3,5-Diiodo-L-thyronine
(Synonyms: 3,5-二碘-L-甲状腺素,3,5-Diiodo-L-thyronine) 目录号 : GC49427
A thyroid hormone metabolite
Cas No.:1041-01-6
Sample solution is provided at 25 µL, 10mM.
;)
,-1-7$$$37316672.jpg');)
;)
;)
$$$36806353.jpg');)
;33(7)%EF%BC%9A546-561$$$37156877.jpg');)
;)
;)
;)
%201124-1138.$$$35908550.jpg');)
%20766-780.$$$37100057.jpg');)
%20418-432.$$$36893736.jpg');)
%EF%BC%9A-240-255.$$$35108512.jpg');)
533-545$$$36543525.jpg');)
%201-13.$$$36600053.jpg');)
;)
Quality Control & SDS
- View current batch:
- Purity: >95.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
3,5-Diiodo-L-thyronine (3,5-T2) is a thyroid hormone metabolite.1 It binds to thyroid hormone receptor α1 (TRα1), TRβ1, and TRβ2 (EC50s = 0.8, 0.79, and 0.1 µM, respectively, in cell-free assays).2 3,5-T2 (1 pM) stimulates oxygen consumption in perfused livers isolated from rats with hypothyroidism induced by sodium iodide.3 It reduces subcutaneous and epididymal fat mass, as well as decreases serum leptin and cholesterol levels, without affecting body weight in high-fat diet-induced obese mice when administered at a dose of 2.5 µg/g per day.1
1.Jonas, W., Lietzow, J., Wohlgemuth, F., et al.3,5-Diiodo-L-thyronine (3,5-T2) exerts thyromimetic effects on hypothalamus-pituitary-thyroid axis, body composition, and energy metabolism in male diet-induced obese miceEndocrinology156(1)389-399(2015) 2.Ball, S.G., Sokolov, J., and Chin, W.W.3,5-Diiodo-L-thyronine (T2) has selective thyromimetic effects in vivo and in vitroJ. Mol. Endocrinol.19(2)137-147(1997) 3.Horst, C., Rokos, H., and Seitz, H.J.Rapid stimulation of hepatic oxygen consumption by 3,5-di-iodo-?-thyronineBiochem. J.261(3)945-950(1989)
| Cas No. | 1041-01-6 | SDF | |
| 别名 | 3,5-二碘-L-甲状腺素,3,5-Diiodo-L-thyronine | ||
| Canonical SMILES | IC(C=C(C=C1I)C[C@H](N)C(O)=O)=C1OC2=CC=C(C=C2)O | ||
| 分子式 | C15H13I2NO4 | 分子量 | 525.1 |
| 溶解度 | 22.22 mg/mL in Ethanol(ultrasonic and adjust pH to 2 with 1M HCl) | 储存条件 | -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
||
| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
 |
1 mg | 5 mg | 10 mg |
| 1 mM | 1.9044 mL | 9.522 mL | 19.044 mL |
| 5 mM | 0.3809 mL | 1.9044 mL | 3.8088 mL |
| 10 mM | 0.1904 mL | 0.9522 mL | 1.9044 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
3,5-Diiodo-L-thyronine: A Possible Pharmacological Agent?
Curr Drug Deliv 2016;13(3):330-8.PMID:26593437DOI:10.2174/1567201813666151123124340.
