| Size | Price | Stock | Qty |
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| 10mg |
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| 100mg |
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| Other Sizes |
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| Targets |
Endogenous Metabolite; synthetic form of the thyroid hormone thyroxine (T4)
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| ln Vitro |
The common ingredient in human serum and amniotic fluid is thyroxine sulfate (T4S). It is mostly produced by peripheral thyroxine and builds up when fetal type I 5-monodeiodination activity is low or is suppressed by medication, like iodates [1].
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| ln Vivo |
Thyroxine sulfate (T4S) has been found in significant concentrations in fetal sheep serum, bile, meconium, amniotic fluid, and allantoic fluid. T4S concentration in women's amniotic fluid at eighteen (19) and fifteen (15) weeks of gestation (25.5 ng/dL and 14.3 ng/dL, respectively). One day after ingesting one gram of ipodate, patients with hyperthyroidism showed a substantial increase in plasma T4S [1]. Prostaglandins are heavily sulfated in the body; biliary excretion of T4S is increased if their type I demyocardial actions are prevented [2]. A decreased demyocardial action of myocardial D1 during critical illness appears to play a role in the increased serum T4S levels, which were considerably higher than those of healthy subjects. function [3].
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| Enzyme Assay |
Recently, we identified significant amounts of thyroxine sulfate (T4S) in fetal sheep serum, meconium, bile, and amniotic and allantoic fluids. Little is known, however, about sulfate conjugation of thyroxine in humans. In this study, we employed a novel, sensitive T4S RIA to address this question. The rabbit antiserum was quite specific; T4, T3, rT3, and 3,3'-T2 showed less than 0.002% cross-reactivity. Other analogs cross-reacted less than 0.0001%. Only rT3S and T3S cross-reacted significantly (9.9% and 2.0%, respectively). The mean serum T4S concentration (ng/dL) was 8.6 in euthyroid subjects, 14.4 in hyperthyroid subjects, 5.0 in hypothyroid subjects, 5.9 in pregnancy, and 4.5 in patients with nonthyroid illnesses. T4S concentration in amniotic fluid from women at 18-19 weeks of gestation (25.5 ng/dL) was higher than that at 14-15 weeks of gestation (14.3 ng/dL). A significant rise in serum T4S was detected in hyperthyroid patients 1 day after ingestion of 1 g of ipodate. These data suggest that T4S is a normal component of human serum and amniotic fluid, and it is mostly derived from T4 peripherally and accumulates when type I 5'-monodeiodinating activity is low in fetuses or inhibited by drugs, such as ipodate[1].
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| Animal Protocol |
A total of 64 blood samples and 65 liver biopsies were obtained within minutes after death from 79 intensive care patients, randomized for intensive or conventional insulin treatment. Serum T4S and the activities of hepatic D1 and 3,3'-diiodothyronine (T2)-SULT and estrogen-SULT were determined.
Results: No differences in T4S or hepatic SULT activities were found between patients treated with intensive or with conventional insulin therapy. T4S levels were significantly elevated compared with healthy references. Furthermore, hepatic D1, but not SULT activity, showed a strong correlation with serum T4S (R = -0.53; P < 0.001) and T4S/T4 ratio (R = -0.62; P < 0.001). Cause of death was significantly correlated with hepatic T2- and estrogen-SULT activities (P < 0.01), with SULT activities being highest in the patients who died of severe brain damage and lowest in the patients who died of a cardiovascular collapse. A longer period of intensive care was associated with higher levels of T4S (P = 0.005), and high levels of bilirubin were associated with low T2-SULT (P = 0.04) activities and high levels of T4S (P < 0.001).
