Biotech Innovator Targets TED

Amgen has a mission to deliver innovative medicines typically addressing conditions with limited treatment options.

TED is a serious, progressive, debilitating and potentially vision-threatening rare autoimmune disease.¹ It often occurs in people living with Graves’ disease, but is a distinct disease that is caused by autoantibodies activating an insulin-like growth factor-1 receptor (IGF-1R)-mediated signalling complex on cells within the retro-orbital space.^2,3

This leads to a cascade of negative effects, which may cause long-term, irreversible damage, including blindness. Signs and symptoms of TED may include dry eyes and grittiness; redness, swelling, and excessive tearing; eyelid retraction; proptosis; pressure and/or pain behind the eyes; and diplopia.^4,5

The real impact of TED goes beyond the eyes. The visible and nonvisible symptoms of TED can have a debilitating impact on patients’ emotional wellbeing, daily activities, and quality of life.^6–8

It can take some patients with TED up to five years to get an accurate diagnosis.⁹ By working together, ophthalmologists and endocrinologists may shorten the time to TED diagnosis. The American Thyroid Association and the European Thyroid Association consensus statement recommends the evaluation and management of TED using a multidisciplinary approach by healthcare professionals who specialise in TED.¹⁰

A spokesperson for Amgen said the company is now targeting TED, and is interested in building a network of physicians, specialising in treating TED.

The company is reaching out to ophthalmologists to better understand the needs, interests, and the type of patients ophthalmologists manage with rare and life impacting eye conditions, the spokesperson said.

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References

1. Barrio-Barrio J, Sabater AL, Galofré JC, et al. Graves’ Ophthalmopathy: VISA versus EUGOGO Classification, Assessment, and Management. J Ophthalmol. 2015;2015:249125. doi: 10.1155/2015/249125.
2. Weightman DR, Perros P, Sherif IH, Kendall-Taylor P. Autoantibodies to IGF-1 binding sites in thyroid associated ophthalmopathy. Autoimmunity. 1993;16(4):251-57. doi: 10.3109/08916939309014643.
3. Pritchard J, Han R, Smith TJ, et al. Immunoglobulin activation of T cell chemoattractant expression in fibroblasts from patients with Graves’ disease is mediated through the insulin-like growth factor I receptor pathway. J Immunol. 2003;170(12):6348-6354. doi: 10.4049/jimmunol.170.12.6348.
4. McKeag D, Lane C, Wiersinga WM, et al.; European Group on Graves’ Orbitopathy (EUGOGO). et al. Clinical features of dysthyroid optic neuropathy: a European Group on Graves’ Orbitopathy (EUGOGO) survey. Br J Ophthalmol. 2007;91(4):455-458. doi: 10.1136/bjo.2006.094607.
5. Bartalena L, Kahaly GJ, Wiersinga WM, et al.; European Group on Graves’ Orbitopathy (EUGOGO). The 2021 European Group on Graves’ orbitopathy (EUGOGO) clinical practice guidelines for the medical management of Graves’ orbitopathy. Eur J Endocrinol. 2021;185(4):G43-G67. doi: 10.1530/EJE-21-0479.
6. Cockerham KP, Padnick-Silver L, Holt RJ, et al., Quality of Life in Patients with Chronic Thyroid Eye Disease in the United States. Ophthalmol Ther. 2021;10(4):975-87. doi: 10.1007/s40123-021-00385-8.
7. Park JJ, Sullivan TJ, Perry-Keene DA, et al. Assessing quality of life in Australian patients with Graves’ ophthalmopathy. Br J Ophthalmol. 2004;88(1):75-78. doi: 10.1136/bjo.88.1.75.
8. Terwee CB, Gerding MN, Wiersinga WM, et al. Development of a disease specific quality of life questionnaire for patients with Graves’ ophthalmopathy: the GO-QOL. Br J Ophthalmol. 1998;82(7):773-79. doi: 10.1136/bjo.82.7.773.
9. Cockerham K, et al. Inactive thyroid eye disease patient journey. Presented at: Endocrine Society; June 15-18, 2023. Chicago, IL.
10. Burch HB, Perros P, Stan MN, et al. Management of thyroid eye disease: A consensus statement by the American Thyroid Association and the European Thyroid Association. Thyroid. 2022;32(12):1439-1470. doi: 10.1089/thy.2022.0251.