestations. This trial is fully enrolled, with participants randomized 1:1 to IMVT-1402 600 mg QW SC or placebo QW SC for 12 weeks during Period 1. Participants who complete Period 1 will enter Period 2, during which all participants will receive IMVT-1402 600 mg QW SC for 14 weeks. After completion of Period 2, participants will be rerandomized 1:1 to blinded IMVT-1402 300 mg or 600 mg SC QW for 26 weeks in Period 3. The primary endpoint will evaluate the efficacy of IMVT-1402 compared to placebo based on percent change from Period 1 baseline in CLASI-A score at week 12. We expect to report top-line results from this trial in the second half of calendar year 2026.

More details on the trial design are described in the figure below:

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Neurological Diseases

Myasthenia Gravis

MG Overview

MG is an autoimmune disorder associated with muscle weakness and fatigue. MG patients develop antibodies that lead to an immunological attack on critical signaling receptor proteins at the junction between nerve and muscle cells, thereby inhibiting the ability of nerves to communicate properly with muscles. This leads to muscle weakness intensified by activity, which can be localized to ocular muscles, or which can be more generalized throughout the body including muscles of respiration.

The symptoms of the disease can be transient and in the early stages of the disease, can remit spontaneously. However, as the disease progresses, symptom-free periods become less frequent and disease exacerbations can last for months or remain chronic. After 15 to 20 years, some weakness often becomes fixed, with the most severely affected muscles frequently becoming atrophic. Many patients find it difficult to perform daily activities due to both insufficient improvement in symptoms even after treatment and in some, the complicating long-term side effects of oral corticosteroids. Approximately 15% to 20% of MG patients will experience at least one myasthenic crisis during which the impairment of muscles required to breathe can become life-threatening.

The prevalence of MG is estimated to be approximately 59,000 to 116,000 cases in the U.S. with 35% of patients not well-controlled on the current standard of care, representing approximately 20,000 to 35,000 patients with significant unmet medical need in the U.S. The majority of these patients demonstrate elevated serum levels of acetylcholine receptor (“AChR”) antibodies.

Current Treatment Paradigm

Very early-stage MG is symptomatically treated with acetylcholinesterase inhibitors. As the disease progresses, patients are typically treated with immunosuppressive agents such as glucocorticoids, azathioprine, mycophenolate mofetil and cyclosporine. Thymectomy may be indicated for treatment in certain patients. As MG becomes more advanced, patients can be treated during exacerbations with IVIg, which provides therapeutic benefit through multiple potential mechanisms including the saturation of FcRn. Physicians direct patients with more advanced chronic disease and patients in times of crisis to therapies that reduce levels of circulating IgG antibodies via PLEX or a variant of PLEX, immunoadsorption. More recent novel mechanism of action therapies include FcRn inhibitors, which generally reduced IgG by 60-70% in their Phase 3 trials at approved doses, and complement inhibitors.

IMVT-1402 as a Potential Treatment for MG

In March 2025, we initiated a potentially registrational trial evaluating IMVT-1402 in adults with MG. This Phase 3 trial (NCT07039916) is a randomized, placebo-controlled, 26-week trial. This study is expected to enroll approximately 230 participants randomized (1:1:1) to one of three blinded treatment groups receiving IMVT-1402 600 mg weekly SC, IMVT-1402 300 mg weekly SC, or matched placebo group for the 12-week induction period. Participants on treatment will continue to be on the same treatment for the 14-week maintenance period, while patients on placebo will receive IMVT-1402 600 mg weekly SC. The study also includes a 52-week long-term extension. The study’s primary endpoint is the change in MG-ADL from baseline at week 12. We expect to report top-line results from this trial in calendar year 2027.

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More details on the trial design are described in the figure below:

Chronic Inflammatory Demyelinating Polyneuropathy

CIDP Overview

CIDP is believed to be an immune-mediated neuropathy characterized by demyelination of peripheral nerves and nerve roots that is driven by pathologic, autoreactive IgG antibodies. The estimated prevalence of CIDP is approximately 58,000 patients in the U.S., with approximately 30% inadequately controlled on treatment, representing approximately 16,000 patients with significant unmet medical need in the U.S.

