TOURMALINE S BUSINESS Overview We are a late-stage clinical biotechnology company developing transformative medicines to dramatically improve the lives of patients with life-altering immune and inflammatory diseases. In

TOURMALINE S BUSINESS

We are a late-stage clinical biotechnology company developing transformative medicines to dramatically improve the lives of patients

with life-altering immune and inflammatory diseases. In doing so, we seek to identify and develop medicines that have the potential to establish new standards-of-care in

areas of high unmet medical need.

Our initial product candidate is TOUR006, a fully human monoclonal antibody that selectively binds to interleukin-6 ( IL-6 ), a key proinflammatory cytokine involved in the pathogenesis of many autoimmune and inflammatory disorders. The

anti-IL-6 and anti-IL-6 receptor

( IL-6R ) antibody class ( IL-6 class ) has over two decades of clinical and commercial experience treating over a million patients with a variety of

autoimmune and inflammatory diseases. To date, four anti-IL-6 or anti-IL-6R antibodies

have been approved in the United States. These four anti-IL-6 or anti-IL-6R antibodies

together generated more than $3.5 billion in global sales in 2022.

TOUR006 is a long-acting anti-IL-6 antibody which we believe has best-in-class properties including a high binding affinity to IL-6, long half-life, and low observed immunogenicity. These characteristics may allow TOUR006 to achieve substantial IL-6 pathway suppression with relatively low amounts of

drug exposure, potentially enabling delivery in a convenient, low volume, infrequently administered, subcutaneous injection.

pursuing two strategic paths for TOUR006, the first of which we refer to as FcRn+ . Neonatal Fc receptor ( FcRn ) inhibitors have emerged as a novel therapeutic class to treat autoantibody-driven diseases. However, FcRn

inhibitors have significant limitations including suboptimal efficacy, lack of durable efficacy, high burden dosing profile, and an unknown long-term safety profile. We believe TOUR006 has the potential to be a superior therapy for a wide range of

autoantibody-driven diseases, compared to FcRn inhibitors. We have identified thyroid eye disease ( TED ) as our beachhead indication for our FcRn+ strategy. TED is an autoimmune disease characterized by autoantibody-mediated activation of

the tissues surrounding the eye, causing inflammation and disfigurement which can be sight-threatening in severe cases. We have identified a substantial body of published clinical observations characterizing the beneficial off-label use of currently marketed IL-6 pathway inhibitors, namely Actemra (tocilizumab), an anti-IL-6R monoclonal antibody, in reducing inflammation, eye-bulging, and levels of autoantibodies in patients with TED. However, no

formal, industry-sponsored development effort studying the IL-6 class for the treatment of TED has been completed to date.

We are currently evaluating TOUR006 in a pivotal Phase 2b trial in first-line TED, which we refer to as the spiriTED trial. We initiated the

spiriTED trial in September 2023 and expect to report topline data in the first half of 2025. Further, we expect to commence a pivotal Phase 3 trial of TOUR006 in first-line TED in 2024, with topline data expected in 2026. This second pivotal trial

will replace the previously-planned open-label basket study in additional TED patient cohorts.

Our second strategic path is

cardiovascular inflammation. We believe TOUR006 has the potential to transform the care of high-risk patients by targeting key inflammatory pathways driving cardiovascular disease. Atherosclerotic cardiovascular disease ( ASCVD ) is a

leading cause of death globally. Preventing major adverse cardiovascular events ( MACE ), such as death, nonfatal myocardial infarction or nonfatal stroke, has the potential to significantly reduce global cardiovascular disease burden. IL-6 has been identified as a promising drug target for addressing the risk of MACE in ASCVD and multiple external Phase 3 cardiovascular outcome trials investigating IL-6

blockade are ongoing. We believe that TOUR006 potentially offers a meaningfully enhanced product profile to these competitor programs with a potential for subcutaneous dosing once every three months. As previously announced in January 2024, we have

reached alignment with the U.S. Food and Drug Administration ( FDA ) on the ASCVD clinical development program, including a Phase 2 trial evaluating the reduction of C-reactive protein

( CRP ), a validated biomarker for inflammation, with quarterly dosing of TOUR006 in patients with elevated cardiovascular risk. This trial is targeted to commence in the first half of 2024, and we expect to report topline data in the

first half of 2025. Pending successful initiation and completion, positive results from the Phase 2 trial are expected to position us to be ready in 2025 to commence a pivotal Phase 3 trial for TOUR006 in cardiovascular disease.

