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Graves’ disease is an autoimmune disorder associated with the overproduction of thyroid hormones and is the most common cause of hyperthyroidism. Although GD can affect any age group or gender, it often occurs in women younger than 40 years of age. A conservative analysis of Inovalon claims data estimates that approximately 880,000 patients in the US suffer from GD and further analysis suggests that there are approximately 330,000 patients who have relapsed on anti-thyroid drugs (ATDs) and who have opted not to pursue surgery.

The disease is mediated by thyroid-stimulating IgG antibodies that cause the thyroid gland to produce an excess of thyroid hormones, resulting in systemic manifestations that affect multiple organs. Patients typically present with classic signs and symptoms of hyperthyroidism, such as heat intolerance, weight loss, anxiety, and frequent bowel movements. The disease can also manifest with ophthalmopathy (e.g., eye redness, swelling, bulging) or dermopathy (e.g., thickened, swollen, and discolored skin). If left untreated, patients may develop arrhythmias, heart failure, or life-threatening thyroid storms.

Thyroid eye disease (TED), also known as Graves’ ophthalmopathy, is an autoimmune disorder affecting the tissues around the eyes. It is a progressive and clinically variable disease that can become debilitating, disfiguring, or sight-threatening. The incidence of TED in the United States is estimated to be approximately 10 per 100,000. TED can be caused by IgG autoantibodies that form against the thyroid-stimulating hormone receptor (TSHR). These antibodies, which also cause Graves’ disease, target the extraocular space and result in clinical manifestations of the disease. Common signs of disease include proptosis (eye bulging), tearing, periorbital edema (swelling around the eyes), redness, dry eyes, eye irritation, and pain behind the eyes; in severe cases, double vision or vision loss may occur.

Myasthenia gravis (MG) ) is a rare, chronic autoimmune disorder characterized by weakness and fatigue of voluntary muscles. The clinical course of MG is variable but usually progressive, and patients tend to experience fluctuating symptoms. 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. For women, disease onset typically occurs around their 20s and 30s, whereas for men it peaks in their 50s and 60s. Overall, MG affects women more frequently than men. The disease is most often caused by autoantibodies that target the acetylcholine receptor or muscle-specific tyrosine kinase receptor at the neuromuscular junction, disrupting normal muscular function. Symptoms typically emerge in the eyes (e.g., drooping eyelids, double vision, blurred vision) and progress into the face, throat, or limbs. Some patients may experience life-threatening respiratory complications due to the weakening of muscles involved in respiration.

Chronic inflammatory demyelinating polyneuropathy (CIDP) is an autoimmune neurological disorder characterized by damage to the myelin sheaths or the nodes on nerve fibers of the peripheral nervous system. Though the clinical course of CIDP can be variable, it is typically a chronic progressive disease if left untreated. CIDP is a rare disease that can occur in any age group, with peak onset being in the 60s and 70s. CIDP affects men twice as much as women. 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 appears to be mediated, at least in some patients, by IgG antibodies that are directed against targets in the myelin sheath; however, the specific target of these antibodies is not yet established. The hallmark signs of CIDP are weakness, tingling sensations, or loss of sensation in the arms and legs that is usually symmetrical and gradually worsens.

Rheumatoid Arthritis (RA) is a chronic, progressive autoimmune disease that causes inflammation in the joints and surrounding tissues. RA is the most common systemic autoimmune disease. The exact cause of RA is not completely understood but is associated with a variety of genetic, hormonal and environmental factors. RA can occur at any age, but it is more commonly diagnosed in middle age and women are more likely to be affected than men.

Difficult-to-treat (D2T) RA is characterized by inadequate response to two or more biologic or targeted synthetic disease-modifying antirheumatic drugs (DMARDs), signs suggestive of active/progressive disease, and symptom management viewed as problematic by the physician or patient.

There are an estimated 70,000 people in the U.S. living with D2T RA. Several autoantibodies may be associated with D2T RA. Symptoms include joint pain, swelling, stiffness and tenderness, fatigue, and fever. Blood vessels and organs like the kidneys, heart, lungs and liver can also be affected by RA. Inadequate control of joint inflammation in RA may lead to irreversible joint erosion.

Sjögren’s disease (SjD) is a chronic autoimmune disease characterized by lymphocytic infiltration of the salivary and lacrimal glands. SjD may occur in isolation (primary SjD) or in association with another systemic autoimmune disease such as Rheumatoid Arthritis (secondary SjD). The estimated prevalence of primary SjD is approximately 290,000 affected individuals in the U.S. It is estimated that up to 30% of primary SjD patients have moderate-to-severe disease. Autoantibodies including anti-Ro/SSA and anti-La/SSB have been detected in approximately 50-70% of patients with primary SjD and can play crucial roles in both the diagnosis and prognosis of the disease. Symptoms include 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 joints and a variety of organ systems such as the skin, lungs, gastrointestinal tract, nervous system, or kidneys.

Cutaneous Lupus Erythematosus (CLE) is a rare, chronic skin disease characterized by skin-specific disease activity, inflammation and eventually scarring and discoloration. Subacute Cutaneous LE (SCLE) and Chronic Cutaneous LE (CCLE) are subtypes of CLE with distinct skin presentation, clinical course and high unmet medical need. The estimated prevalence of SCLE and CCLE is approximately 153,000 affected individuals 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. Triggered by sun exposure, CLE manifests as a recognizable rash and painful skin lesions, often with related symptoms such as itching, burning and alopecia.