Allotetrahydrocortisol
(Synonyms: 异体-3Α-四氢皮质醇,5a-Tetrahydrocortisol) 目录号 : GC38734
Allotetrahydrocortisol (5a-Tetrahydrocortisol) 是一种皮质醇的代谢产物。Cortisol 是皮质醇是人体主要的糖皮质激素，在肾上腺皮质产生，在许多生理过程中起着至关重要的作用。
Cas No.:302-91-0
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
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- Purity: >98.00%
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- Datasheet
Allotetrahydrocortisol (5a-Tetrahydrocortisol) is a metabolite of Cortisol. Cortisol is the main glucocorticoid in human. It is produced in adrenal cortex and plays a crucial role in many physiological processes[1][2].
Allotetrahydrocortisol (5a-Tetrahydrocortisol) is a natural C21 steroid of animal origin, and has the axial configuration of its 3-hydroxyl group[1].
[1]. BUSH IE, et al. The excretion of allo tetrahydrocortisol in human urine. Biochem J. 1957 Dec;67(4):689-700. [2]. Kosicka K, et al. Detailed analysis of cortisol, cortisone and their tetrahydro- and allo-tetrahydrometabolites in human urine by LC-MS/MS. J Pharm Biomed Anal. 2017 Jun 5;140:174-181.
| Cas No. | 302-91-0 | SDF | |
| 别名 | 异体-3Α-四氢皮质醇,5a-Tetrahydrocortisol | ||
| Canonical SMILES | C[C@@]12[C@](C(CO)=O)(O)CC[C@@]1([H])[C@]3([H])CC[C@@]4([H])C[C@H](O)CC[C@]4(C)[C@@]3([H])[C@@H](O)C2 | ||
| 分子式 | C21H34O5 | 分子量 | 366.49 |
| 溶解度 | Soluble in DMSO | 储存条件 | Store at -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。 |
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| 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 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 2.7286 mL | 13.6429 mL | 27.2859 mL |
| 5 mM | 0.5457 mL | 2.7286 mL | 5.4572 mL |
| 10 mM | 0.2729 mL | 1.3643 mL | 2.7286 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。
Simultaneous determination of tetrahydrocortisol, Allotetrahydrocortisol and tetrahydrocortisone in human urine by liquid chromatography-electrospray ionization tandem mass spectrometry
Steroids 2008 Aug;73(7):727-37.PMID:18394666DOI:10.1016/j.steroids.2008.02.009.
Simultaneous quantification method of three major metabolites of cortisone and cortisol, tetrahydrocortisol, Allotetrahydrocortisol and tetrahydrocortisone by liquid chromatography-electrospray ionization tandem mass spectrometry (LC-ESI-MS/MS) was investigated in a positive mode using a recently developed picolinyl derivatization. Conversion of each steroid into the corresponding picolinyl derivatives (1b, 2b or 3b) was performed by mixed anhydride method using picolinic acids and 2-methyl-6-nitrobenzoic anhydride. Derivatization proceeded smoothly to afford the corresponding 3, 21-dipicolinyl derivatives. Positive ion-ESI mass spectra of the picolinyl derivatives were dominated by an appearance of [M+H](+) as base peaks in all cases. The picolinyl derivatives provided 15 to 80-fold higher ESI response in the LC-ESI-MS/MS (selected reaction monitoring: SRM) when compared to those of underivatized molecules in a positive LC-ESI mode. The use of the picolinyl ester, solid-phase extraction, and deuterium labeled internal standards enabled the concentrations of these metabolites in human urine to be determined simultaneously by LC-ESI-MS/MS (SRM) with a small sample volume of less than 1microl urine.
Chemical conversion of corticosteroids to 3 alpha,5 alpha-tetrahydro derivatives. Synthesis of Allotetrahydrocortisol glucuronides and allotetrahydrocortisone glucuronides
Chem Pharm Bull (Tokyo) 1990 Jul;38(7):1949-52.PMID:2268895DOI:10.1248/cpb.38.1949.
The synthesis of the 3- and 21-glucuronides of Allotetrahydrocortisol (allo-THF) and allotetrahydrocortisone (allo-THE) is described. 5 alpha-Dihydrocortisol (5) was prepared by selective hydrogenation of 21-acetoxy-3, 11 beta, 17 alpha-trihydroxy-3,5-pregnadien-20-one 3-ethyl ether (3), followed by acid hydrolysis and saponification. When 5 alpha-dihydrocortisol 21-tetrahydropyranyl ether (6) was treated with potassium tri-sec-butylborohydride in tetrahydrofuran under mild conditions, regioselective and stereoselective reduction at C-3 took place to give allo-THF 21-tetrahydropyranyl either (7). This compound was converted into the 3- and 21-monoacetates of allo-THF and allo-THE, key intermediates. Introduction of the glucuronyl residue at C-3 or C-21 was carried out by means of the Koenigs-Knorr reaction. Prior to saponification yielding the 3-glucuronides (20,23), the alkali-sensitive ketol side chain at C-17 was protected as 20-semicarbazones.
Cortisol metabolism in cirrhosis
J Clin Invest 1967 Nov;46(11):1735-43.PMID:6061746DOI:10.1172/JCI105664.