CIDP typically presents with progressive or relapsing, symmetric involvement of both proximal and distal extremity muscle weakness over the course of several weeks. While the pathophysiology of CIDP is not completely understood, passive serum transfer animal models and the response of CIDP patients to intravenous immunoglobulin, plasma exchange and FcRn blockade suggests that autoantibodies are involved in its pathogenesis. Autoantibody-induced degeneration and demyelination would be expected to cause characteristic electrophysiologic alterations of the peripheral nerves and is clinically manifested by the sensorimotor deficits of CIDP.

Current Treatment Paradigm

IVIg, corticosteroids and PLEX are first-line therapies in the treatment of CIDP. For patients who fail to achieve objective improvement (i.e., of impairment and disability) after three months of treatment with a first-line agent, another agent may be tried. Alternative options include rituximab, cyclophosphamide or cyclosporine, despite limited evidence supporting their use. Once objective improvement is achieved, the patient may be switched to maintenance treatment, the goal of which is to reduce the dose or frequency of treatment while still controlling disease. For maintenance therapy, patients may be switched from IVIg to SCIg, and immunomodulatory agents such as azathioprine, cyclosporine or mycophenolate may be used for IVIg dose-reducing, corticosteroid-sparing or PLEX frequency-reducing effect. For long term management of clinically stable patients, therapy should be periodically reduced or stopped to assess if treatment is still required. An anti-FcRn inhibitor has also been approved for the treatment of CIDP; however, we believe there is still meaningful room to improve on efficacy.

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IMVT-1402 as a Potential Treatment for CIDP

In March 2025, we initiated a potentially registrational trial evaluating IMVT-1402 in adults with CIDP. This trial (NCT07032662) is a randomized, placebo-controlled, 24-week trial in CIDP patients, followed by a 52-week open label extension. The study is expected to enroll approximately 162 participants randomized (2:1) to one either receiving IMVT-1402 600 mg weekly SC, or matched placebo for the 24-week treatment period. The study’s primary endpoint will evaluate the proportion of participants remaining relapse free at week 24, where relapse is defined as worsening on the adjusted inflammatory neuropathy cause and treatment (aINCAT) score at any time point relative to baseline. We expect to report top-line results from this trial in calendar year 2028.

More details on the trial design are described in the figure below:

Key Agreements

License Agreement with HanAll Biopharma Co., Ltd.

In December 2017, Roivant Sciences GmbH (“RSG”), a wholly owned subsidiary of Roivant Sciences Ltd (“RSL”), entered into the HanAll Agreement. Under the HanAll Agreement, RSG received (1) the non-exclusive right to manufacture and (2) the exclusive, royalty-bearing right to (a) develop, import and use (i) the antibody referred to as batoclimab, (ii) certain back-up and next-generation antibodies (including IMVT-1402) and (iii) products containing such antibodies, and (b) to commercialize such products, in the U.S., Canada, Mexico, the EU, the UK, Switzerland, the Middle East, North Africa and Latin America (the “Licensed Territory”) for all human and animal uses during the term of the agreement. With respect to these licenses, RSG also received the right to grant a sublicense, with prior written notice to HanAll of such sublicense, to: (1) a third party in any country in the Licensed Territory outside of the U.S. and EU; (2) an affiliate of RSG in any country in the Licensed Territory; and (3) a third party in the U.S. and EU only after submission of a biologics license application (“BLA”) in the U.S. or a Marketing Authorization Application in the EU. Pursuant to the HanAll Agreement, RSG granted to HanAll an exclusive, royalty-free license under certain RSG patents, know-how and other intellectual property controlled by RSG relating to such antibodies and products to develop, manufacture and commercialize such antibodies and products for use outside of the Licensed Territory. HanAll also reserves the right to conduct discovery or research activities with the batoclimab antibody and certain back-up and next-generation antibodies (including IMVT-1402), with or through a contract research organization or service provider in the Licensed Territory.

In December 2018, we obtained and assumed all of the rights, title, interest and future obligations under the HanAll Agreement from RSG, including all rights to IMVT-1402 and batoclimab in the Licensed Territory, pursuant to an assignment and assumption agreement between RSG and our wholly owned subsidiary, Immunovant Sciences GmbH, (“ISG”), for an aggregate purchase price of $37.8 million. In January 2026, we completed an internal reorganization and transfer of intellectual property rights related to our product candidates between two wholly-owned subsidiaries of the Company. Ownership and rights to such intellectual property remain with us and our subsidiaries.

