Reverse T3 (3,3’,5’-triiodothyronine or rT3) is the third most abundant iodothyronine circulating in human blood and is produced by the inner ring de-iodination of the pro-hormone thyroxine (T4). Unlike the more abundant and active metabolite T3, the measurement of serum rT3 is yet to find a routine clinical application. As rT3 binds weakly to the T3 thyroid nuclear hormone receptors it is thought to represent an inactive end-product of thyroid hormone metabolism, diverting T4 away from T3 production. The analysis of serum rT3 has, up until recently, been measured by competitive radioimmunoassay, but these methods have been superseded by mass-spectrometric methods which are less susceptible to interference from other more abundant iodothyronines. Serum rT3 concentration is increased as part of the non-thyroidal illness syndrome, and by administration of common medications such as amiodarone which inhibit the metabolism of rT3. Serum rT3 concentration is also affected by genetic conditions that affect the iodothyronine deiodinases, as well as thyroid transporters and transport proteins. Analysis of rT3 can provide a useful diagnostic fingerprint for these conditions. rT3 has been shown to bind extra-nuclear iodothyronine receptors with a potential role in cell proliferation however the clinical relevance of these findings awaits further study.

反向T3（3，3′′，5′-三碘甲状腺素或rT3）是人类血液中循环的第三多碘代甲状腺素，由激素原甲状腺素（T4）的内环去碘化产生。与更丰富和活性更高的代谢产物T3不同，血清rT3的测定尚未找到常规的临床应用。由于rT3与T3甲状腺核激素受体的结合较弱，因此它被认为代表了甲状腺激素代谢的非活性终产物，从而使T4脱离了T3的产生。直到最近，血清rT3的分析已通过竞争性放射免疫测定法进行了测定，但是这些方法已被质谱法所取代，质谱法不易受到其他更丰富的碘甲状腺素的干扰。血清rT3浓度升高是非甲状腺疾病综合征的一部分，并通过使用常见药物（如胺碘酮）抑制rT3的代谢。血清rT3浓度还受到影响碘甲状腺素脱碘酶，甲状腺转运蛋白和转运蛋白的遗传条件的影响。rT3的分析可以为这些情况提供有用的诊断指纹。rT3已显示与细胞外增殖具有潜在作用的核外碘甲状腺素受体结合，但是这些发现的临床意义尚待进一步研究。