The core treatments for hyperthyroidism — antithyroid drugs, radioactive iodine, and surgery — remain unchanged in principle, but the fastest-moving area is the immune-targeted therapy of Graves' disease and its ocular complication.
Established therapy
Antithyroid drugs (methimazole preferred, with propylthiouracil reserved for the first trimester of pregnancy and thyroid storm) are first-line for Graves' disease; longer courses of five to ten years reduce recurrence compared with the standard 12–18 months, though recurrence after a standard course still approaches 50%. Radioactive iodine and thyroidectomy remain definitive options, chosen according to goitre size, eye disease, and patient preference. Key risks to counsel on include agranulocytosis and hepatotoxicity with antithyroid drugs, and worsening of active eye disease with radioactive iodine.
Thyroid eye disease: a therapeutic boom
Graves' orbitopathy (thyroid eye disease, TED) has been transformed by targeting the IGF-1 receptor. Teprotumumab, the first such agent (approved in 2020), substantially reduces proptosis and diplopia, at the cost of hyperglycemia, hearing changes, and muscle spasms, delivered as an eight-infusion course over 21 weeks. The field has since expanded rapidly: veligrotug (a full IGF-1R antagonist) was FDA-approved in 2026 on the basis of the THRIVE and THRIVE-2 trials — notable as the first TED therapy with labeled data in both active and chronic disease, and given as a shorter five-infusion, 12-week course. Behind it, the oral small-molecule IGF-1R inhibitor linsitinib (positive Phase 2b/3 LIDS trial) offers the prospect of a pill rather than an infusion, and subcutaneous long-acting antibodies (VRDN-003, lonigutamab) are in late-stage trials aiming for convenient home administration.
Toward disease modification in Graves' hyperthyroidism
For the underlying hyperthyroidism, rather than the eye disease, immunotherapies aimed at the TSH receptor and the autoimmune process remain investigational: the TSH-receptor-blocking antibody K1-70, the anti-CD40 antibody iscalimab, antigen-specific immunotherapy (ATX-GD-59), and FcRn inhibitors (such as batoclimab) that lower pathogenic TSH-receptor antibodies. These hold promise for genuinely modifying the disease rather than just controlling thyroid hormone output, but none has yet replaced antithyroid drugs, radioactive iodine, or surgery.
Further reading: hyperthyroidism review (Lee & Pearce, JAMA 2023); Graves' disease (Chaker et al., Lancet 2024); teprotumumab and IGF-1R therapies for TED (veligrotug THRIVE trials, 2024–2026; linsitinib LIDS, 2025).