Overweight and obesity related metabolic disorders, commonly sharing a pathogenic excess of body adiposity, are world-wide epidemic leading to increasing morbidity and mortality. The related conditions include, among the others, liver steatosis, insulin resistance, and cardiovascular risk. Effective and safe anti-obesity drugs are still needed. Likely without undesirable side effects, an ideal treatment should be able to counteract the numerous causes associated with excess of body adiposity putatively modulating the delicate balance between feeding and energy expenditure, untimely controlling the adipose mass. In the past, thyroid hormones have been tested in reducing weight and lipid accumulation, however, the concomitant induction of a thyrotoxicosis state limited their use. Recent studies in rodents revealed that 3,5- diiodo-L-thyronine (T2), an endogenous metabolite of thyroid hormones, exhibits interesting metabolic activities. Specifically, when exogenously administered, T2 increases the resting metabolic rate and elicits short-term beneficial hypolipidemic effects, without being thyrotoxic, at lest in high fat diet fed rats. Now, a matter of interest is whether T2 can be considered or not a potential anti-obesity pharmacological agent. Actually, very few studies have been performed as far as it concerns the effects of T2 in humans and further analyses on larger cohorts to test time of use- and dose-dependent actions as well as the putative occurrence of T2 induced undesirable side effects, are needed. Here, an updated overview of the current literature on T2 bioactivity is furnished with a particular focus on those effects which may be defined "beneficial" vs. "deleterious" ones above all in view of its putative pharmacological use.
Genomic and Non-Genomic Mechanisms of Action of Thyroid Hormones and Their Catabolite 3,5-Diiodo-L-thyronine in Mammals
Int J Mol Sci 2020 Jun 10;21(11):4140.PMID:32532017DOI:10.3390/ijms21114140.
Since the realization that the cellular homologs of a gene found in the retrovirus that contributes to erythroblastosis in birds (v-erbA), i.e. the proto-oncogene c-erbA encodes the nuclear receptors for thyroid hormones (THs), most of the interest for THs focalized on their ability to control gene transcription. It was found, indeed, that, by regulating gene expression in many tissues, these hormones could mediate critical events both in development and in adult organisms. Among their effects, much attention was given to their ability to increase energy expenditure, and they were early proposed as anti-obesity drugs. However, their clinical use has been strongly challenged by the concomitant onset of toxic effects, especially on the heart. Notably, it has been clearly demonstrated that, besides their direct action on transcription (genomic effects), THs also have non-genomic effects, mediated by cell membrane and/or mitochondrial binding sites, and sometimes triggered by their endogenous catabolites. Among these latter molecules, 3,5-Diiodo-L-thyronine (3,5-T2) has been attracting increasing interest because some of its metabolic effects are similar to those induced by T3, but it seems to be safer. The main target of 3,5-T2 appears to be the mitochondria, and it has been hypothesized that, by acting mainly on mitochondrial function and oxidative stress, 3,5-T2 might prevent and revert tissue damages and hepatic steatosis induced by a hyper-lipid diet, while concomitantly reducing the circulating levels of low density lipoproteins (LDL) and triglycerides. Besides a summary concerning general metabolism of THs, as well as their genomic and non-genomic effects, herein we will discuss resistance to THs and the possible mechanisms of action of 3,5-T2, also in relation to its possible clinical use as a drug.
Proteomic approaches for the study of tissue specific effects of 3,5,3'-triiodo-L-thyronine and 3,5-Diiodo-L-thyronine in conditions of altered energy metabolism
Front Physiol 2014 Dec 17;5:491.PMID:25566089DOI:10.3389/fphys.2014.00491.
In vertebrates and, specifically, in mammals, energy homeostasis is achieved by the integration of metabolic and neuroendocrine signals linked to one another in an intricate network hierarchically responding to the tight modulating action of hormones among which thyroid hormones (THs) play a central role. At the cellular level, 3,5,3'-triiodo-L-thyronine (T3) acts mainly by binding to specific nuclear receptors (TRs) but actually it is becoming more and more evident that some T3- actions are independent of TRs and that other iodothyronines, such as 3,5-Diiodo-L-thyronine (T2), affect energy metabolism and adiposity. In the postgenomic era, clinical and basic biological researches are increasingly benefiting from the recently developed new omics approaches including, among the others, proteomics. Considering the recognized value of proteins as excellent targets in physiology, the functional and simultaneous analysis of the expression level and the cellular localization of multiple proteins can actually be considered fundamental in the understanding of complex mechanisms such as those involved in thyroid control of metabolism. Here, we will discuss new leads (i.e., target proteins and metabolic pathways) emerging in applying proteomics to the actions of T3 and T2 in conditions of altered energy metabolism in animal tissues having a central role in the control of energy balance.
