ArticleThe Journal of clinical endocrinology and metabolism2022
Inhibition of TSH/IGF-1 Receptor Crosstalk by Teprotumumab as a Treatment Modality of Thyroid Eye Disease.
Article in The Journal of clinical endocrinology and metabolism, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.
- Bayesian network analysis of drug treatment strategies for thyroid associated ophthalmopathy.International ophthalmology · 2024Pooled it
- Metformin inhibits PDGFβ signaling to suppress hyaluronan and cytokine production in thyroid eye disease.Experimental eye research · 2026Article
- IL-11 receptor is a novel target for drug development with pharmacological activity in fibro-inflammatory disease.Scientific reports · 2026Review
- Transcriptomic and Neuroimaging Decoding of Brain-Immune Crosstalk in Thyroid Eye Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Teprotumumab for Thyroid Eye Disease: Efficacy and Impact on Orbital Decompression Utilization.Laryngoscope investigative otolaryngology · 2026Article
- Marked and reversible circulating insulin-like growth factor-1 elevation during teprotumumab N01 treatment for thyroid eye disease with limited correspondence to glycemic changes.Frontiers in endocrinology · 2026Article
- Transcriptomic profiling of thyroid eye disease orbital fibroblasts identifies sorafenib as a novel therapeutic.Frontiers in endocrinology · 2026Article
- Unravelling the pathogenic mechanisms in Graves' orbitopathy.European thyroid journal · 2025Review
- Safety, pharmacokinetics, and potential benefits of TSH-receptor-specific monoclonal autoantibody K1-70Endocrine journal · 2025Article
- Teprotumumab for Thyroid Eye Disease: Mechanism, Clinical Efficacy, and Current Challenges.Antibodies (Basel, Switzerland) · 2025Review
- Targeted immunotherapies for Graves' thyroidal & orbital diseases.Frontiers in immunology · 2025Review
- Advances of IGF-1R inhibitors in Graves' ophthalmopathy.International ophthalmology · 2024Review
- Linsitinib inhibits proliferation and induces apoptosis of both IGF-1R and TSH-R expressing cells.Frontiers in immunology · 2024Article
- Current and promising therapies based on the pathogenesis of Graves' ophthalmopathy.Frontiers in pharmacology · 2023Review
- A review of TSHR- and IGF-1R-related pathogenesis and treatment of Graves' orbitopathy.Frontiers in immunology · 2023Review
- Current concepts regarding Graves' orbitopathy.Journal of internal medicine · 2022Review
- Teprotumumab: A Review in Thyroid Eye Disease.Drugs · 2022Review
- Research progress on the pathogenesis of Graves' ophthalmopathy: Based on immunity, noncoding RNA and exosomes.Frontiers in immunology · 2022Review
- The Mysterious Universe of the TSH Receptor.Frontiers in endocrinology · 2022Review
- Therapeutic targets for fibro-inflammation in Graves' orbitopathy.Taiwan journal of ophthalmologyReview
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
contextWe previously presented evidence that TSH receptor (TSHR)-stimulating autoantibodies (TSAbs) bind to and activate TSHRs but do not bind to IGF1 receptors (IGF1Rs). Nevertheless, we showed that IGF1Rs were involved in thyroid eye disease (TED) pathogenesis because TSAbs activated crosstalk between TSHR and IGF1R. Teprotumumab, originally generated to inhibit IGF1 binding to IGF1R, was recently approved for the treatment of TED (Tepezza).
objectiveTo investigate the role of TSHR/IGF1R crosstalk in teprotumumab treatment of TED.
designWe used orbital fibroblasts from patients with TED (TEDOFs) and measured stimulated hyaluronan (HA) secretion as a measure of orbital fibroblast activation by TED immunoglobulins (TED-Igs) and monoclonal TSAb M22. We previously showed that M22, which does not bind to IGF1R, stimulated HA in a biphasic dose-response with the higher potency phase dependent on TSHR/IGF1R crosstalk and the lower potency phase independent of IGF1R. Stimulation by TED-Igs and M22 was measured in the absence or presence of teprotumumab biosimilar (Tepro) or K1-70, an antibody that inhibits TSHR.
resultsWe show: (1) Tepro dose-dependently inhibits stimulation by TED-Igs; (2) Tepro does not bind to TSHRs; (3) Tepro inhibits IGF1R-dependent M22-induced HA production, which is mediated by TSHR/IGF1R crosstalk, but not IGF1R-independent M22 stimulation; and (4) β-arrestin 1 knockdown, which blocks TSHR/IGF1R crosstalk and prevents Tepro inhibition of HA production by M22 and by a pool of TED-Igs.
conclusionWe conclude that Tepro inhibits HA production by TEDOFs by inhibiting TSHR/IGF1R crosstalk and suggest that inhibition of TSHR/IGF1R crosstalk is the mechanism of its action in treating TED.
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