Therapeutic product candidates
Graves’ disease (GD) is an autoimmune disorder caused by auto-reactive T and B lymphocytes targeting the primary auto-antigen, the Thyroid Stimulating Hormone Receptor (TSHR).
TSHR is a G-protein-coupled receptor on thyroid follicular cells in the thyroid gland that stimulates the production of thyroxine (T4) and triiodothyronine (T3) via a cAMP signal cascade upon binding of its ligand, the thyroid-stimulating hormone. Upon internalization, degradation and presentation of the TSHR by antigen presenting cells, T cells become activated and interact with auto reactive B cells, which in turn produce stimulating agonistic auto-antibodies directed against this receptor. These thyroid-stimulating antibodies bind to the same receptor pocket as the thyroid-stimulating hormone, activating the TSHR mediated signal transduction and leading to the production of excess thyroid hormone from the thyroid gland and thyroid growth.
An overactive thyroid gland can be related with hyperthyroid symptoms such as increased heart rate, muscle weakness, disturbed sleep, and irritability. It can also affect the eyes, causing bulging eyes (proptosis). It affects multiple systems of the body, including the skin, heart, circulation and nervous system.
There is a strong hereditary component linked to GD; when one identical twin has Graves' disease, the other twin will have it 25% of the time. It affects up to 2% of the female population, sometimes appears after childbirth, and is five to ten times as common in women as in men.
If you would like to know more, you can visit our Clinical Trials for Graves' Disease page.