Thyroid hormone-binding protein, with a much higher binding affinity for triiodothyronine (T3) than for thyroxine (T4). Probably transports triiodothyronine from the bloodstream to the brain. Homotetramer. Dimer of dimers. In the homotetramer, subunits assemble around a central channel that can accommodate two ligand molecules. Interacts with rbp4. Detected in plasma (at protein level). Expressed during metamorphosis in tadpole liver, but not in tadpole brain nor adult liver. Between 1.5 and 3 days of development, also expressed in the mesoderm of the kidney. Expressed in tadpoles from premetamorphic stage 53 until the end of prometamorphic stage 60. Expression levels reach a maximum at prometamorphic stages 58 to 59, then decline gradually during metamorphic climax stages (61-66). Undetectable in adults. The estrogen ethinylestradiol (EE2) significantly decreases expression in both male and female livers. The environmental contaminants polychlorinated biphenyls (PCBs) result in an increase in gene expression and a delay in metamorphosis. The N-terminus strongly influences thyroid hormone-binding properties. A number of compounds can compete with and disrupt triiodothyronine (T3)-binding. Binds the synthetic estrogen diethylstilbestrol (DES) with the same affinity as T3. Phenolic and phenol compounds can also disrupt T3-binding, with brominated derivatives of bisphenol A (e.g. 3,3'5-tribromobisphenol A) having a higher binding affinity than the chlorinated derivatives (e.g. 3,3'5-trichlorobisphenol A), but with the bromophenols showing lower binding affinity than the chlorophenols. Belongs to the transthyretin family.