ArticleEndocrinology2025
Inhibition of TSH Receptor Expression by a Cyclotriazadisulfonamide as a Potential Treatment of Graves Hyperthyroidism.
Article in Endocrinology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Cytokines and drugs targeting cytokines in Graves' disease and thyroid eye disease.Frontiers in immunology · 2026Review
- Targeted downmodulation of OXTR and Cx43 in the myometrium by SERTIs as a novel tocolytic strategy.Uterine research · 2026Article
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Authors and funding
10 authors.
Funding
Abstract
Graves hyperthyroidism (GH) is a condition in which autoantibodies chronically activate the thyrotropin (TSH) receptor (TSHR). TSHR is one of the few G protein-coupled receptors (GPCRs) predicted to have a signal peptide, making it a potential target for cyclotriazadisulfonamide (CADA) compounds. We sought to determine whether a small-molecule drug that selectively induces nascent protein degradation could decrease TSHR expression in vitro and in vivo at therapeutically relevant levels. We tested several CADA compounds for their ability to reduce TSHR surface expression in HEK 293 cells overexpressing human TSHR (HEK-TSHR cells) using flow cytometry. Inhibition of downstream cAMP production and thyroglobulin (Tg) secretion were measured in HEK-TSHR and human thyrocytes, respectively. Follow-up studies in VGD040-treated BALB/c mice assessed plasma levels of free T4 in response to TSH stimulation. Among a number of CADA analogues, VGD040 decreased TSHR at the surface of HEK-TSHR cells. VGD040 was found to be selective toward TSHR compared to similar glycoprotein hormone receptors. In human thyrocytes, reduction of TSHR surface expression by VGD040 decreased cyclic adenosine monophosphate production and Tg secretion. Most important, VGD040 decreased TH secretion in mice without apparent toxicity at the effective dose studied. VGD040 is an important new lead with potential for developing safe drug treatments for GH.
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