High-Quality Raw Materials Levothyroxine Sodium Thyroid (CAS: 55-03-8)

Levothyroxine sodium;L-Thyroxine Sodium (Steroids) 
Aliases:L-Thyroxine sodium salt; sodium 4-o-(4-hydroxy-3,5-diiodophenyl)-3,5-diiodo-l-tyrosine; sodium (2S)-2-amino-3-[4-(4-hydroxy-3,5-diiodophenoxy)-3,5-diiodophenyl]propanoate hydrate (1:1:5); sodium 2-amino-3-[4-(4-hydroxy-3,5-diiodophenoxy)-3,5-diiodophenyl]propanoate; tyrosine, O-(4-hydroxy-3,5-diiodophenyl)-3,5-diiodo-, sodium salt (1:1)
CAS:55-03-8 
Appearance:almost whtie powder 
EINECS:200-221-4
MF:C15H11I4NNaO4
MW:799.8592
Melting point: 207-210 
Description:

The synthetic four iodine thyroid original acid sodium salt is similar to the role and application of thyroid tablets, oral absorption of 50%, the onset is slow, steady, similar to the physiological hormone replacement treatment for thyroid hormones.
Euthyrox contains 25 ~ 300 μg of T4 and thyroid to produce the same synthetic thyroxine T4. Levothyroxine (iv triiodothyronine, T4) synthesis and secretion by the human thyroid. Thyroxine almost all body tissues have stimulant by increasing the synthesis of proteins and enzymes or enzyme activation, split human embryos and neonatal cells, growth and development. Adult organs physiological role of hormones and energy metabolism, body temperature regulation and protein metabolism of carbohydrates and fat and so on. Thyroxine increased heart rate and cardiac positive inotropic effect, and can increase cardiac output. Levothyroxine sometimes called prohormone, almost all of it is synthesized by the thyroid, iodine thyroid original acid than three metabolic activity is weak. Dependent on thyroid hormone T4 to ensure normal human metabolism, deiodination into T3 (three triiodothyronine). Approximately 45% of the T4 is converted to T3 in peripheral tissues. 80% of thyroid tissue outside T3 by conversion from T4 in. T4 T3 hormone serves as a primary role in thyroid hormone conversion mechanisms. When thyroid hormone deficiency (hypothyroidism), the pituitary secretion of thyroid-stimulating hormone (TSH) increased, thereby promoting the synthesis and secretion of thyroid T4. If too much thyroid hormone (hyperthyroidism), anterior pituitary TSH synthesis and secretion was inhibited. Currently blood TSH concentration has been considered the primary indicator of thyroid hormone-dependent metabolic conditions. Euthyrox endocrine feedback mechanism, inhibiting the secretion of TSH, thereby to reduce the thyroid TSH receptor and blood TSH receptor antibodies, play a role in the prevention of recurrence of hyperthyroidism. Euthyrox also can effectively suppress excessive secretion of pituitary TSH, so as to achieve the role of prevention of postoperative recurrence of goiter.
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