It stimulates the TR-beta receptor for thyroid hormones and thus increases energy expenditure.

[1][2] It has agonistic (thyromimetic) effects at myocardial tissue and pituitary, which results in 3,5-T2 suppressing TSH release.

[3][4] 3,5-T2 is an allosteric regulator of the cytochrome c oxidase, the complex IV of the electron transport chain.

It increases its activity by preventing the interaction of adenosine triphosphate (ATP) as an allosteric inhibitor.

[6][7][8][9] This could explain why patients with low T3 syndrome don't benefit from substitution therapy with thyroid hormones.