Cortodoxone - CAS 152-58-9
Catalog number: 152-58-9
Category: Inhibitor
Please be kindly noted products are not for therapeutic use. We do not sell to patients.
Molecular Formula:
C21H30O4
Molecular Weight:
346.46
COA:
Inquire
Targets:
Glucocorticoid Receptor
Description:
Cortodoxone, a glucocorticoid receptor antagonist, is an intermediate which can be oxygenated to cortisol.
Purity:
>98.0%(LC)
Appearance:
Crystalline solid
Synonyms:
(8R,9S,10R,13S,14S,17R)-17-hydroxy-17-(2-hydroxyacetyl)-10,13-dimethyl-2,6,7,8,9,11,12,14,15,16-decahydro-1H-cyclopenta[a]phenanthren-3-one 11 Deoxycortisol 11 Desoxycortisol 11 Desoxycortisone 11-Deoxycortisol 11-Desoxycortisol 11-Desoxycortisone Cortexo
Solubility:
Soluble in DMSO
Storage:
Store in a cool and dry place and at 0 - 4℃ for short term (days to weeks) or -53℃ for long term (months to years).
MSDS:
Inquire
Application:
Glucocorticoid receptor binding
Shelf Life:
2 years
Quantity:
Grams-Kilos
Boiling Point:
524.5±50.0 °C | Condition: Press: 760 Torr
Melting Point:
215 °C
Density:
1.22 g/cm3
InChIKey:
WHBHBVVOGNECLV-OBQKJFGGSA-N
InChI:
1S/C21H30O4/c1-19-8-5-14(23)11-13(19)3-4-15-16(19)6-9-20(2)17(15)7-10-21(20,25)18(24)12-22/h11,15-17,22,25H,3-10,12H2,1-2H3/t15-,16+,17+,19+,20+,21+/m1/s1
Canonical SMILES:
CC12CCC(=O)C=C1CCC3C2CCC4(C3CCC4(C(=O)CO)O)C
1.Dexamethasone does not exert direct intracellular feedback on steroidogenesis in human adrenal NCI-H295A cells.
Dardis A;Miller WL J Endocrinol. 2003 Oct;179(1):131-42.
Experimental therapy of fetuses affected with congenital adrenal hyperplasia (CAH) has been reported by administering dexamethasone (Dex) to pregnant women at risk for carrying a CAH fetus. Such prenatal therapy can almost wholly eliminate virilization of the external genitalia of affected female fetuses, but only when treatment is started before 9 weeks of gestation. As it is not known whether the hypothalamic-pituitary-adrenal axis is functional at this time, and as the minimal effective doses of Dex are substantially supraphysiologic for the fetus, the mechanism of action of prenatal Dex treatment has been unclear. To assess the possibility that Dex might act directly on the adrenal, we used human adrenocortical NCI-H295A cells, an established model of the human fetal adrenal. Short term (6 h) incubation of these cells with Dex decreased synthesis of 11-deoxycortisol and 17alpha-hydroxyprogesterone and increased synthesis of deoxycorticosterone (DOC), but only at very high concentrations of Dex (> or =10 microM) that affect P450c17 (17alpha-hydroxylase/17,20 lyase) as a competitive inhibitor; no effects were seen at lower concentrations corresponding to those used in prenatal treatment.
2.[Circadian rhythm of cortisol levels and its precursors in different phases of the menstrual cycle in baboons].
Gorlushkin VM;Katsiia GV;Goncharov NP Probl Endokrinol (Mosk). 1981 May-Jun;27(3):67-72.
Radioimmunoassays were used to study in experiments on sacred baboons the circadian rhythms of dehydrocortisone, 11-deoxycortisol, progesterone, pregnenolone and 17-hydroxypregnenolone in the folliculin and luteal phases of the menstrual cycle. The circadian rhythms of dehydrocortisone and 11-deoxycortisol secretion were seen in both phases of the cycle. The maximum content of the plasma steroids were recorded in the morning while the minimum one in the evening and at night. The circadian rhythm of the progesterone level in the folliculin phase correlated with the time course of changes in dehydrocortisone concentration. In the luteal phase, the maximum hormonal levels were seen in the evening and at night. The circadian rhythms of pregnenolone and 17-hydroxypregnenolone secretion were not pronounced in the folliculin phase. However, in the second half of the cycle, the amplitude of circadian rhythms increased, correlating with the dehydrocortisone level rhythm. The daily average concentration of the adrenal steroids tended to decrease in the luteal phase of the baboon menstrual cycle.
3.Aldosterone synthase gene variation and adrenocortical response to sodium status, angiotensin II and ACTH in normal male subjects.
Kennon B;Ingram MC;Friel EC;Anderson NH;MacKenzie SM;Davies E;Shakerdi L;Wallace AM;Fraser R;Connell JM Clin Endocrinol (Oxf). 2004 Aug;61(2):174-81.
OBJECTIVE: ;Aldosterone synthase, a key enzyme in the terminal steps of aldosterone synthesis, is encoded by the CYP11B2 gene. A polymorphism in the 5' coding region of this gene (-344 C/T) is associated with hypertension, particularly with elevation of the aldosterone to renin ratio. A second polymorphism (a conversion in intron 2 to resemble that of the neighbouring 11beta-hydroxylase (CYP11B1) gene) is found in close linkage dysequilibrium with the variant at -344 C/T. The mechanism by which these variants predispose to cardiovascular disease and the precise intermediate phenotype associated with them remains speculative.;DESIGN: ;We performed a focused physiological study in normal volunteers stratified by CYP11B2 genotype.;PATIENTS: ;Twenty-three subjects homozygous for the T allele and 21 homozygous for the C allele of the -344 C/T polymorphism of CYP11B2 were studied.;MEASUREMENTS: ;Basal and angiotensin II stimulated plasma and 24-h urinary steroid excretion during low (60 mmol/day) and high (160 mmol/day) sodium intake and plasma steroids after ACTH stimulation were measured.;RESULTS: ;No influence of polymorphic variation on basal or stimulated plasma cortisol or aldosterone or other plasma steroid concentrations during either dietary phase was seen.
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CAS 152-58-9 Cortodoxone

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