Sobetirome is a selective agonist of the thyroid hormone receptor β (TRβ), with an EC50 of 0.16μM to TRβ-1[1]. Sobetirome readily crosses the blood–brain barrier and is widely used in studies of metabolic, demyelinating, and neurodegenerative diseases[2][3].
In vitro, Sobetirome (10nM; 4 days) reduces proliferation, slows migration, suppresses thyrosphere formation, increases NIS protein and functional iodide uptake, and up-regulates thyroid-differentiation genes in anaplastic thyroid cancer cell lines[4]. Treatment of A549 and MLE12 cells with Sobetirome (10-20nM; 6-16h) upregulates KLF2 and CEBPA, and suppresses the hyperplastic phenotype[5].
In vivo, Sobetirome (3μg/100g/day; i.p.; 6 weeks) reduced fat mass by 20% without increasing food intake or decreasing lean mass in adult female Wistar rats[6]. Sobetirome (97nM/kg/day; i.p.; 8 days) reduced serum cholesterol and triglycerides, elevated SR-BI protein levels, and increased bile acid excretion in euthyroid male C57BL/6 mice[7].
References:
[1] Gierach I, Li J, Wu WY, Grover GJ, Wood DW. Bacterial biosensors for screening isoform-selective ligands for human thyroid receptors α-1 and β-1. FEBS Open Bio. 2012;2:247-253.
[2] Tancevski I, Demetz E, Eller P. Sobetirome: a selective thyromimetic for the treatment of dyslipidemia. Recent Pat Cardiovasc Drug Discov. 2011;6(1):16-19.
[3] Saponaro F, Sestito S, Runfola M, Rapposelli S, Chiellini G. Selective Thyroid Hormone Receptor-Beta (TRβ) Agonists: New Perspectives for the Treatment of Metabolic and Neurodegenerative Disorders. Front Med (Lausanne). 2020;7:331.
[4] Gillis NE, Cozzens LM, Wilson ER, et al. TRβ Agonism Induces Tumor Suppression and Enhances Drug Efficacy in Anaplastic Thyroid Cancer in Female Mice. Endocrinology. 2023;164(10):bqad135.
[5] Pan X, Wang L, Yang J, et al. TRβ activation confers AT2-to-AT1 cell differentiation and anti-fibrosis during lung repair via KLF2 and CEBPA. Nat Commun. 2024;15(1):8672.
[6] Villicev CM, Freitas FR, Aoki MS, et al. Thyroid hormone receptor beta-specific agonist GC-1 increases energy expenditure and prevents fat-mass accumulation in rats. J Endocrinol. 2007;193(1):21-29.
[7] Johansson L, Rudling M, Scanlan TS, et al. Selective thyroid receptor modulation by GC-1 reduces serum lipids and stimulates steps of reverse cholesterol transport in euthyroid mice. Proc Natl Acad Sci U S A. 2005;102(29):10297-10302.
Sobetirome是一种甲状腺激素受体β(TRβ)选择性激动剂,对TRβ-1的EC50为0.16μM[1]。Sobetirome可自由穿过血脑屏障,广泛用于代谢性、脱髓鞘及神经退行性疾病研究[2][3]。
体外实验显示,Sobetirome(10nM;4天)可抑制未分化甲状腺癌细胞系的增殖、迁移和肿瘤球形成,增加NIS蛋白表达及功能性碘摄取,并上调甲状腺分化相关基因[4]。用Sobetirome(10-20nM;6-16小时)处理A549和MLE12细胞可上调KLF2和CEBPA,抑制细胞过度增殖表型[5]。
体内实验中,Sobetirome(3μg/100g/天;腹腔注射;6周)使成年雌性Wistar大鼠脂肪量减少20%,且不增加摄食量或降低瘦体重[6]。Sobetirome(97nM/kg/天;腹腔注射;8天)降低雄性C57BL/6小鼠血清胆固醇和甘油三酯,提升 SR-BI 蛋白水平并增加胆汁酸排泄[7]。
