The following figure summarizes our current development programs:

Note: Hatched bars represent trials that have not yet commenced. The timing of regulatory

submissions and clinical trial milestones are subject to change and additional discussion with the FDA

As can be seen in the chart above, we plan to identify additional indication opportunities for TOUR006. In

addition, we continue to evaluate new in-licensing and acquisition opportunities for assets that we believe have standard-of-care

changing potential for patients with immune, inflammatory and other diseases.

We seek to identify and develop transformative medicines that have the potential to establish new standards-of-care in areas of high unmet medical need. We plan to apply a human data-focused approach to indication selection, identifying diseases where IL-6 pathway

inhibitors have been used successfully in practice despite limited formal industry development and where we believe TOUR006 can potentially bring significant improvements over existing standards of care. We also plan to leverage insights from

clinical trials of competitor IL-6 pathway inhibitor programs with a goal of rapidly bringing TOUR006 into indications that have already been externally de-risked. We

believe this focus on leveraging existing human data could allow us identify indications with high potential for clinical and commercial success and can maximize the value of TOUR006.

The key elements of our strategy include:

Scientific Background

Autoimmune Disorders

The immune system plays a critical role in nearly every aspect of human health. In addition to providing

protection against external pathogens such as viruses, bacteria, and fungi, the immune system is involved in the surveillance and elimination of internal threats such as pre-malignant and malignant lesions.

Beyond providing protection, the immune system regulates key regenerative and homeostatic processes in healthy individuals on an ongoing basis.

In patients with autoimmune diseases, the immune system inappropriately recognizes and attacks normal healthy tissues, resulting in

inflammation, organ damage, debilitating symptoms and, in severe cases, death. To date over 80 autoimmune diseases have been documented, each with a wide range of clinical manifestations, pathophysiology, and severities. It is estimated that

approximately 320 million people globally and approximately 24 million people in the United States are affected by an autoimmune disease.

The standard-of-care for immune-related disorders has been

immunomodulatory and anti-inflammatory agents that are intended to prevent and control immune system overactivity. Recently, improved research and development efforts have resulted in targeted therapies that have shown greater efficacy while

reducing treatment-limiting side effects, including those associated with broad immunosuppression. However, despite these advances, many patients with autoimmune diseases continue to be underserved. Existing targeted therapies may not fully address

underlying disease biology or may have meaningful side effects.

IL-6: Mechanism of Action

IL-6 is a pleiotropic cytokine which plays a key role in driving inflammation

and cellular and humoral immune responses. In typical immunity, IL-6 is produced by various immune cells, including monocytes, macrophages, T cells, and B cells as well as fibroblasts and other non-immune cells, in response to cellular stresses and proinflammatory signals. Increased levels of IL-6 induce the acute phase inflammatory response, activating the innate

immune system and providing a nonspecific response to infections and pathogens. IL-6 also plays a key role in activating the adaptive immune system by inducing proliferation and differentiation of B and T

cells and release of additional inflammatory signals. IL-6 is a critical stimulation factor for B-cell and plasma cell survival, promoting antibody production. In

addition, IL-6 serves as a key differentiating factor for T-cells, specifically promoting the development of Th17 cells and T follicular helper ( Tfh ) cells.

Tfh cells also serve to promote B cell proliferation and antibody production.

Binding of IL-6 to IL-6R leads to recruitment of gp130, resulting in the downstream activation of a JAK/STAT-mediated signaling pathway which, depending on cell type, results in survival, proliferation, differentiation, and/or release

of additional inflammatory signals. IL-6 is the exclusive binding partner of IL-6R and inhibition of either the ligand or the receptor blocks this signaling pathway.

Clinical studies of IL-6 and IL-6R inhibitors have similarly produced observed reductions in C-reactive protein

( CRP ), an acute phase protein commonly used as a biomarker for IL-6 pathway activation and inflammation.

