TGP Levothyroxine Sodium Mechanism of Action

Pharmacology: Pharmacodynamics: Levothyroxine sodium is the monosodium salt of the levorotary isomer of thyroxine.
Thyroxine (T4) is a naturally occurring hormone produced by the thyroid gland and converted to the more active hormone triiodothyronine (T3) in peripheral tissues. The precise signals controlling the conversion of T4 to T3 within the cell are not known. The thyroid hormones are required for normal growth and development, particularly of the nervous system. They increase the resting or basal metabolic rate of the whole organism and have stimulatory effects on the heart, skeletal muscle, liver and kidney. Thyroid hormones enhance lipolysis and the utilization of carbohydrate.
Pharmacokinetics: Levothyroxine sodium is variably but adequately absorbed from the gastrointestinal tract following oral administration. Fasting increases absorption. Once in the circulation, levothyroxine sodium is extensively protein bound, principally to thyroxine-binding globulin (TBG) but also to a lesser extent to thyroxine-binding pre-albumin (TBPA) or to albumin.
Levothyroxine sodium has a plasma half-life in euthyroidism of about 6 to 7 days; the half-life is prolonged in hypothyroidism and reduced in hyperthyroidism.
Levothyroxine sodium is primarily metabolized in the liver and kidney to tri-iodothyronine (liothyronine) and, about 40%, to inactive reverse triiodothyronine (reverse T3) both of which undergo further deiodination to inactive metabolites. Further metabolites result from the deamination and decarboxylation of levothyroxine sodium to tetrac.
Levothyroxine sodium is reported to undergo enterohepatic recycling and excretion in the faeces.
The distribution of thyroid hormones across the placenta and into breast milk is discussed under Pregnancy and Breast feeding.