| Size | Price | Stock | Qty |
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| 5mg |
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| 10mg |
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| 50mg |
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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 via deiodination and binding to T4 glucuronide (T4G), but information on the formation of T4 sulfate (T4S) in vivo is scarce. We examined the excretion of T4G, T4S, T3, and rT3 glucuronide (T3G and rT3G) in the bile of control and 6-propyl-2-thiouracil (PTU) treated rats under pentobarbital anesthesia following intravenous injection of [125I]T4 at 0–8 hours or 17–18 hours. Radioactivity in bile, plasma, feces, and urine was analyzed using Sephadex LH-20 column chromatography and high-performance liquid chromatography (HPLC). PTU increased the total radioactivity excretion in bile by two-fold (26.6% vs. 15.0% dose at 0–8 hours; 2.0% vs. 1.0% dose at 17–18 hours). Seventeen to eighteen hours after T4 injection, the percentage of metabolites in the bile of rats in the control and PTU groups were as follows: T4G, 0.44% vs. 0.75%; T3G, 0.19% vs. 0.07%; rT3G, 0.02% vs. 0.15%; T4S, 0.06% vs. 0.32%. Similar results were obtained in the control group when bile was collected 7-8 hours after intravenous T4 injection. When bile was collected continuously for 8 hours immediately after T4 administration, the excretion rate of T3G was low, while the excretion rate of rT3G was high, possibly due to the prolonged experimental stress time. However, regardless of the bile collection time, PTU reduced the T3G/rT3G ratio by more than 24-fold and increased the excretion of T4S by 5-fold. In animals sacrificed 18 hours after T4 injection, PTU treatment increased plasma T4 retention by 50%, decreased urinary iodine excretion by 74%, and increased fecal radioactivity by 47%. No conjugates were detected in feces. The T4:T3:rT3 ratio in feces of rats in the control group and PTU treatment group was 70:18:2 and 68:7:6, respectively. The results showed that: 1) PTU did not affect the glucuronic acid clearance rate of T4; 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; 4) Inhibition of type I deiodinase of T4 can increase bile excretion of T4S. [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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