IL-6 mediates many autoimmune pathways including production of

autoantibodies and proliferation of autoreactive T-cells; TOUR006 inhibits IL-6 from driving these pathways

Given the multiple roles of IL-6 in inflammation and immune cell activation, inhibiting IL-6 has emerged as an important therapeutic strategy for managing a wide range of immune disorders, including diseases caused by autoantibodies. Based on a review of the scientific literature and publicly reported

clinical evidence, we believe that IL-6 may contribute to the disease pathobiology of over 30 diseases which may affect over 25 million patients in the U.S., including, but not limited to, those listed in

the following figure:

Currently, there are four FDA approved therapies targeting the IL-6/IL-6R

pathway: ACTEMRA (tocilizumab), KEVZARA (sarilumab), ENSPRYNG

(satralizumab-mwge), and SYLVANT (siltuximab). Collectively, these therapies have been approved for nine indications: rheumatoid arthritis ( RA ), giant cell arteritis, juvenile

idiopathic arthritis, polymyalgia rheumatica, cytokine release syndrome, multicentric Castleman s disease, neuromyelitis optica spectrum disorder ( NMOSD ), systemic sclerosis associated interstitial lung disease, and COVID-19. Collectively, these four anti-IL-6 or

anti-IL-6R antibodies generated more than $3.5 billion in global sales in 2022.

Our Product Candidate: TOUR006

We licensed TOUR006, previously known as PF-04236921, from Pfizer Inc. ( Pfizer ) in May

2022. TOUR006 was originally developed from a hybridoma cell line using the Medarex UltiMAb transgenic mouse platform. The UltiMAb platform produces fully human monoclonal antibodies. The IgG1 isotype of the original clone was switched by Pfizer to

IgG2 to reduce Fc receptor binding, thereby creating TOUR006.

To date, TOUR006 has been tested by Pfizer in 448 subjects across six

clinical trials, including over 400 autoimmune patients with RA, systemic lupus erythematosus ( SLE ), or Crohn s disease ( CD ). Across these studies, TOUR006 was generally well-tolerated, consistent with other therapies in

the IL-6 class, and had low rates of anti- drug antibodies ( ADAs ) in the 448 subjects tested. We seek to leverage this large existing clinical dataset for TOUR006, along with the extensive clinical

experience with the IL-6 class, in our development programs. We believe this existing clinical dataset for TOUR006 serves as a basis for which the FDA will allow us to move directly into additional Phase 2

and/or pivotal trials in future selected development indications. To date, the FDA has cleared our Investigational New Drug application ( IND ) to support the initiation of the ongoing pivotal Phase 2b spiriTED study, and we have reached

alignment with the FDA on a Phase 2 study in patients with elevated cardiovascular risk.

Potential Benefits of TOUR006

We believe TOUR006 presents a potentially best-in-class

product profile for a wide range of indications where IL-6 biology is implicated. The potential benefits of TOUR006 may include:

AE: Autoimmune Encephalitis; ASCVD: Atherosclerotic Cardiovascular Disease;

COVID-19: Coronavirus Disease 2019; CRS: Cytokine Release Syndrome; GCA: Giant Cell Arteritis; MCD: Multicentric Castleman s Disease; MG: Myasthenia Gravis; MOGAD: Myelin Oligodendrocyte Glycoprotein

Antibody-Associated Disease; NMOSD: Neuromyelitis Optica Spectrum Disorder; PJIA: Polyarticular Juvenile Idiopathic Arthritis; PMR: Polymyalgia Rheumatica; RA: Rheumatoid Arthritis; SJIA: Systemic Juvenile Idiopathic Arthritis; SSc-ILD: Systemic

Sclerosis-Associated Interstitial Lung Disease; 1 As reported in the label or FDA review documents of the approved products; no head-to-head studies have been conducted

against the approved products shown here, which have each been evaluated in indications other than those we are pursuing

Our FcRn+ Strategy: IL-6 Inhibition for the Treatment of Autoantibody-Driven Disorders

Autoantibody driven disorders are

a type of autoimmune disease in which antibodies erroneously recognize and bind to normal cell-surface or circulating antigens. The binding of autoantibodies to their respective targets can result in inflammation, receptor activation, and further

immune system attack. In some diseases, autoantibodies directed against cell surface receptors may have agonistic or antagonistic activity and aberrantly modulate signaling pathways. Approximately 2.5% of the world s population live with a

disease where autoantibodies are believed to play a role. These disorders impact multiple organs and systems and include TED, Graves disease, NMOSD, MG, and chronic inflammatory demyelinating polyneuropathy, among many others.

Therapeutic strategies that reduce autoantibody levels have been observed to produce clinical benefit in multiple indications. For example,

FcRn inhibition has emerged as a novel therapeutic modality to treat patients with autoantibody driven disorders. Treatment with FcRn inhibitors results in non-disease specific depletion of circulating

antibodies and has been observed to reduce autoantibody levels in patients with autoantibody driven disorders by approximately 60-70%.

Despite these advances, we believe that FcRn inhibitors may have the following limitations:

Given the importance of IL-6 signaling for antibody production and plasma cell