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Subclinical hypothyroidism (SHT), characterized by normal thyroid hormone levels maintained by elevated thyrotropin (TSH), predisposes patients to health problems as they age. Some cases arise from mutations of the TSH receptor (TSHR) that confer TSH resistance. This resistance might be circumvented by TSHR agonists with different modes of binding compared with TSH. We hypothesized that the recently discovered small-molecule TSHR agonist C2, with its unique mode of receptor binding, would activate mutant TSHRs associated with SHT, facilitating their study.

thyroid

Small-Molecule Thyrotropin Receptor Agonist Activates Naturally Occurring Thyrotropin-Insensitive Mutants and Reveals Their Distinct Cyclic Adenosine Monophosphate Signal Persistence