Thyroid hormone analogs with selective actions through specific thyroid hormone 
receptor (TR) subtypes are of great interest. They might offer the possibility 
of mimicking physiological actions of thyroid hormone with receptor subtype or 
tissue specificity with therapeutic aims. They are also pharmacological tools to 
dissect biochemical pathways mediated by specific receptor subtypes, in a 
complementary way to mouse genetic modifications. In this work, we studied the 
in vivo activity in developing rats of two thyroid hormone agonists, the 
TRβ-selective GC-24 and the TRα-selective CO23. Our principal goal was to check 
whether these compounds were active in the rat brain. Analog activity was 
assessed by measuring the expression of thyroid hormone target genes in liver, 
heart, and brain, after administration to hypothyroid rats. GC-24 was very 
selective for TRβ and lacked activity on the brain. On the other hand, CO23 was 
active in liver, heart, and brain on genes regulated by either TRα or TRβ. This 
compound, previously shown to be TRα-selective in tadpoles, displayed no 
selectivity in the rat in vivo.