The production and peripheral metabolism of cortisol have been studied in 10 cirrhotics and 11 controls after i.v. tracers of cortisol-(14)C. The findings were as follows: (a) Total urinary excretion of radioactivity was normal (81% of the dose) but a decreased fraction was present as glucosiduronates: 18-47% of the dose (average 34%) compared to a normal average of 54%. (b) There was a distinctively abnormal pattern of cortisol metabolites, not previously observed in other illnesses: tetrahydrocortisone was decreased to 14% of the enzyme hydrolysate (normal 26%); cortolones were increased to 34% (normal 19%), owing entirely to an increase in cortolone (20alpha) formation, since beta-cortolone (20beta) was not significantly increased; Reichstein's substances U and epi-U were increased, averaging 2.6% for the former and 4.7% for the latter; tetrahydrocortisol, Allotetrahydrocortisol and cortols were normal. This pattern was independent of the degree of decreased glucosiduronate formation and also independent of the presence or absence of a portacaval shunt. (c) Cortisol production, determined by isotope dilution, was normal in each of six cirrhotic patients. From these data, taken in conjunction with our previously reported findings concerning the influence of norethandrolone on cortisol metabolism, the following conclusions were drawn: (a) Cirrhotic patients have decreased A-ring reduction of cortisone to tetrahydrocortisone and correspondingly increased 20-ketone reduction of cortisone to Reichstein's substances U and epi-U and then to the cortolones. (b) Intrahepatic cholestasis, a regular pathophysiological feature of cirrhosis, may be responsible for the observed abnormal cortisol metabolite pattern in this disease. (c) The slowed metabolic turnover rate of cortisol in cirrhosis may be due to decreased transport and/or binding of cortisol to its intracellular metabolic sites rather than to abnormalities of any specific metabolizing enzymes.
Urinary steroid excretion rates in acromegaly
Horm Res 2005;63(5):234-7.PMID:15900108DOI:10.1159/000085840.
Using gas chromatography/mass spectrometry, urinary excretion rates of cortisol, cortisone and of various steroid metabolites were determined in 35 acromegalic patients (18 men, 17 women) and in 45 age- and weight-matched controls. The ratio of excreted cortisol/cortisone was similar in acromegalics (0.75 +/- 0.20) and in controls (0.75 +/- 0.24). Hence, the preponderance of the main cortisone-derived metabolite, tetrahydrocortisone, over the main metabolites of cortisol (tetrahydrocortisol and Allotetrahydrocortisol; p < 0.01), which was seen both in female and in male acromegalics and which was directly correlated with the postglucose concentrations of growth hormone (r = 0.508, p < 0.01), suggests a decreased activity of 11beta-hydroxysteroid dehydrogenase type 1 in acromegaly. Furthermore, the preponderance of etiocholanolone over androsterone (p < 0.01) in men (though not in women) with acromegaly--the ratio androsterone/etiocholanolone being negatively correlated with the serum concentrations of insulin-like growth factor type 1 (r = -0.406, p < 0.05)--suggests a relatively reduced activity of hepatic 5alpha-reductase in male acromegalics.
Effect of Vasopressin on the Hypothalamic-Pituitary-Adrenal Axis in ADPKD Patients during V2 Receptor Antagonism
Am J Nephrol 2020;51(11):861-870.PMID:33147589DOI:10.1159/000511000.
Background: Patients with autosomal dominant polycystic kidney disease (ADPKD) are treated with a vasopressin V2 receptor antagonist (V2RA) to slow disease progression. This drug increases vasopressin considerably in these patients with already elevated baseline levels. Vasopressin is known to stimulate the hypothalamic-pituitary-adrenal (HPA) axis through V1 and V3 receptor activation. It is unknown whether this increase in vasopressin during V2RA treatment affects glucocorticoid production. Methods: Twenty-seven ADPKD patients were studied on and off treatment with a V2RA and compared to age- and sex-matched healthy controls and IgA nephropathy patients, the latter also matched for kidney function. Vasopressin was measured by its surrogate copeptin. Twenty-four-hour urinary excretions of cortisol, cortisone, tetrahydrocortisone, tetrahydrocortisol, Allotetrahydrocortisol, and the total glucocorticoid pool were measured. Results: At baseline, ADPKD patients demonstrated a higher copeptin concentration in comparison with healthy controls, while urinary excretion of cortisol and cortisone was lower (medians of 0.23 vs. 0.34 μmol/24 h, p = 0.007, and 0.29 vs. 0.53 μmol/24 h, p < 0.001, respectively). There were no differences in cortisol and cortisone excretion compared to IgA nephropathy patients. Cortisol, cortisone, and total glucocorticoid excretions correlated with kidney function (R = 0.37, 0.58, and 0.19, respectively; all p < 0.05). Despite that V2RA treatment resulted in a 3-fold increase in copeptin, only cortisone excretion increased (median of 0.44 vs. baseline 0.29 μmol/24 h, p < 0.001), whereas no changes in cortisol or total glucocorticoid excretion were observed. Conclusions: Increased concentration of vasopressin in ADPKD patients at baseline and during V2RA treatment does not result in activation of the HPA axis. The impaired glucocorticoid production in these patients is related to their degree of kidney function impairment.