Conclusion: Serum T4S levels were clearly elevated compared with healthy references, and the decreased deiodination by liver D1 during critical illness appears to play a role in this increase in serum T4S levels.[3]
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| References |
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| Additional Infomation |
The liver metabolizes T4 by deiodination and conjugation to T4 glucuronide (T4G), but little information exists about the formation of T4 sulfate (T4S) in vivo. We have examined the excretion of T4G, T4S, T3 and rT3 glucuronide (T3G and rT3G) in bile, collected under pentobarbital anesthesia 0-8 h or 17-18 h after iv [125I]T4 injection to control and 6-propyl-2-thiouracil (PTU)-treated rats. Radioactivity in bile, plasma, feces, and urine was analyzed by Sephadex LH-20 chromatography and HPLC. PTU induced a 2-fold increase in the biliary excretion of total radioactivity (26.6% vs. 15.0% dose between 0-8 h; 2.0% vs. 1.0% dose between 17-18 h). Biliary metabolites, 17-18 h after T4 injection, in control vs. PTU rats amounted to (percent dose): T4G, 0.44 vs. 0.75; T3G, 0.19 vs. 0.07; rT3G, 0.02 vs. 0.15; and T4S, 0.06 vs. 0.32. Similar results were obtained for control rats when bile was collected between 7-8 h after iv T4. The excretion rate of T3G was lower and that of rT3G higher when bile was continuously collected for 8 h immediately after T4 administration, probably due to prolonged experimental stress. However, regardless of the period of bile collection, PTU induced a more than 24-fold decrease in the T3G/rT3G ratio and a 5-fold increase in T4S excretion. In the animals killed 18 h after T4 injection, PTU treatment increased plasma T4 retention by 50%, reduced urinary I- excretion by 74%, and increased fecal radioactivity by 47%. No conjugates were detected in feces, and the distribution of fecal T4:T3:rT3 was 70:18:2 in control and 68:7:6 in PTU-treated rats. The results indicate that 1) the glucuronidative clearance of T4 is not affected by PTU; 2) the T3G/rT3G ratio in bile is a sensitive indicator of type I deiodinase inhibition; 3) T4 undergoes significant sulfation in rats in vivo, and 4) biliary excretion of T4S is enhanced if its type I deiodination is inhibited.[2]
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| Molecular Formula |
C15H11I4NO7S
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|---|---|
| Molecular Weight |
856.93
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| Exact Mass |
856.644
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| Elemental Analysis |
C, 21.02; H, 1.29; I, 59.24; N, 1.63; O, 13.07; S, 3.74
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| CAS # |
77074-49-8
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| Related CAS # |
L-Thyroxine;51-48-9;L-Thyroxine sodium salt pentahydrate;6106-07-6
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| PubChem CID |
131742
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| Appearance |
White to off-white solid powder
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| LogP |
5.814
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| Hydrogen Bond Donor Count |
3
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| Hydrogen Bond Acceptor Count |
8
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| Rotatable Bond Count |
7
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| Heavy Atom Count |
28
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| Complexity |
625
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| Defined Atom Stereocenter Count |
1
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| SMILES |
C1=C(C=C(C(=C1I)OC2=CC(=C(C(=C2)I)OS(=O)(=O)O)I)I)C[C@@H](C(=O)O)N
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| InChi Key |
QYXIJUZWSSQICT-LBPRGKRZSA-N
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| InChi Code |
InChI=1S/C15H11I4NO7S/c16-8-1-6(3-12(20)15(21)22)2-9(17)13(8)26-7-4-10(18)14(11(19)5-7)27-28(23,24)25/h1-2,4-5,12H,3,20H2,(H,21,22)(H,23,24,25)/t12-/m0/s1
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| Chemical Name |
(2S)-2-amino-3-[4-(3,5-diiodo-4-sulfooxyphenoxy)-3,5-diiodophenyl]propanoic acid
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| Synonyms |
T4 Sulfate; Thyroxine sulphate; L-Tyrosine,O-[3,5-diiodo-4-(sulfooxy)phenyl]-3,5-diiodo-; Thyroxine-4-sulfate; T4 Sulfate; Thyroxine 4'-O-Sulfate; (2S)-2-amino-3-[4-(3,5-diiodo-4-sulfooxyphenoxy)-3,5-diiodophenyl]propanoic acid; Thyroxine sulfate
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: Please store this product in a sealed and protected environment, avoid exposure to moisture. |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
DMSO : ~140 mg/mL (~163.37 mM)
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 5.75 mg/mL (6.71 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 57.5 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: 5.75 mg/mL (6.71 mM) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), suspension solution; with ultrasonication. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 57.5 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly. View More
Solubility in Formulation 3: ≥ 2.58 mg/mL (3.01 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 1.1670 mL | 5.8348 mL | 11.6696 mL | |
| 5 mM | 0.2334 mL | 1.1670 mL | 2.3339 mL | |
| 10 mM | 0.1167 mL | 0.5835 mL | 1.1670 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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