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Pursuant to the HanAll Agreement, we will be responsible for future contingent payments and royalties, including up to an aggregate of $420.0 million upon the achievement of certain regulatory and sales milestone events. We are also obligated to pay HanAll tiered royalties ranging from the mid-single digits to mid-teens percentage of net sales of licensed products, subject to standard offsets and reductions as set forth in the HanAll Agreement. These royalty obligations apply on a product-by-product and country-by-country basis and end upon the latest of: (A) the date on which the last valid claim of the licensed patents expires; (B) the date on which the data or market exclusivity expires; and (C) 11 years after the first commercial sale of the licensed product, in each case, with respect to a given product in a given country.

Except for cost-sharing in connection with the research program, we are solely responsible, at our expense, for all other activities related to the research, development and commercialization of licensed products for the Licensed Territory. We may use a third party for manufacturing activities necessary for the research, development and commercialization of licensed products for the Licensed Territory. In addition, under the HanAll Agreement, we have agreed to use commercially reasonable efforts to develop and commercialize licensed products in the Licensed Territory. Each party to the HanAll Agreement has agreed that neither it nor certain of its affiliates will clinically develop or commercialize certain competitive products in the Licensed Territory.

Under the HanAll Agreement, we have the sole right, but not the obligation, to control the prosecution, defense and enforcement of the licensed patents in the Licensed Territory, and HanAll has backup rights to prosecution, defense and enforcement with respect to any licensed patents for which we elect not to exercise such rights.

The HanAll Agreement will expire on a product-by-product basis on the expiration of the last royalty term with respect to a given licensed product, unless earlier terminated. We may terminate the HanAll Agreement in its entirety without cause upon 180 days’ written notice following 30 days of discussion. Either party may terminate the HanAll Agreement upon 60 days’ written notice for uncured material breach (or 30 days in the case of non-payment), or immediately upon written notice if the other party files a voluntary petition, is subject to a substantiated involuntary petition or for certain other insolvency events. HanAll may terminate the HanAll Agreement if we or our affiliates challenge the validity or enforceability of any of the licensed patents. We have commenced discussions with HanAll regarding the future disposition of batoclimab, including the potential return to HanAll of certain rights for batoclimab. In April 2026, we notified HanAll of our decision to indefinitely delay further development of batoclimab and focus our resources fully on IMVT-1402. Under the HanAll Agreement, we retain final decision-making authority over development and regulatory matters for licensed products in our Licensed Territory, and we believe we have satisfied our obligations under the HanAll Agreement, including with respect to batoclimab. HanAll may disagree with our interpretation of the agreement or our actions thereunder, and we may be unable to reach an agreement with HanAll regarding the future of batoclimab. This could result in a dispute with HanAll involving arbitration or litigation.

We are a Member of the Roivant Family of Companies

We are a majority-owned subsidiary of RSL and have benefited from our ability to leverage the Roivant model and the greater Roivant platform. The period of time between our formation and operational maturation was shortened based on the support from centralized Roivant functions available since creation. Consistent with its model, Roivant has provided us with operational assistance, as well as access to an embedded team of scientific experts, physicians and technologists to help optimize clinical development and commercial strategies. In the future, we may have the ability to benefit from Roivant’s economies of scale and scope, including but not limited to the opportunity to:

•leverage Roivant’s business development engine and vast network of industry relationships for the identification of, and access to, new assets and synergistic partnerships;

•enter channel partnerships with other members of the Roivant family of companies (including but not limited to technology-focused companies built by Roivant), with the goal of delivering efficiencies in the development and commercialization process;

•access Roivant’s human capital engine to recruit new employees from within and beyond the biopharmaceutical industry;

•enable our employees to participate in Roivant’s career development program which facilitates employee mobility across members of the Roivant family of companies;

•benefit from shared learnings best practices, and external industry relationships across the Roivant family of companies; and

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•derive certain benefits of scale upon becoming a commercial-stage company.

For a description of our transactions under agreements with related parties, refer to Part II, Item 8. Financial Statements and Supplementary Data, Note 5 – Related Party Transactions.

For a discussion on RSL’s significant ownership of our shares of common stock and related possible risks, please refer to