• 65 Mario Capecchi Drive, Salt Lake City, Utah,84132
  • 175N 400W, #C10, Orem, Utah,84057
  • 2255N 1700W, Layton, Utah,84041
  • 617 E. Riverside Drive, St. George, Utah,84790
  • 552 N. Dixie Drive, St. George, Utah,84770
  • Harley Street, London, ,W1G8
  • 1025 E. 3300 S., Suite B, Salt Lake City, Utah,84106



Thyroid-associated ophthalmopathy, a condition commonly associated with Graves’
disease, remains inadequately treated. Current medical therapies, which primarily
consist of glucocorticoids, have limited efficacy and present safety concerns. Inhibition
of the insulin-like growth factor I receptor (IGF-IR) is a new therapeutic
strategy to attenuate the underlying autoimmune pathogenesis of ophthalmopathy

Current treatments are inconsistently beneficial and often associated with side effects,

  • Previous clinical trials  suggest that high dose glucocorticoids, alone3-5 or with radiotherapy can reduce inflammation-related signs and symptoms in patients with active ophthalmopathy.
  • However, glucocorticoids and orbital radiotherapy minimally affect proptosis and can cause dose-limiting adverse reactions.5 In many patients


  • in patients with Graves’ disease, Immunoglobulins that activate insulin-like growth factor I (IGF-I) receptor (IGF-IR) signaling have been detected
  • IGF-I synergistically enhances the actions of thyrotropin  IGF-IR is a membraneespanning tyrosine kinase receptor with roles in development and metabolism
  • IGF-IR is overexpressed by orbital fibroblasts18 and by T cells and B cells in persons with Graves’ disease.
  • (IGF-I)  regulates immune function and thus might be targeted therapeutically in autoimmune diseases.

Mechanism of Action

Teprotumumab-trbw’s mechanism of action in patients with Thyroid Eye Disease has not been fully characterized. Teprotumumab-trbw binds to IGF-1R and blocks its activation and signaling.