3,5-Diiodo-L-thyronine Exerts Metabolically Favorable Effects on Visceral Adipose Tissue of Rats Receiving a High-Fat Diet
Nutrients 2019 Jan 27;11(2):278.PMID:30691227DOI:10.3390/nu11020278.
When administered to rats receiving a high-fat diet (HFD), 3,5-Diiodo-L-thyronine (3,5-T2) [at a dose of 25 μg/100 g body weight (BW)] is known to increase energy expenditure and to prevent HFD-induced adiposity. Here, we investigated which cellular and molecular processes in visceral white adipose tissue (VAT) contributed to the beneficial effect of 3,5-T2 over time (between 1 day and 4 weeks following administration). 3,5-T2 programmed the adipocyte for lipolysis by rapidly inducing hormone sensitive lipase (HSL) phosphorylation at the protein kinase A-responsive site Ser563, accompanied with glycerol release at the 1-week time-point, contributing to the partial normalization of adipocyte volume with respect to control (N) animals. After two weeks, when the adipocyte volumes of HFD-3,5-T2 rats were completely normalized to those of the controls (N), 3,5-T2 consistently induced HSL phosphorylation at Ser563, indicative of a combined effect of 3,5-T2-induced adipose lipolysis and increasing non-adipose oxidative metabolism. VAT proteome analysis after 4 weeks of treatment revealed that 3,5-T2 significantly altered the proteomic profile of HFD rats and produced a marked pro-angiogenic action. This was associated with a reduced representation of proteins involved in lipid storage or related to response to oxidative stress, and a normalization of the levels of those involved in lipogenesis-associated mitochondrial function. In conclusion, the prevention of VAT mass-gain by 3,5-T2 occurred through different molecular pathways that, together with the previously reported stimulation of resting metabolism and liver fatty acid oxidation, are associated with an anti adipogenic/lipogenic potential and positively impact on tissue health.
3,5-Diiodo-L-thyronine increases de novo lipogenesis in liver from hypothyroid rats by SREBP-1 and ChREBP-mediated transcriptional mechanisms
IUBMB Life 2019 Jul;71(7):863-872.PMID:30707786DOI:10.1002/iub.2014.
Hepatic de novo lipogenesis (DNL), the process by which carbohydrates are converted into lipids, is strictly controlled by nutritional and hormonal status. 3,5-Diiodo-L-thyronine (T2), a product of the 3,5,3'-triiodo-L-thyronine (T3) peripheral metabolism, has been shown to mimic some T3 effects on lipid metabolism by a short-term mechanism independent of protein synthesis. Here, we report that T2, administered for 1 week to hypothyroid rats, increases total fatty acid synthesis from acetate in isolated hepatocytes. Studies carried out on liver subcellular fractions demonstrated that T2 not only increases the activity and the expression of acetyl-CoA carboxylase and fatty acid synthase but also of other proteins linked to DNL such as the mitochondrial citrate carrier and the cytosolic ATP citrate lyase. Parallelly, T2 stimulates the activities of enzymes supplying cytosolic NADPH needed for the reductive steps of DNL. With respect to both euthyroid and hypothyroid rats, T2 administration decreases the hepatic mRNA level of SREBP-1, a transcription factor which represents a master regulator of DNL. However, when compared to hypothyroid rats T2 significantly increases, without bringing to the euthyroid value, the content of both mature (nSREBP-1), and precursor (pSREBP-1) forms of the SREBP-1 protein as well as their ratio. Moreover, T2 administration strongly augmented the nuclear content of ChREBP, another crucial transcription factor involved in the regulation of lipogenic genes. Based on these results, we can conclude that in the liver of hypothyroid rats the transcriptional activation by T2 of DNL genes could depend, at least in part, on SREBP-1- and ChREBP-dependent mechanisms. © 2019 IUBMB Life, 2019.